More people are catching coronavirus a second time, heightening long COVID risk, experts say

Authors: Rong-Gong Lin II, Luke Money Mon, August 1, 2022  LA Times

Emerging evidence suggests that catching the coronavirus a second time can heighten long-term health risks, a worrisome development as the circulation of increasingly contagious Omicron subvariants leads to greater numbers of Californians being reinfected.

Earlier in the pandemic, it was assumed that getting infected afforded some degree of lasting protection, for perhaps a few months.

As the coronavirus mutates, though, that’s no longer a given. And each individual infection carries the risk not only for acute illness but the potential to develop long COVID.

“The additive risk is really not trivial, not insignificant. It’s really substantial,” said Dr. Ziyad Al-Aly, clinical epidemiologist at Washington University in St. Louis and chief of research and development at the Veterans Affairs Saint Louis Healthcare System.

According to a preprint study examining U.S. veterans, of which Al-Aly was the lead author, getting infected twice or more “contributes to additional risks of all-cause mortality, hospitalization and adverse health outcomes” in various organ systems, and can additionally worsen risk for diabetes, fatigue and mental health disorders.

“Reinfection absolutely adds risk,” Al-Aly said. The study suggested that, compared with those infected only once, individuals who caught the coronavirus a second time were at 2½ times greater risk of developing heart or lung disease and blood clotting issues. Subsequent infections also were associated with a higher risk of potentially serious health problems, as well as death from COVID-19.

It’s possible that a repeat coronavirus infection will leave someone just fine, which is what happens to most people, Al-Aly said. “But you might be one of the unlucky ones and … get some really serious health problem with an infection.”

Los Angeles County Public Health Director Barbara Ferrer recently cited Al-Aly’s pre-print study as rationale for wearing masks in indoor public settings to avoid reinfection.

“They also saw that those with repeat infections had a higher risk of gastrointestinal, kidney, mental health, musculoskeletal and neurologic disorders, as well as diabetes,” Ferrer said of the study. “Moreover, the risk of developing a long-term health problem increased further with each reinfection. The risk of having long-term health conditions was three times higher for those infected compared to those who were uninfected.”

Older viruses, such as those that cause measles and chickenpox, are quite stable — meaning that the vaccinations are highly effective and surviving either illness typically confers lifelong immunity.

Not so with the coronavirus, which has mutated wildly since the pandemic began. Someone who got infected with the variant that dominated California in late 2020, for instance, was vulnerable to catching the Delta variant the following summer. And those who survived Delta faced the risk of catching the later Omicron variant.

But the reinfection landscape has been upended even further as California has been walloped with a family of increasingly transmissible Omicron subvariants. The most recent of those, BA.5, has shown particular proficiency for reinfection — with the ability to target even those who survived an earlier Omicron case mere weeks before.

“This concept of building immunity, it really only works if you’re encountering the same beast again and again and again,” Al-Aly said. But in the world of COVID-19, BA.5 is actually a “very different beast” than earlier variants.

It’s possible that the acute phase of a second bout of COVID-19 could be milder than the first. But a subsequent attack can still leave more extensive cumulative damage to the body than if there had been only one infection.

Think of coronavirus infections like earthquake sequences: It’s possible an aftershock could be less severe than the first temblor but cumulatively could add more damage. And just because your home is still standing after one quake doesn’t mean you shouldn’t explore ways to make it seismically safer.

“Part of the reason why things, for many people, feel like they’re not so bad right now is because we are being very aggressive in countering the virus with vaccines, with treatments,” Dr. Ashish Jha, the White House COVID-19 response coordinator, said during a healthcare summit hosted by the Hill. “If we took our foot off the pedal, we’re going to see this virus come back in a way that’s much more dangerous. So we’ve got to stay on that front footing and continue fighting this thing.”

As it relates specifically to long COVID — a condition in which symptoms can persist months or even years after an initial infection — getting vaccinated and boosted likely reduces risk, but studies differ as to the degree of protection.

