How many times can you get COVID? What experts know about reinfection

Authors:  Hannah Sparks May 18, 2022  The New York Post

The new normal is now.

In what seemed like an instant, COVID-19 became an inevitable aspect of everyday life more than two years ago — with no signs to suggest that we’ll ever see otherwise again.

As we look at our lives ahead with waves of new variants and “stealth” sub-variants, and seasonal vaccine boosters to match, it begs the question: Should we fear reinfection?

Doctors have recently confirmed that those infected with an earlier Omicron variant, which first appeared and spread rapidly last summer, can indeed test positive again for the new sub-variant.

Last week, as the latest strain — BA.2 or BA2.12.1 — made its presence known in New York City and clusters throughout the Northeast and Midwest, the US crossed a grim milestone: 1,000,000 COVID deaths. Globally, we’ve lost more than 6,000,000.

The Post spoke to NYU Langone Health infectious diseases expert Dr. Michael Phillips about what we can expect from life with COVID as we know it.

Can you get infected with COVID twice — and who’s at risk?

There is no such thing as perfect immunity from COVID. Regardless of severity or immunization, someone who tests positive for the virus can become infected again at some point.

“Our hospitalizations have crept up over the past several weeks, particularly with this newer variant of Omicron,” Dr. Phillips told The Post. “But thankfully, the vast majority of people [who] get the infection tend to recover without too much problems.”

But there’s more at stake for some. People who have not received two doses of the mRNA vaccine, as well as those with weakened immune systems due to age, medications, preexisting illness or other clinical factors, such as poor physical fitness, are at a higher risk of reinfection and becoming severely sick with COVID-19.

But Phillips warns against us “develop[ing] a laissez faire attitude about it.” While some relatively young, healthy and vaccinated individuals may become reinfected with only a mild case, the person they pass it to — potentially, someone with a weakened immune system due to age, medications, preexisting illness or other clinical factors, such as poor physical fitness — may not fare so well.

Omicron is “very, very different from prior waves of Delta,” Phillips added. “I think it shifted our game plan for sure.” Now more than ever the focus of prevention efforts is on protecting those the ones at a greater risk of severe illness — and protecting yourself from COVID reinfection means also “protect[ing] the vulnerable.”

Can you be reinfected with the same COVID variant?

It’s certainly possible, particularly in those who are not vaccinated. Unlike earlier variants, Omicron has rapidly evolved into several sub-types, prompting simultaneous localized outbreaks. Meanwhile, there’s no telling how many positive cases of COVID-19 go unreported, whether due to lack of testing or symptoms to warrant alarm. So whether to fear reinfection with the same niche strain may not be a pragmatic question to ask — because, by the time it’s answered, a new strain may already be here.

“There are so many of these other variants within that big family of coronaviruses, and we’re typically infected with three to four a year,” Phillips explained, most of which present as a mild cold.

Ideally, SARS-CoV-2 could fade into coronavirus obscurity like many of the others — but we aren’t there yet, and it’s too soon to say whether that’s a feasible outlook. “It’s still severe enough that that we have to be pretty mindful about,” said Phillips. “We just don’t know enough about future variants for us to take our guard down yet.”

How long after getting COVID can you be reinfected?

This is another complicated question — especially for sufferers of long COVID, who appear to harbor low, even undetectable levels of the virus for weeks and months. For mild to moderate cases, people who test positive for COVID can expect their infection to clear within five to 10 days after their symptoms arose, or since their confirmed test result.

Nascent research suggests that the average immune system can fend off COVID reinfection for three to five months after the previous bout. That’s why, according to the Centers for Disease Control and Prevention, people who had a confirmed infection within the previous 90 days are not expected to quarantine after coming in contact with another infected individual.

But all bets are off about six months later, when antibodies are known to start waning — regardless of vaccination.

How long do COVID antibodies last?

Experts don’t know exactly. While those survive COVID appear to be largely protected from repeat or severe illness for up to five months after the previous infection, there isn’t enough data available yet to be certain how long those COVID-specific antibodies linger, or even to confirm that the presence of antibodies guarantees immunity, according to the Food and Drug Administration.

Immune system B cells give rise to COVID-specific antibodies, designed to attack the virus on sight, before it can penetrate tissue cells and reproduce. They begin to form within the first few days infection or vaccination, and continue to build for several weeks until they peak at around three months thereafter — when your COVID defenses are at their strongest.

The good news is that waning antibodies doesn’t mean we’re totally defenseless, as some B cells will remember the tools it previously took to create COVID antibodies during re-invasion. (Boosters, furthermore, helps our immune system remember how. to fight.) Meanwhile, our killer T-cells, the immune system’s backup line of defense, may not so good at preventing the virus from entering the body, but they can spot an infected host cell — and destroy before it multiplies to another cell. And while they’re more difficult to track, they do appear to be more faithful than fleeting antibodies.

“Those appear to stay be much more robust,” said Phillips, adding, that “the T cell response is probably more important for response to viral infections” in the long run.

Are COVID vaccines still effective?

“We don’t have to be paranoid about the emergence of a new strain … but we have to be thoughtful and ready for that.”

Dr. Michael Phillips, MD, NYU Langone Health

More or less. Vaccines remain the best way to build-up antibodies, the body’s primary line of defense against severe COVID-19 illness. While allowing oneself to become infected can also give rise to antibodies, it’s not worth the risk.

“I’m strongly pro vaccine, because of the the problems that happen when you don’t get it,” said Phillips, who hinted at alternative forms of vaccination technology on the horizon as well.

Regardless of type, antibodies are known to wane afer about six months since last infection or booster, making reinfection more likely to occur.

How often can you get a COVID booster?

For those on the two-dose regimen, a second round should be completed about six weeks after the first. However, it’s been well over a year since the vaccine was introduced, which means many patients completed those two rounds back in 2021.

Doctors expect that annually, even seasonally redesigned boosters against COVID-19 could become the norm — kind of like influenza, only different, and more troubling: One flu season sees just one or two major strains globally, allowing researchers time to prepare vaccines. “It’s not this, sort of, constant changing during a ‘season’,” said Phillips, like COVID-19 has done.

Currently, only those who have a weakened immune system and people age 50 or older are being recommended for a third shot by the CDC — which is, altogether, a good sign.

Said Phillips, “We don’t have to be paranoid about the emergence of a new strain … but we have to be thoughtful and ready for that.”

Clinical update on risks and efficacy of anti-SARS-CoV-2 vaccines in patients with autoimmune hepatitis and summary of reports on post-vaccination liver injury

Authors: Ana Lleo 1Nora Cazzagon 2Cristina Rigamonti 3Giuseppe Cabibbo 4Quirino Lai 5Luigi Muratori 6Marco Carbone 7Italian Association for the Study of the LiverAffiliations expand PMID: 35410851 PMCID: PMC8958090DOI: 10.1016/j.dld.2022.03.014 Published:March 27, 2022DOI:


Patients with liver diseases, especially those with cirrhosis, have an increased mortality risk when infected by SARS-CoV-2 and therefore anti-SARS-CoV-2 vaccine has been recommended by leading Scientific Associations for all patients with chronic liver diseases. However, previous reports have shown a reduced antibody response following the full course of vaccination in immunosuppressed patients, including liver transplant recipients and several rheumatic diseases.This document, drafted by an expert panel of hepatologists appointed by the Italian Association for the Study of the Liver (AISF), aims to present the updated scientific data on the safety and efficacy of anti-SARS-CoV-2 mRNA vaccines in patients with autoimmune hepatitis (AIH). Furthermore, given the recent reports of sporadic cases of AIH-like cases following anti-SARS-CoV-2 mRNA vaccines, we summarize available data. Finally, we provide experts recommendations based on the limited data available.

1. 2022 AISF recommendation on anti-SARS-CoV-2 vaccines for patients with known autoimmune hepatitis

Patients with chronic liver diseases (CLD), especially those with cirrhosis, have an increased mortality risk when infected by SARS-CoV-2 [[1]]. One of the largest international studies currently available, showed an observed mortality of 32% in patients with cirrhosis compared to 8% in those without [[2]]. Therefore, the European Association for the Study of the Liver (EASL) has recommended vaccination against SARS-CoV-2 for all patients with CLD [[3]]. Although contrasting data have been published, patients with AIH with or without cirrhosis under immunosuppressive therapy represent an at-risk category of developing severe COVID-19 when infected [[4],[5]]. Therefore, based on the data available, the benefit of anti-SARS-CoV-2 vaccination outweighs the potential risk for disease exacerbation in AIH.Although the registration trials of mRNA vaccines enrolled patients with CLD (217 patients in Pfizer trial and 196 patients in Moderna trial), subjects under immunosuppressive therapy were excluded. A recent study by Thuluvath and colleagues found that 75% of patients with CLD without cirrhosis and 77% of patients with cirrhosis had adequate antibody response to anti-SARS-CoV2 vaccines [[6]]. The authors included 233 patients with CLD with 61 being affected by immune mediated liver diseases, including AIH, primary biliary cholangitis, and primary sclerosing cholangitis. Also 62 patients were liver transplant (LT) recipients, 79 had cirrhosis, and 92 had CLD without cirrhosis. Antibody levels were undetectable in 11 patients who had LT, 3 with cirrhosis, and 4 without liver cirrhosis. LT and treatment with two or more immunosuppressive drugs were associated with poor antibody responses. However, only 3 patients out of 18 with undetectable antibody were AIH patients on immunosuppression (2 on prednisone plus mycophenolate mofetil (MMF) and 1 on prednisone plus azathioprine).Reports have shown a reduced antibody response following the full course of vaccination in liver transplant recipients [[7]]. It has also been formerly demonstrated that specific drugs (i.e. methotrexate, abatacept, and rituximab) reduced the immune response to influenza or pneumococcal vaccines in a number of different rheumatic diseases [8910]. The efficacy of anti-SARS-CoV-2 vaccination in preventing COVID-19 in patients with AIH on immunosuppressive therapies [[11],[12]], as well as the risk of disease reactivation after anti-SARS-CoV-2 vaccination, have been poorly investigated. Similarly, cellular immunity to SARS-CoV-2 in AIH patients has not been studied.The American College of Rheumatology (ACR) has recently proposed a guidance [[13]] suggesting a short-term withdrawal of methotrexate, JAK inhibitors, abatacept, and MMF, and deferral of rituximab and cyclophosphamide infusion if possible before anti SARS-Cov-2 vaccination, according to rheumatic disease activity. However, there is no solid evidence as to whether it is appropriate or not to suspend or reduce the dose of immunosuppressive drugs immediately before or following the administration of the vaccine in AIH patients. Importantly, this strategy may be potentially associated with an increased risk of AIH reactivation particularly dangerous in patients with cirrhosis. Of interest, high doses of MMF and rituximab remain independent predictors of failure to develop an antibody response after vaccination in rheumatic diseases [[14]]; however, no data are available in AIH. At the present time, the available data do not justify withdraw or reduction of immunosuppression before or immediately after vaccination in patients with AIH.Finally, no clear evidence of reactivation of AIH after anti-SARS-CoV-2 vaccination has been reported in the literature. Interestingly, the presence of significant fibrosis at the liver histology of a small number of newly diagnosed AIH following anti-SARS-CoV-2 vaccination might suggest the possibility of disease reactivation [151617]. However, until new multicenter studies are available there is no current indication for routine testing of transaminases levels in AIH patients after vaccination.