“I think having some preexisting immunity — whether it’s natural or from a vaccine — appears to reduce your risk of long COVID, but it’s still there. It’s not zero,” said Dr. Steven Deeks, a professor of medicine at UC San Francisco and principal investigator of the Long-term Impact of Infection With Novel Coronavirus, or LIINC, study.

Another report, observing triple-vaccinated Italian healthcare workers who weren’t hospitalized for COVID-19, found that two or three doses of vaccine were associated with a lower prevalence of long COVID.

A separate report suggested that even adults who had received a booster dose still have to consider the risk of long COVID. A British report said that, during the initial Omicron wave, about 1 in every 25 triple-vaccinated adults self-reported having long COVID three to four months after their first infection.

Still, some clinicians say that long COVID sufferers tend to be either unvaccinated or missing their boosters.

“The number of patients I’m seeing who were vaccinated and boosted who are coming in with long COVID is very low,” said Dr. Nisha Viswanathan, director of the UCLA Health Long COVID Program.

Long COVID also doesn’t prevent you from becoming infected with the coronavirus again. Viswanathan said she’s had patients who have seen their long COVID symptoms improve, then get sickened with another bout of COVID-19, and then see long COVID signs return.

The best way to prevent long COVID is to not get COVID-19. Many officials and experts cite non-pharmaceutical interventions such as masking as key tools, since vaccinations reduce, but do not entirely eliminate, the risk.

Masking is not a terrible thing to ask of people, especially in probably the places that are the most crowded, and the places that maybe are the highest risk of transmission,” Viswanathan said. Taking activities outside is also safer than being unmasked indoors.

Some of Viswanathan’s patients have downplayed the risk of COVID-19, commenting how it’s become a mild illness, and adding they don’t see the point of taking precautions. But, she said, better knowledge about long COVID and its disabling effects would help people understand the importance of masking and getting vaccinated and boosted.

A UCLA study published in the Journal of General Internal Medicine, of which Viswanathan was a co-author, found that of 1,038 patients with symptomatic COVID-19 between April 2020 and February 2021, nearly 30% developed long COVID. The most common symptoms were fatigue and shortness of breath among hospitalized patients.

While many are weary of COVID-19 preventive measures after nearly two and a half years, they remain important, said Dr. Anne Foster, vice president and chief clinical strategy officer for the University of California Health system.

The burden of long COVID following this wave is unknown. The official case tallies are likely vast undercounts, given that so many at-home tests are being used, and that could suggest that the burden of long COVID in subsequent months will be hard to predict, Foster said.

“I know everyone has moved on and people are going back to the way things were, and I sort of get it,” Deeks said. “But people do need to be aware that there is this additional risk that’s not going away and they might adjust their lives accordingly.

“But everyone’s going to figure this out on their own.”

Adverse effects of COVID-19 vaccines and measures to prevent them

Authors: Kenji Yamamoto Virol J. 2022; 19: 100. Published online 2022 Jun 5. doi: 10.1186/s12985-022-01831-0 PMCID: PMC9167431PMID: 35659687


Recently, The Lancet published a study on the effectiveness of COVID-19 vaccines and the waning of immunity with time. The study showed that immune function among vaccinated individuals 8 months after the administration of two doses of COVID-19 vaccine was lower than that among the unvaccinated individuals. According to European Medicines Agency recommendations, frequent COVID-19 booster shots could adversely affect the immune response and may not be feasible. The decrease in immunity can be caused by several factors such as N1-methylpseudouridine, the spike protein, lipid nanoparticles, antibody-dependent enhancement, and the original antigenic stimulus. These clinical alterations may explain the association reported between COVID-19 vaccination and shingles. As a safety measure, further booster vaccinations should be discontinued. In addition, the date of vaccination should be recorded in the medical record of patients. Several practical measures to prevent a decrease in immunity have been reported. These include limiting the use of non-steroidal anti-inflammatory drugs, including acetaminophen to maintain deep body temperature, appropriate use of antibiotics, smoking cessation, stress control, and limiting the use of lipid emulsions, including propofol, which may cause perioperative immunosuppression. In conclusion, COVID-19 vaccination is a major risk factor for infections in critically ill patients.