2. 2022 aisf recommendation on autoimmune hepatitis like onset following anti-SARS-CoV-2 vaccination

The COVID-19 pandemics has necessitated the development and registration of several vaccines in record time. The monitoring for safety, side effect and efficacy is ongoing in the post-marketing surveillance. Recent reports inform on the possible occurrence of immune mediated hepatitis or AIH-like disease in predisposed individuals. Autoimmunity is widely accepted to develop in genetically predisposed individuals and some polymorphisms have been identified in AIH [[18]]; unfortunately, they are not yet of clinical use and cannot be of help to identify individuals at risk.Considering that 58% of the world population has received at least one dose of anti-SARS-CoV-2 vaccine, with 9.2 billion doses been administered globally, it is unclear whether this is a pure coincidence rather than a causality.The fact that someone developed immune-mediated acute hepatitis after vaccination does not necessarily mean that this was caused by the vaccine.The European Medicine Agency (EMA)’s Pharmacovigilance Risk Assessment Committee (PRAC) has recently started an assessment following the very small number of cases reported after vaccination with Spikevax and Comirnaty (known as Moderna and Pfizer vaccines, respectively) in the medical literature and EudraVigilance ( Further data and analyses have been requested from the marketing authorization holder to support the ongoing assessment by PRAC. Given the small number of cases currently reported, the issue seems to be rare; however, specific studies should be performed to define the number and severity of cases.At the time these recommendations are drafted, 17 reports have been published in the medical literature that overall include 31 cases of suspected AIH-like triggered by the vaccine (Table 1). Patients were more often women (F:M 21:10), age ranging from 32 to 89 years old (median 58 years). In eleven cases a pre-existent autoimmune condition (i.e., seven Hashimoto thyroiditis, one primary biliary cholangitis, two rheumatoid arthritis, one systemic lupus erythematosus) is reported. Two patients had experienced COVID-19 infection before the vaccine. All except four presented with an acute onset of AIH-like with jaundice. All patients underwent liver biopsy and in six of them fibrosis was already present, which might suggest that they had a previous liver disease, possibly an undiagnosed AIH. All were treated with steroid therapy, and all improved the liver function tests (LFTs), although details on the biochemical response are not thoroughly reported.Table 1Cases of suspected AIH triggered by the vaccine reported in the literature.

ReferenceVaccinePatient’s characteristicsClinical presentation and laboratory dataTherapyOutcome
Age, genderAutoimmune comorbiditiesPrevious COVID-19 infectionOther comorbidities
Avci & Abasiyanik [15]mRNAPfizer/BioNTech,1 month before61, FHashimoto thyroiditisYes, mild, 8 months beforeHypertensionAcute icteric ANA, ASMA, hyper-IgG, fibrosis F2,Prednisolone + azathioprine add-on35 days follow-up, mild transaminases and bilirubin
Bril et al. [16]mRNAPfizer/BioNTech,7 days before35, FNot reportedNoGestational hypertension and cesarian section 3 months beforeAcute icteric, normal IgG, no fibrosisPrednisone 20 mg/day50 days follow-up, transaminases normalization
Cao et al. [17]Inactivated whole-virion SARS-CoV2 (Coronavac)57, FNot reportedNoNot reportedAcute icteric, pruritus IgG slight elevation, ANA+, Fibrosis F2Methylprednisolone, UDCA + azathioprine add-on5 months follow-up, no relapse
Clayton-Chubb et al. [23]ChAdOx1 nCoV-19 vaccine (Oxford-AstraZeneca), 26 days before36, MNoNoHypertension, laser eye surgery 2 weeks beforeAcute, sub-icteric, asymptomatic, ANA+, normal IgG, no fibrosisPrednisolone 60 mg/day24 days, normalization of bilirubin, marked reduction of ALT
Garrido et al. [24]mRNA Moderna, 2 weeks before65, FNoNoPolycythemia vera under PEG-IFNAcute icteric severe, ANA, hyper-IgG, no fibrosisPrednisolone 60 mg/day1 month, improvement of LFTs and IgG normalization
Ghielmetti et al. [25]mRNA-1273, 7 days before63, MNoNo, unknown but anti-cardiolipin+Type 2 diabetes, ischemic heart diseaseAcute icteric, hyper-IgG, ANA+, AMA+ (different from PBC) APCA+, no fibrosisPrednisone 40 mg/day, rapidly tapered14 days follow-up
Goulas et al. [26]mRNA Moderna, 2 weeks before52, FNoNoAcute icteric, ANA+, ASMA+, hyper-IgG, no fibrosis reportedPrednisolone 50 mg/day, azathioprine add-onUnknown
Londono et al. [27]mRNA Moderna, 7 days after the II dose41, FNot reportedNoHormonal therapy for premature ovarian failureAcute icteric, ANA, ASMA, anti-SLA/LC+, hyper-IgG, no fibrosisPrednisone 1 mg/KgNormalization of LFTs
Palla et al. [28]mRNAPfizer/BioNTech 1 month after II dose40, FSarcoidosisTransaminases 3–4 x ULN fluctuation, ANA+, hyper-IgG, active hepatitis, fibrosis with septaPrednisolone 40 mg/dayTransaminases decline after 7 days of prednisolone
Rela et al. [29]ChAdOx1 nCoV-19 vaccine (Oxford-AstraZeneca), 20 days before38, FNo (hypothyroidism?)NoHypothyroidismAcute icteric, ANA+, IgG mildly elevated, multiacinar hepatic necrosis, no fibrosisPrednisolone 30 mg/day and tapering after 4 weeks1 month of follow-up normal LFTs
ChAdOx1 nCoV-19 vaccine (Oxford-AstraZeneca), 16 days before62, M2 episodes of jaundice resolved with native medicationAcute severe AIH, autoantibodies negative, mild fibrosisPrednisolone 30 mg/day + plasma exchange 5 cyclesPersistent cholestasis → death in 21 days for economic constraints regarding liver transplantation
Rocco et al. [30]Pfizer/BioNTech 1 week before (II dose)89, FHashimoto thyroiditisNoPrevious acute glomerulonephritis, pravastatin and low-dose aspirin for primary preventionAcute icteric, ANA+, hyper-IgG, no fibrosisPrednisone 1 mg/Kg/day and tapering3 months of follow-up, progressive improvement
Tan et al. [31]mRNA Moderna, 6 weeks before56, FNot reportedNoRosuvastatinAcute icteric, ANA+, ASMA+, hyper-IgG, also eosinophil, early fibrosisBudesonide1 week of follow-up
Tun et al. [32]mRNA Moderna, 3 days before (I dose) and 2 days before (II dose)47, MNot reportedNoNot reportedAcute icteric, ANA+ hyper-IgG, rapidly resolved and then reappeared 2 days after the II dose, minimal fibrosisPrednisolone 40 mg/day2 weeks of follow-up PT normalized
Vuille-Lessard et al. [33]mRNA Moderna, 3 days before76, FHashimoto thyroiditisYes, 3 months before (mild disease)Prior urothelial carcinomaAcute icteric, hyper-IgG, ANA+, ASMA+, ANCA+, steatosis, active AIH, fibrosis not evaluablePrednisolone 40 mg/day + azathioprine add-on 2 weeks after4 months follow-up: LFTs normalization after 4 weeks, stop azathioprine and 6 weeks after no relapse
Suzuki Y et al. [34]mRNA Pfizer/BioNTech 10 days before (II dose)80, FNot reportedNot reportedGastroesophageal reflux esophagitisAcute icteric, ANA+, hyper-IgGPrednisone at an initial dose of 0.8 mg/kg/day, then tapered to 10 mg/week50 days of follow-up: transaminases normalization
mRNA Pfizer/BioNTech 4 days before (II dose)75, FNot reportedNot reportedDyslipidemiaAcute icteric, ANA+, AMA +, hyper-IgGPrednisone at an initial dose of 1 mg/kg/day, then tapered to 10 mg/week105 days of follow-up: transaminases normalization
mRNA Pfizer/BioNTech 7 days before (I dose)78, FPrimary biliary cholangitisNot reportedNoAcute, ANA+, AMA+, hyper IgGPrednisone at an initial dose of 0.6 mg/kg/day, then tapered to 10 mg/week103 days of follow-up: transaminases normalization
Torrente et al. [35]ChAdOx1 nCoV-19 vaccine (Oxford-AstraZeneca), 3 weeks before49, FHypothyroidism (?), ANA+NoHypothyroidism treated with levothyroxineAcute AIH, ANA+, hyper-IgG, no fibrosisPrednisone 30 mg/day then tapering and azathioprine add-onTransaminases decrease after 2 weeks
Rigamonti C et al. [36]mRNAPfizer/BioNTech, 7 patientsmRNA Moderna, 2 patientsChAdOx1 nCoV-19 vaccine (Oxford-AstraZeneca),3 patientsmedian age 62 years (range 32–80)6 F, 6 M3 thyroiditis,2 rheumatoid arthritis,1 systemic lupus erythematosus10 acute onset,8 jaundice,8 positive autoantibodies (6 ANA, 1 SMA, 1 LKM-1)Prednisone / prednisolone +/- azathioprinemedian follow-up 3 months: 58% complete biochemical response
Efe C et al. [37]mRNAPfizer/BioNTech, 1 patient53, MNoneNot reportedNoneAcute icteric hepatitis, no ANA, hyper-IgG, no fibrosisprednisolone (40 mg/day) and plasma exchangeLiver transplantation

Adverse effects of the vaccine are possible, and abnormal liver function tests following vaccination represent an important clinical issue. AIH is a relatively rare, chronic immune-mediated liver disease, which develops in genetically predisposed individuals following environmental triggers; viral infections and drug exposures have been suggested to trigger the disease, but not definitive evidence is available [[19],[20]]. AIH-like onset after vaccination – other than anti-SARS-CoV-2 – has been also previously reported [[21]]. However, even if it can be speculated that the vaccines can disturb self-tolerance and trigger autoimmune responses through cross-reactivity with host cells, it might be hard to definitively state that AIH is induced by a vaccine. Considering the reported AIH-like cases following SARS-CoV-2 vaccination, timing of occurrence of acute hepatitis from vaccination in some of them is very short (less than 7 days), suggesting that a dysregulation of immune system has already occurred before vaccination in those cases. So far, given the availability of only observational literature without a structured collection of AIH-like cases after anti-SARS-CoV-2 vaccines, no definitive conclusions can be drawn. There is a need for population-based studies to gather data on the incidence, severity, and clinical features of anti-SARS-Cov-2 vaccination-induced AIH under the umbrella of the national and European Scientific Societies.In the meantime, while intensive vaccination against SARS-CoV-2 continues, healthcare providers should include the diagnosis of AIH triggered by vaccines in the differential diagnosis in cases of acute hepatitis of unexplained etiology and manage them as drug-induced AIH or AIH-like liver injury as recommended by current guidelines [[22]].


*These recommendations will be reviewed periodically as further information becomes available.

  • •AIH patients should receive anti-SARS-CoV-2 vaccination consistent with the age restriction of the local approval. In Italy, as recommended by the Italian Ministry of Health for all immunosuppressed patients, mRNA vaccines should be used. Based on the data for the mRNA vaccines available, there is no preference for one vaccine over another.
  • Patients with AIH are suggested to undergo vaccination when the disease activity is controlled by immunosuppressive therapy. To date there are no data available to establish variations on the interval between doses of anti-SARS-Cov2 vaccine.
  • There is no current evidence to recommend suspension or reduction of immunosuppressive drugs in AIH patients before or immediately after anti-SARS-CoV-2 vaccination.
  • The risk of AIH flare or disease worsening following anti-SARS-Cov-2 vaccination has not been assessed to date and specific studies are required before defining a line of recommendation. Based on available data routine testing of transaminases levels in AIH patients after vaccination could be suggested in selected patients although the timing needs to be defined.
  • •Testing of antibody levels for IgM and/or IgG to spike or nucleocapsid proteins to assess immunity to SARS-Cov2 after vaccination in AIH patients is not recommended, nor to assess the need for vaccination in an unvaccinated AIH patients.
  • Patients with new acute onset of liver injury following anti-SARS-Cov-2 vaccine should be managed as suggested by current guidelines and known clinical algorithms, including the indication to liver biopsy. Considering the lack of evidence currently available to exclude drug induced AIH in this setting, immunosuppressive therapy should be carefully considered and used if AIH diagnosis is confirmed; long-term immunosuppressive therapy needs to be assessed on a patient-by-patient basis.
  • Patients with newly diagnosed AIH or AIH flare after anti-SARS-Cov-2 vaccine should be consider for vaccine booster; however, the timing of the booster could be personalised based on the disease activity and ongoing therapy and discussed case-by-case with an expert center in autoimmune liver diseases.
  • Given the limited number of cases compared to the number of vaccinated subjects, extended testing of transaminases level after vaccination in the general population is not sustainable nor suggested.
  • EMA’s PRAC encourages all healthcare professionals and patients to report any cases of autoimmune hepatitis and other adverse events in people after vaccination.

Association of Prior BNT162b2 COVID-19 Vaccination With Symptomatic SARS-CoV-2 Infection in Children and Adolescents During Omicron Predominance

Authors: Katherine E. Fleming-Dutra, MD1Amadea Britton, MD1,2Nong Shang, PhD1et al May 13, 2022 JAMA. Published online May 13, 2022. doi:10.1001/jama.2022.7493

Key Points

Question  Does the estimated effectiveness of 2 doses of the BNT162b2 COVID-19 vaccine against symptomatic SARS-CoV-2 Omicron variant infection (based on the odds ratio for the association of prior vaccination and infection) wane rapidly among children and adolescents, as has been observed for adults?

Findings  In a test-negative, case-control study conducted from December 2021 to February 2022 during Omicron variant predominance that included 121 952 tests from sites across the US, estimated vaccine effectiveness against symptomatic infection for children 5 to 11 years of age was 60.1% 2 to 4 weeks after dose 2 and 28.9% during month 2 after dose 2. Among adolescents 12 to 15 years of age, estimated vaccine effectiveness was 59.5% 2 to 4 weeks after dose 2 and 16.6% during month 2; estimated booster dose effectiveness in adolescents 2 to 6.5 weeks after the booster was 71.1%.

Meaning  Among children and adolescents, estimated vaccine effectiveness for 2 doses of BNT162b2 against symptomatic infection decreased rapidly, and among adolescents increased after a booster dose.Abstract

Importance  Efficacy of 2 doses of the BNT162b2 COVID-19 vaccine (Pfizer-BioNTech) against COVID-19 was high in pediatric trials conducted before the SARS-CoV-2 Omicron variant emerged. Among adults, estimated vaccine effectiveness (VE) of 2 BNT162b2 doses against symptomatic Omicron infection was reduced compared with prior variants, waned rapidly, and increased with a booster.

Objective  To evaluate the association of symptomatic infection with prior vaccination with BNT162b2 to estimate VE among children and adolescents during Omicron variant predominance.

Design, Setting, and Participants  A test-negative, case-control analysis was conducted using data from 6897 pharmacy-based, drive-through SARS-CoV-2 testing sites across the US from a single pharmacy chain in the Increasing Community Access to Testing platform. This analysis included 74 208 tests from children 5 to 11 years of age and 47 744 tests from adolescents 12 to 15 years of age with COVID-19–like illness who underwent SARS-CoV-2 nucleic acid amplification testing from December 26, 2021, to February 21, 2022.

Exposures  Two BNT162b2 doses 2 weeks or more before SARS-CoV-2 testing vs no vaccination for children; 2 or 3 doses 2 weeks or more before testing vs no vaccination for adolescents (who are recommended to receive a booster dose).

Main Outcomes and Measures  Symptomatic infection. The adjusted odds ratio (OR) for the association of prior vaccination and symptomatic SARS-CoV-2 infection was used to estimate VE: VE = (1 − OR) × 100%.

Results  A total of 30 999 test-positive cases and 43 209 test-negative controls were included from children 5 to 11 years of age, as well as 22 273 test-positive cases and 25 471 test-negative controls from adolescents 12 to 15 years of age. The median age among those with included tests was 10 years (IQR, 7-13); 61 189 (50.2%) were female, 75 758 (70.1%) were White, and 29 034 (25.7%) were Hispanic/Latino. At 2 to 4 weeks after dose 2, among children, the adjusted OR was 0.40 (95% CI, 0.35-0.45; estimated VE, 60.1% [95% CI, 54.7%-64.8%]) and among adolescents, the OR was 0.40 (95% CI, 0.29-0.56; estimated VE, 59.5% [95% CI, 44.3%-70.6%]). During month 2 after dose 2, among children, the OR was 0.71 (95% CI, 0.67-0.76; estimated VE, 28.9% [95% CI, 24.5%-33.1%]) and among adolescents, the OR was 0.83 (95% CI, 0.76-0.92; estimated VE, 16.6% [95% CI, 8.1%-24.3%]). Among adolescents, the booster dose OR 2 to 6.5 weeks after the dose was 0.29 (95% CI, 0.24-0.35; estimated VE, 71.1% [95% CI, 65.5%-75.7%]).

Conclusions and Relevance  Among children and adolescents, estimated VE for 2 doses of BNT162b2 against symptomatic infection was modest and decreased rapidly. Among adolescents, the estimated effectiveness increased after a booster dose.Introduction

In December 2021 and January 2022, the spread of the SARS-CoV-2 Omicron variant led to the highest rates of COVID-19 cases among children 5 to 15 years old1 and the highest rate of pediatric hospitalizations (age ≤17 years) with COVID-19 to this point in the pandemic.2,3 Randomized trials of the BNT162b2 mRNA COVID-19 vaccine (Pfizer-BioNTech), the only COVID-19 vaccine authorized for use in children and adolescents 5 to 15 years of age, were conducted before the emergence of the Omicron variant and demonstrated high efficacy of 2 doses against COVID-19 (100% and 91% among those aged 12-15 and 5-11 years, respectively).4,5 The US Food and Drug Administration issued Emergency Use Authorization for BNT162b2 (2 doses of 30 μg) for those aged 12 to 15 years on May 10, 2021,6 and for those aged 5 to 11 years (2 doses of 10 μg) on October 29, 2021.7 Evidence that estimated vaccine effectiveness (VE) waned over time among adults and adolescents8 contributed to a recommendation on January 5, 2022, for a booster (30-μg dose) 5 months or more after the second dose for adolescents 12 to 15 years old.9

Observational studies in adults documented lower protection from mRNA vaccines against the Omicron variant compared with the Delta variant and rapid waning of protection.10,11 However, observational estimates of VE among children 5 to 11 years old and adolescents 12 to 15 years old during Omicron variant predominance are lacking but needed to inform COVID-19 vaccine policy and use of nonpharmaceutical interventions in these age groups. The objectives of this analysis were to use the odds ratio (OR) for the association of prior vaccination and symptomatic infection to estimate BNT162b2 VE during Omicron variant predominance of (1) 2 doses among children 5 to 11 years old and adolescents 12 to 15 years old over time since the second dose and (2) 3 doses among adolescents 12 to 15 years old.Methods

This activity was determined to be public health surveillance as defined in 45 CFR §46.102(l) (US Department of Health and Human Services [HHS], Title 45 Code of Federal Regulations, §46 Protection of Human Subjects); thus, it was not submitted for institutional review board approval and informed consent was not needed.Data Source

Data from the Increasing Community Access to Testing (ICATT) platform were used. ICATT is an HHS program that contracts with 4 commercial pharmacy chains to facilitate drive-through SARS-CoV-2 testing nationally.8,10,12,13 No-cost testing is available to anyone regardless of symptom or exposure status, and sites were selected to address COVID-19 health disparities by increasing access in racially and ethnically diverse communities and areas with moderate to high social vulnerability based on the Social Vulnerability Index (SVI).14 During the analysis period, contracted pharmacy chains used different versions of the registration questionnaire and not all captured data on booster doses. This analysis was, therefore, limited to a single chain, which collected data on booster doses and provided 82% of tests platform-wide for children and adolescents aged 5 to 15 years during the analysis period.

When registering for SARS-CoV-2 testing, individuals or parents/guardians of minors answered a questionnaire (available in English or Spanish) to self-report demographic information (including race and ethnicity selected from fixed categories, shown in the Table), COVID-19–like illness symptoms (fever, cough, shortness of breath, recent loss of sense of smell or taste, muscle pain, fatigue, chill, headache, sore throat, congestion or runny nose, vomiting, or diarrhea; reported to HHS as asymptomatic or symptomatic with ≥1 symptom), and vaccination status.10 Race and ethnicity were collected as part of the HHS COVID-19 laboratory reporting requirements.15 Self-reported COVID-19 vaccination data included number of doses received up to 4, and for each dose, vaccine product and month and year received. For doses reported in the same month or the month before test registration, the registrant was asked whether the most recent dose was administered at least 2 weeks before the test date. Reporting of vaccination status was neither mandatory nor verified. Test registrants were also asked to self-report underlying health conditions, including immunocompromising conditions (defined in the questionnaire as “immunocompromising medications, solid organ or blood stem cell transplant, HIV, or other immunocompromising conditions”), and whether they had previously tested positive for SARS-CoV-2 (within 90 days and/or >90 days before test registration); answers were not verified.

Nasal swabs were self-collected at drive-through sites and tested for SARS-CoV-2 either onsite with the ID Now (Abbott Diagnostics Scarborough Inc) rapid nucleic acid amplification test (NAAT) or at contracted laboratories using laboratory-based NAAT (TaqPath COVID-19 Combo Kit [Thermo Fischer Scientific Inc] or COVID-19 RT-PCR Test [Laboratory Corporation of America]). Deidentified questionnaire data, specimen collection date, test type, test result, and testing site location and census tract SVI14 were reported to HHS with an approximate 3-day lag.Study Design

A test-negative, case-control analysis16 was conducted to estimate BNT162b2 VE against symptomatic infection. This analysis used rapid and laboratory-based NAATs from children and adolescents aged 5 to 15 years reporting 1 or more symptoms tested at the pharmacy chain from December 26, 2021, to February 21, 2022 (data downloaded February 22, 2022). The unit of analysis was tests, because unique identifiers for individuals were not available. Cases were defined as those with positive SARS-CoV-2 NAAT results, and controls were those with negative NAAT results. Tests from children and adolescents meeting any of the following criteria were excluded: indeterminate test results, missing assay type, reported an immunocompromising condition (because COVID-19 vaccine recommendations differ for these individuals),9 unknown vaccination status, vaccine product other than BNT162b2, receipt of 1 vaccine dose or receipt of the second or third dose within 2 weeks of the test date, vaccination before the month of the recommendation by the Advisory Committee on Immunization Practices (for children 5-11 years, November 2021; for adolescents 12-15 years, May 2021 for the primary series and January 2022 for the booster dose),9,17,18 receipt of more than the authorized number of doses for nonimmunocompromised individuals (>2 for children 5-11 years, >3 for adolescents 12-15 years), receipt of a third dose less than 4 months after the second dose (for adolescents 12-15 years),9 or inconsistent vaccination information (eg, reported vaccine receipt but missing dose dates, reported no vaccine receipt but doses reported).Exposure

The exposures of interest were 2 BNT162b2 doses for children 5 to 11 years old and 2 or 3 BNT162b2 doses for adolescents 12 to 15 years old. Cases and controls were considered unvaccinated if tests were from children and adolescents who received no COVID-19 vaccine before the SARS-CoV-2 test. Cases and controls were considered vaccinated with 2 or 3 doses if tests were from children and adolescents who reported receiving the second or third dose 2 weeks or more before their SARS-CoV-2 test.Outcome

The outcome measure was symptomatic SARS-CoV-2 infection determined by positive NAAT result in a person reporting COVID-19–like illness.Statistical Analysis

Associations between symptomatic SARS-CoV-2 infection and BNT162b2 vaccination were estimated by comparing the odds of prior vaccination with 2 or 3 doses (exposed) vs no vaccination (unexposed) in cases vs controls using multivariable logistic regression. The OR was used to estimate VE, where VE = (1 – OR) × 100%. Logistic regression models were adjusted for calendar day of test (continuous variable), race, ethnicity, sex, testing site region, and testing site census tract SVI (continuous variable).14 Tests with missing sex and site census tract SVI were not included in adjusted analyses. Unknown race and ethnicity were coded as categorical levels within each variable to retain those tests in regression models.