COVID Vaccines Increase Adverse Events and Weaken The Immune System

The coronavirus disease (COVID-19) pandemic has led to the widespread use of genetic vaccines, including mRNA and viral vector vaccines. In addition, booster vaccines have been used, but their effectiveness against the highly mutated spike protein of Omicron strains is limited. Recently, The Lancet published a study on the effectiveness of COVID-19 vaccines and the waning of immunity with time [1]. The study showed that immune function among vaccinated individuals 8 months after the administration of two doses of COVID-19 vaccine was lower than that among unvaccinated individuals. These findings were more pronounced in older adults and individuals with pre-existing conditions. According to the European Medicines Agency’s recommendations, frequent COVID-19 booster shots could adversely affect the immune response and may not be feasible [2]. Several countries, including Israel, Chile, and Sweden, are offering the fourth dose to only older adults and other groups rather than to all individuals [3].

The decrease in immunity is caused by several factors. First, N1-methylpseudouridine is used as a substitute for uracil in the genetic code. The modified protein may induce the activation of regulatory T cells, resulting in decreased cellular immunity [4]. Thereby, the spike proteins do not immediately decay following the administration of mRNA vaccines. The spike proteins present on exosomes circulate throughout the body for more than 4 months [5]. In addition, in vivo studies have shown that lipid nanoparticles (LNPs) accumulate in the liver, spleen, adrenal glands, and ovaries [6], and that LNP-encapsulated mRNA is highly inflammatory [7]. Newly generated antibodies of the spike protein damage the cells and tissues that are primed to produce spike proteins [8], and vascular endothelial cells are damaged by spike proteins in the bloodstream [9]; this may damage the immune system organs such as the adrenal gland. Additionally, antibody-dependent enhancement may occur, wherein infection-enhancing antibodies attenuate the effect of neutralizing antibodies in preventing infection [10]. The original antigenic sin [11], that is, the residual immune memory of the Wuhan-type vaccine may prevent the vaccine from being sufficiently effective against variant strains. These mechanisms may also be involved in the exacerbation of COVID-19.

Some studies suggest a link between COVID-19 vaccines and reactivation of the virus that causes shingles [1213]. This condition is sometimes referred to as vaccine-acquired immunodeficiency syndrome [14]. Since December 2021, besides COVID-19, Department of Cardiovascular Surgery, Okamura Memorial Hospital, Shizuoka, Japan (hereinafter referred to as “the institute”) has encountered cases of infections that are difficult to control. For example, there were several cases of suspected infections due to inflammation after open-heart surgery, which could not be controlled even after several weeks of use of multiple antibiotics. The patients showed signs of being immunocompromised, and there were a few deaths. The risk of infection may increase. Various medical algorithms for evaluating postoperative prognosis may have to be revised in the future. The media have so far concealed the adverse events of vaccine administration, such as vaccine-induced immune thrombotic thrombocytopenia (VITT), owing to biased propaganda. The institute encounters many cases in which this cause is recognized. These situations have occurred in waves; however, they are yet to be resolved despite the measures implemented to routinely screen patients admitted for surgery for heparin-induced thrombocytopenia (HIT) antibodies. Four HIT antibody-positive cases have been confirmed at the institute since the start of vaccination; this frequency of HIT antibody-positive cases has rarely been observed before. Fatal cases due to VITT following the administration of COVID-19 vaccines have also been reported [15].

As a safety measure, further booster vaccinations should be discontinued. In addition, the date of vaccination and the time since the last vaccination should be recorded in the medical record of patients. Owing to the lack of awareness of this disease group among physicians and general public in Japan, a history of COVID-19 vaccination is often not documented, as it is in the case of influenza vaccination. The time elapsed since the last COVID-19 vaccination may need to be considered when invasive procedures are required. Several practical measures that can be implemented to prevent a decrease in immunity have been reported [16]. These include limiting the use of non-steroidal anti-inflammatory drugs, including acetaminophen, to maintain deep body temperature, appropriate use of antibiotics, smoking cessation, stress control, and limiting the use of lipid emulsions, including propofol, which may cause perioperative immunosuppression [17].