Adjusted OR and corresponding VE of 2 doses were estimated by age group (5-11 years and 12-15 years) and month since the second dose. Because only vaccination month and year but not exact calendar dates of each dose were reported, month since the second dose was calculated as the difference between the month and year of testing and the month and year of the second vaccine dose (at least 2 weeks after the second dose). The range of possible days after the second dose for month 0 was 14 to 30 days; month 1, 14 to 60 days; month 2, 30 to 90 days; month 3, 60 to 120 days, and so on (assuming 30 days per month). Because of potential imprecision of month since vaccination based on calendar month of vaccination and testing rather than exact dates, a simulation analysis (of scenarios with rapid vs slow vaccine uptake and varying date of vaccine introduction) and an analysis of previously published data from this platform8 were conducted to compare VE estimates using this approach with those with exact number of days since the second dose (eAppendix in the Supplement).

The maximum difference between calendar month of SARS-CoV-2 test and calendar month of the second dose was 3 months for children 5 to 11 years old (tested during February 2022 and second dose received in November 2021) and 9 months for adolescents 12 to 15 years old (tested during February 2022 and second dose received in May 2021). However, VE was not calculated for the last month since the second dose (month 3 for children and month 9 for adolescents) because the number of possible days since the second dose was limited in the last month. This was a result of both the timing of vaccine authorization (children became eligible for second doses in late November 202118 and adolescents in late May 202117) and by the timing of the end of the study period (test dates were only included through February 21, 2022) (eAppendix in the Supplement). For adolescents 12 to 15 years of age, the maximum possible time after a booster was 6.5 weeks (tested February 21, 2022, and booster dose received after recommendation by the Advisory Committee on Immunization Practices on January 5, 2022).9

To assess the effect of reported prior SARS-CoV-2 infection on estimated 2-dose VE (by age group and month since the second dose), 3 sensitivity analyses were conducted. The first analysis included only tests from individuals without any reported prior SARS-CoV-2–positive test result. The second analysis included only tests from individuals without reported prior SARS-CoV-2–positive test result within 90 days, because a recent prior positive test result could have been due to prolonged NAAT positivity,19 multiple tests within the same illness episode (eg, confirming an at-home test), or reinfection with a different variant in the setting of Omicron variant emergence. The third analysis included only tests from individuals without reported prior SARS-CoV-2–positive test result more than 90 days prior to the test date, because prior SARS-CoV-2 infection provides infection-induced immunity in both vaccinated and unvaccinated individuals.20

The adjusted OR and corresponding VE of 3 doses among adolescents 12 to 15 years old were estimated overall (ie, not by month since the second dose) due to the short timeframe (6.5 weeks) since booster recommendation.

Statistical analyses were performed in R (version 4.1.2; R Foundation) and SAS (version 9.4; SAS Institute Inc). OR and VE estimates were presented with 95% CIs. To compare the waning pattern for estimated VE since the second dose between children and adolescents, an interaction term between age group (5-11 vs 12-15 years) and month after the second dose (for months 0, 1, and 2) was added to the model; a likelihood ratio test comparing the models with and without the interaction term was used to evaluate the interaction. Two-sided P values comparing the magnitude of the association of vaccination and infection between the 2 age groups and across study months were estimated; a P value less than .05 was considered significant. Because of the potential for type I error due to multiple comparisons, findings should be interpreted as exploratory.Results

A total of 121 952 tests from children and adolescents aged 5 to 15 years at 6897 sites across 49 states (all states except North Dakota), Washington, DC, and Puerto Rico, met inclusion criteria (Figure 1), including 53 272 cases (43.7%) and 68 680 controls (56.3%). The median age among individuals with included tests was 10 years (IQR, 7-13); 61 189 (50.2%) were female, 75 758 (70.1%) were White, and 29 034 (25.7%) were Hispanic/Latino. Among 74 208 included tests from children 5 to 11 years old, 58 430 (78.4%) were from unvaccinated children and 15 778 (21.3%) from those vaccinated with 2 doses. Among 47 744 included tests from adolescents 12 to 15 years old, 24 767 (51.9%) were from unvaccinated adolescents, 22 072 (46.2%) from those vaccinated with 2 doses, and 905 (1.9%) from those with booster doses.

Included tests were more frequently rapid NAAT (66.3%) than laboratory-based NAAT (33.7%), and controls were more often tested by rapid NAAT than cases (70.5% vs 60.2% for children; 71.5% vs 60.8% for adolescents) (Table). Cases vs controls were more often tests from persons from the South Atlantic region (27.6% vs 22.3% for children; 27.9% vs 23.7% for adolescents). Report of prior positive SARS-CoV-2 test result within 90 days of the test date was more common among cases than controls (22.0% vs 13.0% for children; 21.1% vs 15.5% for adolescents), while report of a positive test result more than 90 days before the test date was less common among cases than controls (4.9% vs 11.1% for children; 6.5% vs 13.4% for adolescents).

Among children 5 to 11 years old, the adjusted OR for symptomatic infection for tests performed during month 0 after the second dose was 0.40 (95% CI, 0.35-0.45; estimated VE, 60.1% [95% CI, 54.7%-64.8%]) and during month 2 after the second dose was 0.71 (95% CI, 0.67-0.76; estimated VE, 28.9% [95% CI, 24.5%-33.1%]) (Figure 2). For adolescents 12 to 15 years old, the adjusted OR during month 0 after the second dose was 0.40 (95% CI, 0.29-0.56; estimated VE, 59.5% [95% CI, 44.3%-70.6%]), during month 2 after the second dose was 0.83 (95% CI, 0.76-0.92; estimated VE, 16.6% [95% CI, 8.1%-24.3%]), and was no longer significantly different from 0 during month 3 after the second dose (OR, 0.90 [95% CI, 0.82-1.00]; estimated VE, 9.6% [95% CI, −0.1% to 18.3%]). Estimated VE was not significantly different between children and adolescents during months 0 and 1 after the second dose, but estimated VE in children was significantly higher than in adolescents during month 2 (P value for month 0: .99; month 1: .40; month 2: .01; and for months 0-2 combined: .06).

The simulation analysis showed that estimated VE waning curves that used either the exact number of days or calculated months since the second dose were in close agreement in scenarios with rapid and slow vaccine uptake and vaccine introduction on day 1 and day 16 of month 0 (eFigures 1-2 in the Supplement). The analysis of previously published data from this platform showed estimated monthly VE waning curves aligned well with daily VE waning curves (eFigures 3-4 in the Supplement).

Sensitivity analyses limited to those without any prior SARS-CoV-2–positive test result (eFigure 5 in the Supplement), without prior SARS-CoV-2–positive test result within 90 days of test date (eFigure 6 in the Supplement), and without prior SARS-CoV-2–positive test result more than 90 days prior to test date (eFigure 7 in the Supplement) yielded estimated VE at month 0 of 60.4% to 66.4% among children 5 to 11 years old and 58.3% to 64.3% among adolescents 12 to 15 years old. These were similar to the main analysis results that did not take prior infection into account. However, estimated VE in the sensitivity analyses was somewhat more sustained over time relative to the main analysis, particularly for the model limited to tests from individuals without any reported prior infection (estimated VE among children was 39.8% during month 2; among adolescents, estimated VE was significantly different from 0 until month 7) and the model limited to tests from those without infection within 90 days (estimated VE among children was 39.8% at month 2; among adolescents, estimated VE was significantly different from 0 until month 5).

Among adolescents, the adjusted OR for a booster dose 2 to 6.5 weeks after the dose was 0.29 (95% CI, 0.24-0.35; estimated VE, 71.1% [95% CI, 65.5%-75.7%]).Discussion

This analysis estimated BNT162b2 VE among children 5 to 11 years old and adolescents 12 to 15 years old with COVID-19–like illness tested for SARS-CoV-2 using NAAT at drive-through US pharmacy sites from December 26, 2021, to February 21, 2022. It found the estimated VE of the BNT162b2 2-dose primary series against symptomatic infection with the Omicron variant was modest and decreased over time since vaccination in both age groups, similar to the pattern observed in adults during Omicron variant predominance.10 A booster dose was associated with increased protection against symptomatic infection in adolescents.

Previous analyses among adults have shown lower estimated VE against the Omicron variant than against the Delta variant and waning of mRNA vaccine protection against symptomatic infection, regardless of predominant variant.8,10,11 A recent analysis from the same testing platform as this analysis demonstrated the estimated VE of the 2-dose BNT162b2 primary series against symptomatic Omicron infection among adults 18 years or older was 42% at 2 to 4 weeks after the second dose. This decreased to not significantly different from 0 by 3 months after the second dose.10 In this analysis, the estimated VE against symptomatic infection among adolescents 12 to 15 years old also was not significantly different from 0 during month 3 after the second dose. Among children 5 to 11 years old, the duration of protection could only be assessed up through month 2 since the second dose, and continued monitoring will be important.

Among adolescents 12 to 15 years old, the estimated VE against symptomatic infection increased after a booster dose. This finding is consistent with data on adults from this platform and from other studies among adults and adolescents during Omicron variant predominance, which provide evidence of increased protection following mRNA vaccine booster dose.10,21,22 Given the well-established pattern of waning mRNA VE after 2 doses and early evidence of waning of booster dose protection in adults,22 monitoring the duration of protection from booster doses in adolescents will be important. Booster doses may be needed to optimize protection against symptomatic infection with the Omicron variant in children 5 to 11 years old as well.

Children aged 5 to 11 years receive a lower-dose formulation (10 μg) of BNT162b2 than adolescents and adults (30 μg), and limited observational data are available on VE with the 10-μg dose. In this analysis, the similar starting VE among children and adolescents and slower waning seen in children than adolescents suggest the 10-μg dose performed as well or better in children than the 30-μg dose in adolescents. These findings are consistent with the phase 2-3 trial in which immunogenicity of the 10-μg dose among children 5 to 11 years old, as measured by geometric mean titers of neutralizing antibodies 1 month after the second dose, was not significantly different from that generated by 30 μg in persons 16 to 25 years old.4 Furthermore, recent studies indicate estimated 2-dose BNT162b2 VE is similar among children 5 to 11 years old and adolescents 12 to 15 years old against any Omicron infection with or without symptoms (31% and 59%, respectively, with overlapping CIs)23 and against emergency department and urgent care visits due to COVID-19 (51% among children 5-11 years vs 45% among adolescents 12-15 years, with overlapping CIs).21

Prior SARS-CoV-2 infection may influence estimated VE in various ways. Unvaccinated persons with prior infection may have infection-induced immunity, which could bias VE estimates toward the null, whereas vaccinated persons with prior infection may have higher levels of protection than those with vaccination alone.20 Additionally, the proportion of the population with prior infection and how protective prior infection from a previous variant is against currently circulating variants can also influence estimated VE. The sensitivity analysis including only children and adolescents without any reported prior infection showed that waning of estimated VE was less pronounced than in the main analysis, which may provide the clearest picture of protection provided by vaccination. However, prior SARS-CoV-2 infection is increasingly common; the estimated SARS-CoV-2 infection–induced antibody seroprevalence among US children 0 to 17 years old who had blood specimens tested at commercial laboratories (for reasons unrelated to COVID-19) was 45% in December 2021.24 Although history of SARS-CoV-2 infection was self-reported in this analysis and is an imperfect measure, 27% of tests were from persons reporting prior infection. Thus, inclusion of tests from persons with prior infection may more accurately reflect vaccine performance under current conditions in the US.

Although estimated VE against symptomatic infection waned quickly in this analysis, vaccine protection against symptomatic infection is harder to achieve than protection against severe disease. For mRNA vaccines including BNT162b2, estimated VE against severe disease and hospitalization has been higher and waned more slowly than estimated VE against infection among adolescents and adults during Delta predominance25 and Omicron predominance.21,22 While estimated VE against symptomatic infection is an important end point to inform nonpharmaceutical intervention policy decisions and can provide an early warning signal of declining VE, estimated VE against severe disease is needed for children and adolescents during Omicron variant predominance.Limitations

This analysis is subject to several limitations. First, vaccination status was self-reported, which may lead to misclassification. Second, approximately 12% of tests were from people who did not report vaccination status, and 8% had missing symptom data. Exclusion of these tests may have biased results. Third, vaccination dose dates were provided as month and year rather than exact calendar date, which could affect the estimated VE over time through imprecise classification of months since vaccination. A simulation analysis and an analysis of previously published data from this platform8 (eAppendix in the Supplement) suggested that the magnitude and patterns of estimated VE over time would be similar when estimated by day or month since second dose and additionally would be robust to different speeds of vaccine uptake and timing of vaccine authorization.

Fourth, person-level identifiers were not available; therefore, the unit of analysis was tests, not individuals. The analysis was restricted to symptomatic children and adolescents tested within a 2-month timeframe, likely reducing the number of individuals contributing multiple tests. Fifth, these data are from children and adolescents who sought testing at ICATT sites and may not be generalizable to the US population. Nonetheless, these data represent a large sample of children and adolescents 5 to 15 years old tested at 6897 sites nationally. Sixth, primary series vaccine coverage among children 5 to 11 years old and booster coverage among adolescents 12 to 15 years old remained low in the US during the time of this study.26 Children who received the primary series and boosted adolescents may differ in meaningful and unmeasured ways from unvaccinated children and unboosted adolescents.

Seventh, due to the short time (6.5 weeks) since adolescents 12 to 15 years old were recommended for a booster dose, this analysis was unable to estimate booster VE over time in adolescents. Eighth, this analysis includes both rapid and laboratory-based NAAT. While there may be slight variation in the sensitivity of assays performed at different laboratories, NAAT, including rapid NAAT, is the most sensitive method available for detection of SARS-CoV-2 infection.27 Simulations of the effect of test sensitivity on influenza VE estimates using the test-negative design suggest that estimated VE remains relatively stable over a range of test sensitivity from 80% to 100%.28Conclusions

Among children and adolescents, estimated VE for 2 doses of BNT162b2 against symptomatic infection was modest and decreased rapidly. Among adolescents, the estimated effectiveness increased after a booster dose.

References1.Centers for Disease Control and Prevention. COVID data tracker: COVID-19 weekly cases and deaths per 100,000 population by age, race/ethnicity, and sex. Accessed January 20, 2022.

2.Centers for Disease Control and Prevention. COVID data tracker: new admissions of patients with confirmed COVID-19, United States. Accessed January 20, 2022.

3.Marks  KJ, Whitaker  M, Anglin  O,  et al; COVID-NET Surveillance Team.  Hospitalizations of children and adolescents with laboratory-confirmed COVID-19: COVID-NET, 14 states, July 2021-January 2022.   MMWR Morb Mortal Wkly Rep. 2022;71(7):271-278. doi:10.15585/mmwr.mm7107e4PubMedGoogle ScholarCrossref

4.Walter  EB, Talaat  KR, Sabharwal  C,  et al; C4591007 Clinical Trial Group.  Evaluation of the BNT162b2 COVID-19 vaccine in children 5 to 11 years of age.   N Engl J Med. 2022;386(1):35-46. doi:10.1056/NEJMoa2116298PubMedGoogle ScholarCrossref

5.Frenck  RW  Jr, Klein  NP, Kitchin  N,  et al; C4591001 Clinical Trial Group.  Safety, immunogenicity, and efficacy of the BNT162b2 COVID-19 vaccine in adolescents.   N Engl J Med. 2021;385(3):239-250. doi:10.1056/NEJMoa2107456PubMedGoogle ScholarCrossref

6.Food and Drug Administration. Pfizer-BioNTech COVID-19 vaccine EUA letter of authorization. Accessed October 4, 2021.

7.Food and Drug Administration. FDA authorizes Pfizer-BioNTech COVID-19 vaccine for emergency use in children 5 through 11 years of age. Accessed February 25, 2022.

8.Britton  A, Fleming-Dutra  KE, Shang  N,  et al.  Association of COVID-19 vaccination with symptomatic SARS-CoV-2 infection by time since vaccination and Delta variant predominance.   JAMA. 2022;327(11):1032-1041. doi:10.1001/jama.2022.2068
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9.Centers for Disease Control and Prevention. Interim use of COVID-19 vaccines in the United States: interim clinical considerations. Accessed February 11, 2022.

10.Accorsi  EK, Britton  A, Fleming-Dutra  KE,  et al.  Association between 3 doses of mRNA COVID-19 vaccine and symptomatic infection caused by the SARS-CoV-2 Omicron and Delta variants.   JAMA. 2022;327(7):639-651. doi:10.1001/jama.2022.0470
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11.UK Health Security Agency. COVID-19 vaccine surveillance report: week 6, 10 February 2022. Accessed February 13, 2022.

12.Miller  MF, Shi  M, Motsinger-Reif  A, Weinberg  CR, Miller  JD, Nichols  E.  Community-based testing sites for SARS-CoV-2: United States, March 2020-November 2021.   MMWR Morb Mortal Wkly Rep. 2021;70(49):1706-1711. doi:10.15585/mmwr.mm7049a3PubMedGoogle ScholarCrossref

13.Centers for Disease Control and Prevention. Increasing Community Access to Testing (ICATT) for COVID-19. Accessed February 26, 2022.

14.Agency for Toxic Substances and Disease Registry. CDC/ATSDR Social Vulnerability Index. Accessed September 24, 2021.

15.Centers for Disease Control and Prevention. 07/31/2020: Lab advisory: update on COVID-19 laboratory reporting requirements. Accessed January 11, 2022.

16.Chua  H, Feng  S, Lewnard  JA,  et al.  The use of test-negative controls to monitor vaccine effectiveness: a systematic review of methodology.   Epidemiology. 2020;31(1):43-64. doi:10.1097/EDE.0000000000001116PubMedGoogle ScholarCrossref

17.Wallace  M, Woodworth  KR, Gargano  JW,  et al.  The Advisory Committee on Immunization Practices’ interim recommendation for use of Pfizer-BioNTech COVID-19 vaccine in adolescents aged 12-15 years: United States, May 2021.   MMWR Morb Mortal Wkly Rep. 2021;70(20):749-752. doi:10.15585/mmwr.mm7020e1PubMedGoogle ScholarCrossref

18.Woodworth  KR, Moulia  D, Collins  JP,  et al.  The Advisory Committee on Immunization Practices’ interim recommendation for use of Pfizer-BioNTech COVID-19 vaccine in children aged 5-11 years: United States, November 2021.   MMWR Morb Mortal Wkly Rep. 2021;70(45):1579-1583. doi:10.15585/mmwr.mm7045e1PubMedGoogle ScholarCrossref

19.Centers for Disease Control and Prevention. Overview of testing for SARS-CoV-2, the virus that causes COVID-19. Accessed March 10, 2022.

20.Hall  V, Foulkes  S, Insalata  F,  et al; SIREN Study Group.  Protection against SARS-CoV-2 after COVID-19 vaccination and previous infection.   N Engl J Med. 2022;386(13):1207-1220. doi:10.1056/NEJMoa2118691PubMedGoogle ScholarCrossref

21.Klein  NP, Stockwell  MS, Demarco  M,  et al.  Effectiveness of COVID-19 Pfizer-BioNTech BNT162b2 mRNA vaccination in preventing COVID-19-associated emergency department and urgent care encounters and hospitalizations among nonimmunocompromised children and adolescents aged 5-17 years: VISION Network, 10 states, April 2021-January 2022.   MMWR Morb Mortal Wkly Rep. 2022;71(9):352-358. doi:10.15585/mmwr.mm7109e3PubMedGoogle ScholarCrossref

22.Ferdinands  JM, Rao  S, Dixon  BE,  et al.  Waning 2-dose and 3-dose effectiveness of mRNA vaccines against COVID-19-associated emergency department and urgent care encounters and hospitalizations among adults during periods of Delta and Omicron variant predominance: VISION Network, 10 states, August 2021-January 2022.   MMWR Morb Mortal Wkly Rep. 2022;71(7):255-263. doi:10.15585/mmwr.mm7107e2PubMedGoogle ScholarCrossref

23.Fowlkes  AL, Yoon  SK, Lutrick  K,  et al.  Effectiveness of 2-dose BNT162b2 (Pfizer BioNTech) mRNA vaccine in preventing SARS-CoV-2 infection among children aged 5-11 years and adolescents aged 12-15 years: PROTECT cohort, July 2021-February 2022.   MMWR Morb Mortal Wkly Rep. 2022;71(11):422-428. doi:10.15585/mmwr.mm7111e1PubMedGoogle ScholarCrossref

24.Centers for Disease Control and Prevention. COVID data tracker: nationwide COVID-19 infection-induced antibody seroprevalence (commercial laboratories). Accessed March 9, 2022.

25.Tartof  SY, Slezak  JM, Fischer  H,  et al.  Effectiveness of mRNA BNT162b2 COVID-19 vaccine up to 6 months in a large integrated health system in the USA: a retrospective cohort study.   Lancet. 2021;398(10309):1407-1416. doi:10.1016/S0140-6736(21)02183-8PubMedGoogle ScholarCrossref

26.Centers for Disease Control and Prevention. COVID data tracker: trends in demographic characteristics of people receiving COVID-19 vaccinations in the United States. Accessed February 13, 2022.

27.Food and Drug Administration. In vitro diagnostics EUAs: molecular diagnostic tests for SARS-CoV-2. Accessed March 17, 2022.

8.Jackson  ML, Rothman  KJ.  Effects of imperfect test sensitivity and specificity on observational studies of influenza vaccine effectiveness.   Vaccine. 2015;33(11):1313-1316. doi:10.1016/j.vaccine.2015.01.069PubMedGoogle ScholarCrossref

Pfizer Jab In Young People Only 20% Effective After 60 Days, 0% After 5 Months

Authors:  Zachary Stieber May 14, 2022 The Epoch Times

The Pfizer COVID-19 vaccine turned negatively effective after five months, according to a new study

The Pfizer COVID-19 vaccine turned negatively effective after five months, according to a new study.

Researchers with the U.S. Centers for Disease Control and Prevention (CDC) analyzed test results from sites across the United States and determined that the vaccine was 60 percent effective two to four weeks after 12- to 15-year-olds got the second of the two-dose primary regimen.

But the effectiveness, measured against symptomatic illness, quickly plummeted, hitting 20 percent around month two and zero around month five.

After that, recipients in the age group were more likely to be infected by the disease caused by the CCP (Chinese Communist Party) virus, also known as SARS-CoV-2, the virus causes COVID-19.

Vaccine effectiveness “was no longer significantly different from 0 during month 3 after the second dose,” the researchers wrote in the study, which was published by the Journal of the American Medical Association.

Pfizer, its partner BioNTech, and the CDC didn’t respond to requests for comment.

The analyzed tests were performed between Dec. 26, 2021, and Feb. 21, 2022. Some 47,700 tests among 12- to 15-year-olds were included, with about half being unvaccinated. The testing data was on the Increasing Community Access to Testing, a program funded by the U.S. Department of Health and Human Services that contracts with pharmacy chains to perform drive-through testing. The testing data was supplemented by information in questionnaires filled out by adults with the adolescents.

Limitations of the study included vaccination being self-reported.

The study was funded by the U.S. government.

The study also found that vaccine effectiveness against symptomatic infection plunged quickly for those 5 to 11 years old, starting at 60 percent but hitting 23 percent just one month later.

One way to combat the negative effectiveness, researchers said, was to get a booster dose.

Of the 906 12- to 15-year-olds who got a third, or booster, dose, the effectiveness was measured at 71 percent two to six weeks after receipt.

Other studies, though, show that the protection from a booster, like that from the primary regimen, quickly wanes.

“Given the well-established pattern of waning mRNA VE after 2 doses and early evidence of waning of booster dose protection in adults, monitoring the duration of protection from booster doses in adolescents will be important,” researchers said.

Both the Pfizer and Moderna vaccines are built on messenger RNA (mRNA) technology. VE refers to vaccine effectiveness.

In another study published by the same journal on May 13, New York researchers reported the gap of infection and hospitalization risk between unvaccinated and vaccinated youth narrowing over time, with vaccinated 5- to 11-year-olds being infected at a rate of 62 per 100,000 and unvaccinated being infected at a rate of 70 per 100,000.