To date, when comparing the advantages and disadvantages of mRNA vaccines, vaccination has been commonly recommended. As the COVID-19 pandemic becomes better controlled, vaccine sequelae are likely to become more apparent. It has been hypothesized that there will be an increase in cardiovascular diseases, especially acute coronary syndromes, caused by the spike proteins in genetic vaccines [1819]. Besides the risk of infections owing to lowered immune functions, there is a possible risk of unknown organ damage caused by the vaccine that has remained hidden without apparent clinical presentations, mainly in the circulatory system. Therefore, careful risk assessments prior to surgery and invasive medical procedures are essential. Randomized controlled trials are further needed to confirm these clinical observations.

In conclusion, COVID-19 vaccination is a major risk factor for infections in critically ill patients.


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Duration of Shedding of Culturable Virus in SARS-CoV-2 Omicron (BA.1) Infection

Authors: Julie Boucau, Ph.D. Caitlin Marino, B.S. Ragon Institute, Cambridge, MA

James Regan, B.S. Brigham and Women’s Hospital, Boston, MA Rockib Uddin, B.S.
Massachusetts General Hospital, Boston, MA Manish C. Choudhary, Ph.D.
James P. Flynn, B.S. Brigham and Women’s Hospital, Boston, MA Geoffrey Chen, B.A.
Ashley M. Stuckwisch, B.S. Josh Mathews, A.B. May Y. Liew, B.A. Arshdeep Singh, B.S.
Taryn Lipiner, M.P.H. Massachusetts General Hospital, Boston, MA Autumn Kittilson, B.S. Meghan Melberg, B.S. Yijia Li, M.D. Brigham and Women’s Hospital, Boston, MARebecca F. Gilbert, B.A. Zahra Reynolds, M.P.H. Surabhi L. Iyer, B.A. Grace C.Chamberlin, B.A. Tammy D. Vyas, B.S. Marcia B. Goldberg, M.D.Jatin M. Vyas, M.D., Ph.D.Massachusetts General Hospital, Boston, MAJonathan Z. Li, M.D.Brigham and Women’s Hospital, Boston, MA Jacob E. Lemieux, M.D., D.Phil. Mark J. Siedner, M.D., M.P.H.Amy K. Barczak, M.D.Massachusetts General Hospital, Boston, MA

July 21, 2022 N Engl J Med 2022; 387:275-277 DOI: 10.1056/NEJMc2202092

The B.1.1.529 (omicron) variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has a shorter incubation period and a higher transmission rate than previous variants.1,2 Recently, the Centers for Disease Control and Prevention recommended shortening the strict isolation period for infected persons in non–health care settings from 10 days to 5 days after symptom onset or after the initial positive test, followed by 5 days of masking.3 However, the viral decay kinetics of the omicron variant and the duration of shedding of culturable virus have not been well characterized.

We used longitudinal sampling of nasal swabs for determination of viral load, sequencing, and viral culture in outpatients with newly diagnosed coronavirus disease 2019 (Covid-19).4 From July 2021 through January 2022, we enrolled 66 participants, including 32 with samples that were sequenced and identified as the B.1.617.2 (delta) variant and 34 with samples that were sequenced and identified as the omicron subvariant BA.1, inclusive of sublineages. Participants who received Covid-19–specific therapies were excluded; all but 1 participant had symptomatic infection. This study was approved by the institutional review board and the institutional biosafety committee at Mass General Brigham, and informed consent was obtained from all the participants. Figure 1.Viral Decay and Time to Negative Viral Culture.

The characteristics of the participants were similar in the two variant groups except that more participants with omicron infection had received a booster vaccine than had those with delta infection (35% vs. 3%) (Tables S1 and S2 in the Supplementary Appendix, available with the full text of this letter at In an analysis in which a Cox proportional-hazards model that adjusted for age, sex, and vaccination status was used, the number of days from an initial positive polymerase-chain-reaction (PCR) assay to a negative PCR assay (adjusted hazard ratio, 0.61; 95% confidence interval [CI], 0.33 to 1.15) and the number of days from an initial positive PCR assay to culture conversion (adjusted hazard ratio, 0.77; 95% CI, 0.44 to 1.37) were similar in the two variant groups (Figure 1A through 1C and S1 through S3, and Tables S3 through S5). The median time from the initial positive PCR assay to culture conversion was 4 days (interquartile range, 3 to 5) in the delta group and 5 days (interquartile range, 3 to 9) in the omicron group; the median time from symptom onset or the initial positive PCR assay, whichever was earlier, to culture conversion was 6 days (interquartile range, 4 to 7) and 8 days (interquartile range, 5 to 10), respectively. There were no appreciable between-group differences in the time to PCR conversion or culture conversion according to vaccination status, although the sample size was quite small, which led to imprecision in the estimates (Figure 1D and 1E).

In this longitudinal cohort of participants, most of whom had symptomatic, nonsevere Covid-19 infection, the viral decay kinetics were similar with omicron infection and delta infection. Although vaccination has been shown to reduce the incidence of infection and the severity of disease, we did not find large differences in the median duration of viral shedding among participants who were unvaccinated, those who were vaccinated but not boosted, and those who were vaccinated and boosted.

Our results should be interpreted within the context of a small sample size, which limits precision, and the possibility of residual confounding in comparisons according to variant, vaccination status, and the time period of infection. Although culture positivity has been proposed as a possible proxy for infectiousness,5 additional studies are needed to correlate viral-culture positivity with confirmed transmission in order to inform isolation periods. Our data suggest that some persons who are infected with the omicron and delta SARS-CoV-2 variants shed culturable virus more than 5 days after symptom onset or an initial positive test.

How immune response triggered by COVID-19 may damage the brain

Findings could give insight into long-term neurological symptoms of COVID-19

Date:July 5, 2022Source:NIH/National Institute of Neurological Disorders and Stroke

Summary:A new study describes the immune response triggered by COVID-19 infection that damages the brain’s blood vessels and may lead to short- and long-term neurological symptoms. The study examined brain changes in nine people who died suddenly after contracting the virus.

A study from the National Institutes of Health describes the immune response triggered by COVID-19 infection that damages the brain’s blood vessels and may lead to short- and long-term neurological symptoms. In a study published in Brain, researchers from the National Institute of Neurological Disorders and Stroke (NINDS) examined brain changes in nine people who died suddenly after contracting the virus.

The scientists found evidence that antibodies — proteins produced by the immune system in response to viruses and other invaders — are involved in an attack on the cells lining the brain’s blood vessels, leading to inflammation and damage. Consistent with an earlier study from the group, SARS-CoV-2 was not detected in the patients’ brains, suggesting the virus was not infecting the brain directly.

Understanding how SARS-CoV-2 can trigger brain damage may help inform development of therapies for COVID-19 patients who have lingering neurological symptoms.

“Patients often develop neurological complications with COVID-19, but the underlying pathophysiological process is not well understood,” said Avindra Nath, M.D., clinical director at NINDS and the senior author of the study. “We had previously shown blood vessel damage and inflammation in patients’ brains at autopsy, but we didn’t understand the cause of the damage. I think in this paper we’ve gained important insight into the cascade of events.”

Dr. Nath and his team found that antibodies produced in response to COVID-19 may mistakenly target cells crucial to the blood-brain barrier. Tightly packed endothelial cells help form the blood-brain barrier, which keeps harmful substances from reaching the brain while allowing necessary substances to pass through. Damage to endothelial cells in blood vessels in the brain can lead to leakage of proteins from the blood. This causes bleeds and clots in some COVID-19 patients and can increase the risk of stroke.