That was an incidence rate ratio of 1.1; the rate ratio for 12- to 17-year-olds was 2.

The protection also waned considerably against hospitalization over time, researchers found.

They said that the findings support “efforts to increase vaccination coverage in children and adolescents.”

A Case of Hepatotoxicity After Receiving a COVID-19 Vaccine

Authors: Muath M. AlqarniAmmar Z. FaloudahAmjad S. AlsulaihebiHassan K. HalawaniAbdulmajeed S. Khan Published: December 16, 2021  DOI: 10.7759/cureus.20455


The coronavirus disease 2019 (COVID-19) has led to a global health crisis. Its clinical manifestations are well-documented, and severe complications among patients who survived the infection are being continuously reported. Several vaccines with well-established efficacies and excellent safety profiles have also been approved. To date, few side effects of vaccines have been reported. Drug-induced hepatotoxicity is an extremely rare side effect of these vaccines, with few reported instances. In this case report, we describe a patient who experienced hepatotoxicity after receiving the COVID-19 vaccine from Pfizer BioNTech.


The coronavirus disease 2019 (COVID-19) has caused an unprecedented global health crisis. Its most common symptoms include fever, cough, fatigue, and myalgia. Rarely, patients may develop an acute respiratory distress syndrome or multiple organ failure [1]. Other conditions, such as liver injury, may occur. Various factors can lead to liver injury, including severe inflammatory responses, severe hypoxia, drug-induced liver injury (DILI), and worsening of pre-existing metabolic conditions [2]. The manifestations of liver injury vary from elevated serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin to hepatic dysfunction in severe cases [3]. In May 2020, the Pfizer‐BioNTech COVID‐19 vaccine received emergency authorization for use among adolescents aged 12-15 years [4]. Clinical trials have demonstrated that its efficacy in this age group may be as high as 100%. The vaccine’s side effects are typically mild and non-life-threatening, including headache, fatigue, myalgias, and chills [5]. However, there have been reports on extremely rare yet life-threatening side effects, such as anaphylactic shock, deep venous thromboembolism, and pulmonary embolism [1,6].

Case Presentation

A 14-year-old female, not known to have any chronic illnesses, presented to the emergency department with epigastric pain, diarrhea, nausea, and vomiting for the past four days. Three days prior to her current presentation, the patient received the second dose of the Pfizer/BioNTech BNT162b2 mRNA COVID-19 vaccine. The patient denied the use of any pharmaceutical, herbal, or recreational drugs. Upon arrival to the emergency room, the patient had a temperature of 36.9°C, a pulse rate of 128 bpm, a blood pressure of 90/63 mmHg, a respiratory rate of 18 rpm, and oxygen saturation of 97% on room air. On physical examination, the patient was conscious, oriented, and had a Glasgow coma scale (GCS) score of 15/15. In addition, she had mild epigastric tenderness and jaundice. No signs of chronic liver disease were evident.

On the first day of admission, vital signs returned to normal after resuscitation with intravenous fluids. The patient’s urine was dark as observed after urinary catheter insertion. The hematology panel showed Leukopenia, neutropenia, and lymphopenia among others as seen in Table 1. Biochemical and coagulation profile workups are shown in Table 2. Abdominal ultrasound was unremarkable except for a minimal rim of free fluid in the pelvic cavity. Along with conservative treatment, the patient was started on N-acetylcysteine, lactulose, and Vitamin K. In addition, ceftriaxone was given as an empirical antibiotic. On the second day, the results of AST, ALT, and alkaline phosphatase decreased, yet remained abnormally high (Figures 12).

DateWhite blood cellsNeutrophilsLymphocytesPlateletsTotal bilirubinDirect bilirubin
09/08/20211.670.9 (53.9%)0.68 (40.7%)107121.186.1
10/08/20211.220.58 (47.6%)0.56 (45.9%)107117.981.1
11/08/20211.080.37 (34.3%)0.66 (61.1%)101156.694.3
12/08/20211.250.49(39.2%)0.69 (55.2%)101179.6106.8
13/08/20211.090.53(48.6%)0.53 (48.6%)86213.4122.2
14/08/20211.000.52 (52.0%)0.45 (45.0%)87231.6154.0
15/08/20211.380.72 (52.2%)0.60 (43.5%)83291.4187.5
Table 1: Trend of the complete blood counts and bilirubin

Normal ranges: White blood cells: 4-10 x 109/L, Neutrophils: 2-7×103/µL (40%-75%), Lymphocytes: 1-3.5×103/µL (20%-45%), Platelets: 150-400×103/µL, Total bilirubin: 0-21 µmol/L, Direct bilirubin: 0-3.4 µmol/L

DateProthrombin timeAPTTinternational normalized ratioPotassiumSodium  Ammonia  Creatine  
Table 2: Trends of the chemical and coagulation profiles

Abbreviations: APTT: Activated Partial prothrombin time, INR: international normalized ratio

Normal ranges: Prothrombin time: 11-13 seconds, Partial prothrombin time 28-40 seconds, INR: 0.9-1.2, Potassium: 3.5-5.1 mmol/L, Sodium: 136-145 mmol/L, Ammonia: 11-51 µmol/L

Figure 1: AST and ALT trends

Normal ranges: AST – Aspartate transaminase (0-40 U/L), ALT – Alanine transaminase (0-41 U/L)

Figure 2: Alkaline phosphatase and albumin trends

Normal ranges: Albumin: 39.7-49.4 mmol/L, Alkaline phosphate: 35-104 mmol/L

On the fourth day, the patient became agitated and non-responsive, when assessed, her GCS score dropped to 8/15. Consequently, she was transferred to the intensive care unit, where she was intubated. Consultations from gastroenterology, infectious disease, neurology, and hematology departments were requested. Following this, a wide range of infectious, immunological, and toxicological tests were ordered (Tables 3,4). Nevertheless, all the results were unremarkable. To rule out structural brain pathologies, a brain computed tomography without contrast was performed. A suspicious hypodense lesion in the right temporal lobe was identified. However, the findings from the brain magnetic resonance imaging were unremarkable.

Blood culture and sensitivity Negative
Cytomegalovirus immune globulin M (CMV IgM)Negative
Indirect Coombs testNegative
Direct Coombs testNegative
Hepatitis A virus immune globulin M (HAV IgM)Negative
Hepatitis C virus antibodies (enzyme immunoassays) Negative
Hepatitis B surface antigen (HBsAg)Negative
Urine culture and sensitivityNegative
human immunodeficiency virus serology (HIV)Negative
Stool Culture and sensitivityNegative
Chikungunya PCRNegative
Alkhurma virus PCRNegative
Dengue virus PCRNegative
Dengue virus serotypeNegative
Dengue virus IgGNegative
Dengue virus nonstructural protein 1 (NS1)Negative
Dengue virus IgMNegative
Rift valley fever PCRNegative
Anti-Smooth Muscle Antibody (ASMA)Negative
Antinuclear Antibodies (ANA)Negative
Anti-Liver-Kidney Microsomal Antibody (LKM)Negative
Table 3: Immunologic and infectious work-up for liver disease

Abbreviations: Ig: immunoglobulin, PCR: polymerase chain reaction

Name of the tested substanceResult
Salicylic acidNegative
Narcotic alkaloids and its derivativesNegative
Barbituric acidNegative
Tricyclic antidepressants Negative
Organophosphorus pesticidesNegative
Table 4: Urine and blood toxicology panel

The patient’s level of consciousness returned to normal by the seventh day, her liver enzyme levels continued to decline, and her symptoms have resolved. Afterward, she was transferred to a liver transplant center for further investigation and management.


DILI is the most common cause of acute liver injury in developed countries [7]. Its presentation ranges from an incidental elevation of liver enzymes to outright acute liver failure [8]. There are two types of DILI: idiosyncratic and intrinsic. The most common type of which is the intrinsic type that has a short latency period and is dose-dependent. An example of an offending agent in this type is acetaminophen. Contrarily, the idiosyncratic type is less common and has a longer latency. A few examples of idiosyncratic drugs are amoxicillin, nonsteroidal anti-inflammatory drugs, and isoniazid [9]. In our case, we hypothesized the type of DILI to be idiosyncratic, due to the short latency period.

The diagnosis of DILI is made by identifying a relationship between drug exposure and the onset of liver disease. It is important to exclude any infectious, autoimmune, or other forms of liver disease. A thorough medical history and a high clinical suspicion are the basis for a correct diagnosis. A recovery following withdrawal from an offending agent may indicate DILI [10]. A diagnostic criterion that can be utilized in diagnosing DILI is the Rousse Uclaf Causality Assessment Method of the Council of International Organization of Medical Science (RUCAM/CIOMS) [11]. This criterion was applied to our patient’s case, and a total of 6 was calculated, indicating that DILI is probable.

Currently, there is no effective treatment for DILI other than discontinuing the offending drug and providing patients with supportive measures until their condition improves [12]. The exception is acetaminophen intoxication in which an antidote can be used in management, namely N-acetylcysteine. Early transfer of patients with idiosyncratic DILI to tertiary liver centers is important. Liver transplantation increases overall survival from 27.8% to 66.2% [13]. Withholding the transplantation can result in infection, brain damage, organ failure, and even death [14].

There have been three reports of patients having hepatic failure, with one case being acute, after receiving the Pfizer/BioNTech BNT162b2 mRNA vaccine in the United Kingdom between September 12, 2020 and September 4, 2021. Moreover, there have been 17 reported cases of liver injury, with two cases being drug-induced [15]. The possible side effects of the COVID-19 vaccines on the liver are not limited to one type. Two case reports suggested that the ChAdOx1 nCoV-19 vaccine (Oxford-AstraZeneca) may trigger acute autoimmune hepatitis [16]. Mann et al. reported a case of a 61-year-old female who developed generalized weakness and low-grade fever after receiving the second dose of Pfizer/BioNTech BNT162b2 mRNA vaccine. The patient had an ALP of 207 µ/L, total bilirubin of 6.2 mg/dL, direct bilirubin of 3.9 mg/dL, a WBC of 17 x 109, and AST of 37 U/L. All laboratory workup and imaging to investigate possible etiologies were unremarkable. As compared to our case, there were significant differences in age group, initial presentation, and degree of liver injury [17].

Prior to her recent presentation, our patient had no chronic illnesses. Given that her history, physical examination, and laboratory workups were unremarkable, the patient’s clinical picture was attributed to hepatotoxicity secondary to the Pfizer/BioNTech BNT162b2 mRNA vaccine, the only pharmacological agent that she was exposed to before her current presentation.


This is a case of hepatotoxicity in a 14-year-old patient that occurred after receiving the second dose of the Pfizer/BioNTech BNT162b2 mRNA vaccine. The exhaustive clinical and laboratory evaluation failed to establish any other plausible etiology besides the vaccine. The purpose of this report is to raise awareness of this uncommon but potentially life-threatening side effect.


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Covid Failure

What we did didn’t work. Let’s learn from that.

Authors: PETER VAN BUREN MAY 16, 2022| The American Conservative

We were swindled, fooled, bamboozled, and lied to during the pandemic. The public-health establishment misled the American people about the value of masking, closures, and social distancing. No one has accepted blame. Understanding how badly we failed is not only an inevitable part of the “told you so” process, but, more importantly, a lesson for next time. Just ask the Swedes.

Sweden had zero excess deaths associated with Covid-19. The U.S. had the most excess deaths of all nations. New York had more than Florida. That’s the whole story right there in a handful of words.

Let’s unpack it.

The key element of misdirection in the American swindle was case counts, those running numbers on screens telling us how many Americans had tested positive for Covid. If you’re curious, it looks like some 60 percent of us have had Covid at some point, with most of us experiencing mild or no symptoms.

How high the case numbers went in your neck of the woods depended a lot on the amount of testing taking place. More testing meant more “cases.” For me, when I had a very mild set of symptoms all clearly in line with Covid, I never even bothered to test. Like most people, I just sat around the house for a few days until I got better. My spouse, who had no symptoms, never got tested, either. Neither of us were included in the ever-growing case counts that dominated the headlines for years.

Not that it matters. The case count tells us very little. Hospitalization totals are useful for managing caseload, but often are indicative of protocols like testing patients upon entry to the hospital. Many hospital treatments changed, too. Initially, many Covid-positive people were hospitalized and put on respirators. Before long, many doctors realized infections associated with long-term respirator use were killing people, too.

Eventually, hospitalization numbers went down. That stat, too, only told you so much. Since Covid proved fatal primarily to the elderly, many hospitalizations began with something else only to end with Covid. My own father suffered a blinding, massive stroke, went into hospital, and caught Covid there, to officially die of respiratory failure. I’m not sure if he counted as a Covid death or not.

Now the bad news: Modern medicine cannot cure death. Everybody dies. Most Americans who don’t die earlier in life in accidents typically die after the age of 77. In 2020, heart disease and cancer each killed about double the number of people that Covid did.

The only statistic that really matters then when talking about the roughly two years of the pandemic is “excess deaths,” deaths beyond the usual couple of million that occur every year.

Sweden had zero excess deaths. The U.S. had the most excess deaths of all nations. New York had more than Florida.

Sweden did very little in terms of halting work and school, or forcing masking and social distancing. The U.S. did quite a bit more. The U.S. states known for their Covid “efforts,” particularly New York, had excess deaths worse than or similar to do-little Florida. These states expended an awful lot of effort and angst, and suffered great collateral damage (addiction, suicide, unemployment, social unrest, failing grades), for very little benefit.

And we were lied to by the Covidians. In July 2020, the New York Times stated Sweden’s “decision to carry on in the face of the pandemic has yielded a surge of deaths without sparing its economy from damage. Sweden’s grim result—more death, and nearly equal economic damage—suggests that the supposed choice between lives and paychecks is a false one: failure to impose social distancing can cost lives and jobs at the same time.”

Tsktsk, said the media. And they’re still saying it. Despite Florida having 148 excess deaths per 100,000 to New York’s 248, Politico‘s May 1, 2022, headline read: “Florida lost 70,000 people to Covid. It’s still not prepared for the next wave.”

Much as Florida did, Sweden allowed restaurants, gyms, shops, and most schools to stay open. People went to work; some voluntarily masked, some not. Their decision stood in stark contrast to the U.S., where, by April 2020, the CDC recommended draconian lockdowns, throwing millions out of work and school.

The U.S. is the only major Western nation that still demands a negative Covid test for entry, including for its own citizens. The U.S. is the only nation where every Covid therapeutic, such as new anti-viral drugs that lessen the severity of a positive case, is filtered through the lens of partisan politics.

In addition to leaving our economy in shambles, America’s Covid strategy apparently did not consider the age disparity in excess deaths. Globally, most Covid deaths occured among persons age 77 and older. People exposed to Covid in their 70s have twice the mortality rate of those exposed in their 60s, and 3,000 times that of Covid-exposed children. But everyone was made to wear a mask as though everyone were at equal risk of Covid, and without solid evidence that mask mandates significantly lower viral spread in the community.

The data were clear in China from the early days of the pandemic. Death rates for elderly Chinese in the early days of the pandemic, who were not social distancing, and elderly Americans, who were social distancing, were very similar. Swedish intensive-care-admission rates showed sharp declines after early pandemic peaks despite a lack of state-imposed shutdowns.

Age-specific solutions were needed for a virus with age-specific effects. We ignored or overlooked the data. We are paying for that mistake now. Savings lives or saving the economy? Both, please. Ask the Swedes.

America’s pandemic response was wrong across the board. Its failure is attributable in part to red-blue politics and a pathetic desire for control by Democratic governors.

It was also exacerbated by Americans’ underlying health, which is worse than most other developed countries. Our underlying health woes are exacerbated by income inequality and high rates of poverty, and maddening levels of obesity, diabetes, and “deaths of despair,” especially among the underclass. Black Americans were hit harder by Covid than white Americans. The poor were hit harder than the well-to-do.

Whatever we did, whether we masked or locked down or stayed open and maskless, we still would have suffered because of these underlying issues. Fixing the next pandemic means fixing America first.

Autoimmune hepatitis after SARS-CoV-2 vaccine: New-onset or flare-up?

Authors: Enver Avci 1Fatma Abasiyanik 2

Autoimmune 2021 Dec;125: 102745. doi: 10.1016/j.jaut.2021.102745  Epub 2021 Nov 11. PMID:  34781161PMCID: PMC8580815DOI: 10.1016/j.jaut.2021.102745


Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been reported to trigger several autoimmune diseases. There are also recent reports of autoimmune diseases that develop after SARS-CoV-2 vaccines. Autoimmune hepatitis is a polygenic multifactorial disease, which is diagnosed using a scoring system. A 61-year-old woman presented with malaise, fatigue, loss of appetite, nausea and yellow eyes. She had a Pfizer/BioNTech BNT162b2 mRNA vaccine a month ago. Her physical examination revealed jaundice all over the body, especially in the sclera. The laboratory tests showed elevated liver enzymes and bilirubin levels. Antinuclear antibody and anti-smooth muscle antibody were positive and immunoglobulin G was markedly elevated. The liver biopsy revealed histopathological findings consistent with autoimmune hepatitis (AIH). The patient was diagnosed with AIH and initiated on steroid therapy. She rapidly responded to steroid therapy. A few cases of AIH have been reported after the COVID-19 vaccine so far. Although the exact cause of autoimmune reactions is unknown, an abnormal immune response and bystander activation induced by molecular mimicry is considered a potential mechanism, especially in susceptible individuals. As intensive vaccination against SARS-CoV-2 continues, we would like to emphasize that clinicians should be cautious and consider AIH in patients presenting with similar signs and symptoms.


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CDC: No Documents Supporting Claim Vaccines Don’t Cause Variants

Authors:  Zachary Stieber May 13, 2022 The Epoch Times

The Centers for Disease Control and Prevention (CDC) says it does not have documents backing its claim that COVID-19 vaccines do not cause variants of the virus that causes COVID-19.

The CDC’s website calls it a myth that the vaccines cause variants.

“FACT: COVID-19 vaccines do not create or cause variants of the virus that causes COVID-19. Instead, COVID-19 vaccines can help prevent new variants from emerging,” the website states.

“New variants of a virus happen because the virus that causes COVID-19 constantly changes through a natural ongoing process of mutation (change). As the virus spreads, it has more opportunities to change. High vaccination coverage in a population reduces the spread of the virus and helps prevent new variants from emerging,” it also says.

The Informed Consent Action Network (ICAN), a nonprofit, asked the CDC in Freedom of Information Act requests for documentation supporting the claim.

In one request, the group asked for “All documents sufficient to support that COVID-19 vaccines do not create or cause variants of the virus that causes COVID-19.”

Another requested “All documents sufficient to support that the immunity conferred by COVID-19 vaccines does not contribute to virus evolution and the emergence of variants.”

The CDC has now responded to both requests, saying a search “found no records responsive” to them.

The first response came in January (pdf); the second came on May 4 (pdf).

If the CDC is making declaratory statements, the agency should have documents supporting them, Aaron Siri, an attorney representing ICAN, told The Epoch Times.

The responses are “very troubling,” Siri said. “I thought the CDC was a data-driven organization, that they made their decisions based on the studies and the science and the data.”

The CDC did not respond to a request for comment.

ICAN has been one of the more prolific requesters of information from the CDC during the pandemic. Many requests have yielded information. Others have not.

In this case, the CDC should act to ensure continued public trust, Siri says.

“Remove the language or provide the evidence,” he said. “There obviously are going to be instances where recommendations from the CDC might prove helpful or useful. And I think they do a disservice to everybody by hurting their own credibility by making statements that they either don’t have support or won’t produce the support for.”

Scientists outside the CDC have also said that vaccines can help prevent new variants.

“As more people get vaccinated, we expect virus circulation to decrease, which will then lead to fewer mutations,” the World Health Organization says on its site.

But many of the claims relied on the vaccines being able to stop infection from the CCP (Chinese Communist Party) virus, which causes COVID-19. The vaccines are increasingly unable to do so, particularly against the newest dominant strain, Omicron.

Dr. Geert Vanden Bossche, a virologist, is among those who say that the vaccines themselves are behind new variants.

“All COVID-19 vaccines fail in blocking viral transmission, especially transmission of more infectious variants. This is a huge problem as viral transmission is now increasingly taking place among healthy people in general and vaccinees in particular (as their S-specific Abs do not sufficiently neutralize S variants),” Vanden Bossche says on his website. “The resulting suboptimal S-directed immune pressure serves as a breeding ground for even more infectious variants.”

Growing Number Of COVID-19 Deaths Among Vaccinated People: Federal Data

Authors: Katabella Roberts via The Epoch Times MY 13, 2022

An increasing number of COVID-19 deaths are occurring among individuals in the United States who have been vaccinated, according to federal data.

In August of 2021, roughly 18.9 percent of COVID-19 deaths happened among individuals who were vaccinated, an ABC News analysis of the data shows. Six months later in February 2022, that figure had risen to over 40 percent as the highly-transmissible Omicron variant made its way across the globe.

Similarly, in September 2021, just 1.1 percent of COVID-19 deaths occurred among Americans who had been fully vaccinated and boosted once. Five months later in February, that percentage had jumped to about 25 percent, according to ABC News.

A separate analysis of federal data by CNN shows that in the second half of September 2021—when the Delta variant was at its peak—less than a quarter of all COVID-19 deaths were among individuals who were vaccinated with at least two doses of the Moderna or Pfizer/BioNTech mRNA vaccines or a single dose of the Johnson & Johnson vaccine. However, just months later in January and February as Omicron surged, that figure had jumped to 40 percent.

Some experts believe the increase in deaths among fully vaccinated people or “breakthrough infections” in those who have received all their shots is not overly concerning, saying it is because while more and more people become fully vaccinated, new variants emerge and vaccine protection begins to wane as fewer people continue to get booster shots.

These data should not be interpreted as vaccines not working. In fact, these real-world analyses continue to reaffirm the incredible protection these vaccines afford especially when up to date with boosters,” said John Brownstein, an epidemiologist at Boston Children’s Hospital and an ABC News contributor.

Despite an increasing number of deaths among the vaccinated, the Centers for Disease Control and Prevention (CDC) states that vaccines are safe and effective. Data from the government agency says that overall, the risk of death from COVID-19 is roughly five times higher in unvaccinated individuals than in those who have had at least their initial dose of a vaccine.

However, in some cases, serious adverse events such as thrombosis with thrombocytopenia syndrome (blood clots), myocarditis (inflammation of the heart muscle), and pericarditis (inflammation of the outer lining of the heart) have been documented.

As of May 4, around 257.9 million people in the United States, or 77.7 percent of the total population in the nation have received at least one dose of vaccine, while roughly 219.9 million people, or 66.2 percent of the total U.S. population, have been fully vaccinated.

Around 100.9 million of those who are fully vaccinated have received a booster shot, while 49.4 percent of those eligible for booster shots have not yet had one.

As the Omicron variant swept through the nation, an increasing number of vulnerable, older populations were being hospitalized, and 73 percent of deaths have been among those 65 and older, despite the fact that 90 percent of seniors have had all of their vaccine shots.

However, a large percentage—a third of them—have not yet had their booster jab.

“This trend in increased risk among the elderly further supports the need for community-wide immunization,” Brownstein said. “Older populations, especially those with underlying conditions, continue to be at great risk of severe complications, especially as immunity wanes. The best way to protect them is to make sure everyone around them is fully immunized.”

The data comes a month after pharmaceutical and biotechnology company Moderna said that preliminary results from its study on a COVID-19 vaccine intended to protect against variants showed that it outperformed the company’s currently authorized booster shot, mRNA-1273.

Moderna said on April 19 that its mRNA-1273.211 shot, its first bivalent booster vaccine candidate, showed “superiority” against the Beta, Delta, and Omicron variants of the virus one month after being administered, compared to the booster shot of its original vaccine currently in use.