For the first time, researchers observed deposits of immune complexes — molecules formed when antibodies bind antigens (foreign substances) — on the surface of endothelial cells in the brains of COVID-19 patients. Such immune complexes can damage tissue by triggering inflammation.

The study builds on their previous research, which found evidence of brain damage caused by thinning and leaky blood vessels. They suspected that the damage may have been due to the body’s natural inflammatory response to the virus.

To further explore this immune response, Dr. Nath and his team examined brain tissue from a subset of patients in the previous study. The nine individuals, age 24 to 73, were chosen because they showed signs of blood vessel damage in the brain based on structural brain scans. The samples were compared to those from 10 controls. The team looked at neuroinflammation and immune responses using immunohistochemistry, a technique that uses antibodies to identify specific marker proteins in the tissues.

As in their earlier study, researchers found signs of leaky blood vessels, based on the presence of blood proteins that normally do not cross the blood brain barrier. This suggests that the tight junctions between the endothelial cells in the blood brain barrier are damaged.

Dr. Nath and his colleagues found evidence that damage to endothelial cells was likely due to an immune response — discovering deposits of immune complexes on the surface of the cells.

These observations suggest an antibody-mediated attack that activates endothelial cells. When endothelial cells are activated, they express proteins called adhesion molecules that cause platelets to stick together. High levels of adhesion molecules were found in endothelial cells in the samples of brain tissue.

“Activation of the endothelial cells brings platelets that stick to the blood vessel walls, causing clots to form and leakage to occur. At the same time the tight junctions between the endothelial cells get disrupted causing them to leak,” Dr. Nath explained. “Once leakage occurs, immune cells such as macrophages may come to repair the damage, setting up inflammation. This, in turn, causes damage to neurons.”

Researchers found that in areas with damage to the endothelial cells, more than 300 genes showed decreased expression, while six genes were increased. These genes were associated with oxidative stress, DNA damage, and metabolic dysregulation. This may provide clues to the molecular basis of neurological symptoms related to COVID-19 and offer potential therapeutic targets.

Together, these findings give insight into the immune response damaging the brain after COVID-19 infection. But it remains unclear what antigen the immune response is targeting, as the virus itself was not detected in the brain. It is possible that antibodies against the SARS-CoV-2 spike protein could bind to the ACE2 receptor used by the virus to enter cells. More research is needed to explore this hypothesis.

The study may also have implications for understanding and treating long-term neurological symptoms after COVID-19, which include headache, fatigue, loss of taste and smell, sleep problems, and “brain fog.” Had the patients in the study survived, the researchers believe they would likely have developed Long COVID.

“It is quite possible that this same immune response persists in Long COVID patients resulting in neuronal injury,” said Dr. Nath. “There could be a small indolent immune response that is continuing, which means that immune-modulating therapies might help these patients. So these findings have very important therapeutic implications.”

The results suggest that treatments designed to prevent the development of the immune complexes observed in the study could be potential therapies for post-COVID neurological symptoms.

This study was supported by the NINDS Division of Intramural Research (NS003130) and K23NS109284, Roy J. Carver Foundation, and the Iowa Neuroscience Institute.

make a difference: sponsored opportunity

Story Source:

Materials provided by NIH/National Institute of Neurological Disorders and StrokeNote: Content may be edited for style and length.

Journal Reference:

  1. Myoung Hwa Lee, Daniel P Perl, Joseph Steiner, Nicholas Pasternack, Wenxue Li, Dragan Maric, Farinaz Safavi, Iren Horkayne-Szakaly, Robert Jones, Michelle N Stram, Joel T Moncur, Marco Hefti, Rebecca D Folkerth, Avindra Nath. Neurovascular injury with complement activation and inflammation in COVID-19Brain, 2022; DOI: 10.1093/brain/awac151

Researchers are working together to better understand and treat the syndrome


Robin Macnofsky’s first symptoms, in April 2020, were so mild she didn’t take a test for COVID-19, preferring to save it for someone who really needed it.