Autoimmune Hepatitis Following Vaccination for SARS-CoV-2 in Korea: Coincidence or Autoimmunity?

Authors: Seong Hee Kang 1 2Moon Young Kim 1 3Mee Yon Cho 4Soon Koo Baik 1 5Affiliations expandPMID: 35437965PMCID: PMC9015903DOI: 10.3346/jkms.2022.37.e116

J Korean Med Sci 2022 Apr 18;37(15):e116. doi: 10.3346/jkms.2022.37.e116.


Autoimmune hepatitis (AIH) is a chronic, autoimmune disease of the liver that occurs when the body’s immune system attacks liver cells, causing the liver to be inflamed. AIH is one of the manifestations of a coronavirus disease 2019 (COVID-19), as well as an adverse event occurring after vaccination against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Few cases of AIH have been described after vaccination with two messenger RNA (mRNA)-based vaccines—BTN162b2 (Pfizer-BioNTech) and mRNA-1273 (Moderna)—against SARS-CoV-2. Herein, we report a case of AIH occurring after Pfizer-BioNTech COVID-19 vaccine. A 27-year-old female presented with jaundice and hepatomegaly, appearing 14 days after receiving the second dose of Pfizer-BioNTech vaccine. Her laboratory results showed abnormal liver function with high total immunoglobulin G level. She was diagnosed with AIH with histologic finding and successfully treated with oral prednisolone. We report an AIH case after COVID-19 vaccination in Korea.
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The coronavirus disease 2019 (COVID-19) pandemic, putatively caused by the widespread transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in 257,469,528 laboratory-confirmed cases of infection and 5,158,211 deaths globally as of November 28, 2021.1 Rapid vaccine development, however, has significantly mitigated severe COVID-19 illness. Two messenger RNA (mRNA) COVID-19 vaccines, BNT162b2 (Pfizer-BioNTech, New York, NY, USA/Mainz, Germany) and mRNA-1273 (Moderna, Cambridge, MA, USA), were granted emergency use authorization by the United States Food and Drug Administration in December 2020. SARS-CoV-2 infection has been associated with the development of autoimmune processes.2 Because SARS-CoV-2 harbors the same protein motif the mRNA vaccine codes for, it is plausible that these vaccines could trigger autoimmune diseases in predisposed patients.34 Autoimmune hepatitis (AIH) is a polygenic multifactorial disease that may be triggered by specific environmental factors, such as viral infections, resulting in the loss of self-tolerance to autoantigens in genetically susceptible individuals.5


We treated a 27-year-old female nurse who developed AIH after COVID-19 vaccination. She had no known history of liver disease and did not use herbal remedies or alcohol. She received a second dose of the Pfizer-BioNTech COVID-19 vaccine on March 30, 2021, and, since April 6, 2021, symptoms of nausea, vomiting, headache, fever, and dark urine continued. Accordingly, she was hospitalized via the emergency room 14 days after COVID-19 vaccination. A COVID-19 polymerase chain reaction test, performed at the local hospital on April 7 and 12, 2021, was negative. The physical examination was unremarkable, except for scleral icterus, jaundice, and palpable hepatomegaly. In the emergency room, laboratory investigations were significant for the following: bilirubin, 8.6 mg/dL; aspartate aminotransferase (AST), 1,004 U/L; alanine aminotransferase (ALT), 1,478 U/L; alkaline phosphatase, 182 U/L, white blood cell count, 6,720/μL (neutrophils, 46.8%); hemoglobin, 13.0 g/dL; platelet count 373,000/μL; blood urea nitrogen/creatinine, < 5.0/0.54 mg/dL (estimated glomerular filtration rate, 145.0 mL/min/1.73 m2); and prothrombin international normalized ratio, 1.1. Laboratory results were negative for hepatitis A, B, C, and E, Epstein-Barr virus, cytomegalovirus, herpes simplex virus types 1 and 2, and human immunodeficiency virus. Antinuclear antibody (ANA) was positive (1:80; mixed pattern). Other antibodies (including anti-mitochondrial, anti-smooth muscle, liver-kidney microsomal, and antineutrophil cytoplasmic antibodies) were negative. Total immunoglobulin G (IgG) level was 1,641 mg/dL (normal range, 549–1,584 mg/dL). Ceruloplasmin, transferrin saturation, thyroid function test, and serum protein electrophoresis were all normal. Abdominal ultrasound revealed splenomegaly (12.5 cm) without cirrhosis and gallbladder wall thickening.

Liver dynamic computed tomography revealed no evidence of biliary lithiasis or biliary dilation, and ultrasound-guided transabdominal liver biopsies were obtained. In microscopic examination, 17 portal tracts were identified. Although there was a focal bridging, the overall lobular architecture was preserved in the low magnification. Some portal tracts were widened by moderate inflammation with periportal fibrosis (Fig. 1). The portal inflammation was composed of mainly lymphocytes, clusters of plasma cells and few eosinophils, extending into proto-lobular interface (interface hepatitis) (Fig. 2A). The immunohistochemical staining for plasma cell markers, MUM1 and CD138 confirmed significant plasma cell infiltration in portal tracts as well as in lobules (Fig. 2B). Diffuse moderate necroinflammatory damage in lobules, associated with perivenular hepatocytes degeneration, mild cholestasis with hepatocytic rosettes (Fig. 2C) and sinusoidal inflammation were found. Other than COVID-19 vaccination, no other drug, herbal supplement, or toxin use were reported by the patient. The revised original score for AIH pretreatment was 18 (results > 15 suggest definite AIH). Treatment with oral prednisolone (40 mg daily) was initiated. Plasma ALT, AST, and total bilirubin levels over time, and before and after treatment, are summarized in Fig. 3. After three weeks of treatment, diarrhea and fever developed, and she was transferred to the hospital’s emergency room. Treatment with prednisolone (20 mg daily) was discontinued with the diagnosis of enteritis. Four days after admission, symptoms were relieved, and she was discharged from hospital with steroid discontinuation. Two weeks after stopping therapy, there were biochemical signs of an AIH relapse; therefore, treatment with oral prednisolone (10 mg daily) was restarted. Liver enzyme levels were completely normalized and the patient’s symptoms significantly improved.

Fig. 1
The microphotograph of low magnification of liver biopsy shows portal widening with periportal fibrosis (A) hematoxylin and eosin ×100, (B) Masson trichrome ×100.Click for larger imageDownload as PowerPoint slide

Fig. 2
Histological finding. (A) The porto-lobular interface shows severe inflammation composed of lymphocytes, clausters of plasma cells (circle) and a few eosinophils. Bile ducts (closed arrow) are not damaged (H&E, ×400). (B) The photomicrography of MUM1 immunohistochemical stain demonstrates numerous plasma cell infiltration (×400). (C) The lobules show diffuse degeneration of hepatocytes, mild cholestasis in hepatocytic rosettes (opened arrow) and sinusoidal lymphoplasma cells infiltration (H&E ×400).
H&E = hematoxylin and eosin.Click for larger imageDownload as PowerPoint slide

Fig. 3
Trends of serum ALT, AST and total bilirubin over time.
ALT = alanine aminotransferase, AST = aspartate aminotransferase.Click for larger imageDownload as PowerPoint slide

We described a case of AIH that developed in a patient after vaccination with the Pfizer-BioNTech COVID-19 vaccine, which was resolved with steroid treatment. To date, four cases of AIH have been reported after Pfizer-BioNTech COVID-19 vaccination in the literature (Table 1)678, the first of which was reported by Bril et al.3 The patient was a 35-year-old woman in her third month postpartum who developed AIH after COVID-19 vaccination. In this case, AIH exhibited some atypical features: autoantibodies other than ANA were negative and eosinophils were present on liver histology. Similarly, Lodato et al.6 reported a case of AIH occurring after vaccination, with no development of autoantibodies and eosinophil infiltrate in liver histology. Thereafter, two patients had a history of Hashimoto’s disease, high IgG levels, and typical findings on biopsy, unlike the above cases.78 Although our patient had no autoimmune disease, autoantibodies were positive, and IgG level was high. In addition, our case had typical findings on biopsy and responded well to steroid therapy. It is thought to be a new-onset AIH triggered by COVID-19 vaccination, but periportal fibrosis was observed in histological examination. However, in case with acute onset, there may be minimal fibrosis. Moreover, symptoms developed after the second vaccination in this patient, but there is a possibility that inflammation may have occurred even though there were no symptoms after the first vaccination.

Table 1
Characteristics of patients with autoimmune hepatitis after Pfizer-BioNTech COVID-19 vaccineClick for larger imageClick for full tableDownload as Excel file

Because causality cannot be definitively confirmed, it is possible that this association was coincidental. However, severe cases of SARS-CoV-2 infection are characterized by autoinflammatory dysregulation.9 Because the viral spike protein appears to be responsible, it is plausible that spike-directed antibodies induced by vaccination may also trigger autoimmune conditions in predisposed individuals.10 In support of this, several cases of immune thrombocytopenia have been reported days after COVID-19 vaccination. Vaccines protect the host from the virus by inducing antibody generation against viral peptides.11 Autoimmunity can develop due to cross-reactivity to the generated antibodies. The epitopes used for induction of the host immune system may mimic the structure of self-peptides, and antibodies that develop after vaccination may cause cross-reactivity directed to the self.12

Given the close temporal relationship between vaccination and onset of symptoms, we hypothesized that vaccination against COVID-19 could have triggered the development of AIH in our patient. To the best of our knowledge, this is the first reported episode of AIH that developed post-COVID-19 vaccination in Korea. Whether a causal relationship exists between COVID-19 vaccination and the development of AIH remains to be determined. Nevertheless, it is necessary to raise awareness about potential side effects that will likely emerge as more individuals are vaccinated.

1. World Health Organization. Global surveillance for COVID-19 caused by human infection with COVID-19 virus: interim guidance 2020. [Updated 2020]. [Accessed November 28, 2021]. Liu Y, Sawalha AH, Lu Q. COVID-19 and autoimmune diseases. Curr Opin Rheumatol 2021;33(2):155–162.

3. Bril F, Al Diffalha S, Dean M, Fettig DM. Autoimmune hepatitis developing after coronavirus disease 2019 (COVID-19) vaccine: causality or casualty? J Hepatol 2021;75(1):222–224.

4. Lee EJ, Cines DB, Gernsheimer T, Kessler C, Michel M, Tarantino MD, et al. Thrombocytopenia following Pfizer and Moderna SARS-CoV-2 vaccination. Am J Hematol 2021;96(5):534–537.

5. Czaja AJ. Autoimmune liver disease. Curr Opin Gastroenterol 2004;20(3):231–240.

6. Lodato F, Larocca A, D’Errico A, Cennamo V. An unusual case of acute cholestatic hepatitis after m-RNABNT162b2 (Comirnaty) SARS-CoV-2 vaccine: coincidence, autoimmunity or drug-related liver injury. J Hepatol 2021;75(5):1254–1256.

7. Rocco A, Sgamato C, Compare D, Nardone G. Autoimmune hepatitis following SARS-CoV-2 vaccine: may not be a casuality. J Hepatol 2021;75(3):728–729.

8. Avci E, Abasiyanik F. Autoimmune hepatitis after SARS-CoV-2 vaccine: new-onset or flare-up? J Autoimmun 2021;125:102745

9. Ehrenfeld M, Tincani A, Andreoli L, Cattalini M, Greenbaum A, Kanduc D, et al. COVID-19 and autoimmunity. Autoimmun Rev 2020;19(8):102597

10. Vojdani A, Kharrazian D. Potential antigenic cross-reactivity between SARS-CoV-2 and human tissue with a possible link to an increase in autoimmune diseases. Clin Immunol 2020;217:108480

11. Sadarangani M, Marchant A, Kollmann TR. Immunological mechanisms of vaccine-induced protection against COVID-19 in humans. Nat Rev Immunol 2021;21(8):475–484.

12. Malonis RJ, Lai JR, Vergnolle O. Peptide-based vaccines: current progress and future challenges. Chem Rev 2020;120(6):3210–3229.