A few weeks later her chest tightened and her temperature spiked. These ebbed, but an even stronger wave hit: a high fever and exhaustion that left her bedbound in a days-long “zombie sleep.” Macnofsky tested positive for COVID-19 (likely from remaining viral genetic material). Her symptoms endured.

Previously a champion multi-tasker who could split her concentration in four directions, the then-59-year-old could no longer follow the plot of a TV episode or walk her dog. Her temperature waxed and waned.

A realization dawned: The end was nowhere in sight, and no one could tell her why.

Scientists studying the unfamiliar and unfurling COVID-19 pandemic also began to realize that for Macnofsky and many other COVID-19 patients, a long hospital stay or a short, mild illness were not the only outcomes. For some people, mild symptoms, quickly resolved, were just the beginning.

Researchers worldwide, including many at Fred Hutchinson Cancer Research Center and the University of Washington, are working to understand long COVID-19, the long-lasting effects of COVID-19 infection that can affect adults, teens and children. Hutch and UW investigators are building on deep expertise in immunology and infectious diseases like HIV to figure out what causes long COVID-19, who is at risk, and how to treat it. To do so, they’re tackling challenges that range from basic questions about how best to measure symptoms to uncovering the complex immunological interplay that may drive symptoms.

‘Something is different’

In March 2020, Julie Czartoski, a nurse practitioner working with Fred Hutch virology expert and Joel D. Meyers Endowed Chair holder Dr. Julie McElrath, helped McElrath quickly put together a study, the Seattle COVID Cohort Study, to look at COVID-19 in first responders and those infected with SARS-CoV-2, the virus that causes COVID-19. They wanted to know who was getting it, and how badly. Soon they opened the study to others in the community. Luckily, few participants who contracted the coronavirus had symptoms that warranted hospitalization. Most had relatively mild infections that cleared up quickly.

But that wasn’t the end. For many, symptoms persisted, even worsened. Participants reported lingering fevers, new joint pain, exhaustion and brain fog, among a grab bag of other symptoms. When an unexpected number of young, healthy firefighters reported atrial fibrillation — a rapid, abnormal heart rhythm — Czartoski knew something was up.

“It’s not unheard of in young adults, but to have so many was weird,” she said. “I remember texting Julie McElrath and saying, ‘Something is different, because these people are still sick.’”

Because of their fast action and prompt study enrollment, Czartoski and McElrath were early to recognize a truth that would eventually become clear to other scientists: COVID-19 can cast a long shadow.

More research and resources 

Many of the people in McElrath’s study who reported lasting problems had experienced mild, almost cold-like infections with SARS-CoV-2. Very few had been hospitalized.

It takes time to know for sure that a patient is suffering from long COVID-19. A week or two is not long enough to be sure their symptoms won’t clear up soon. Eventually, McElrath and her team found that about 30% of the coronavirus-positive participants in their study had lasting symptoms, or new symptoms attributed to COVID-19, that extended at least 60 days past their initial infection, Czartoski said.

Long COVID-19 dogs some patients, like Macnofsky, much longer, and their symptoms can be severe. After two different week-long hospital stays, in which she underwent terrifying procedures to remove nearly a liter of fluid pressing on her heart and then her lungs, Macnofsky took a leave of absence from her career as a community organizer. By early 2022, she still rations her energy and has yet to regain her prior multi-tasking abilities.

Time defines the syndrome and time challenges those suffering from it and the scientists working to untangle it. Also known as PASC, for post-acute sequelae of SARS-CoV-2 infection, long COVID-19 refers to symptoms that endure long after someone has recovered from their initial coronavirus infection. (The term “sequelae” refers to a disease’s aftereffects.) Symptoms can include fatigue, shortness of breath, brain fog, fever, anxiety and depression. COVID-19 patients who were sick enough to need ICU care may also be dealing with post-ICU syndrome, and it’s not yet clear how their experience will unfold differently from patients who were treated in the ICU for other causes.

For a health problem as mysterious and as complex as long COVID-19, progress requires scientific teamwork.

That’s why, in summer 2021, Dr. Rachel Bender Ignacio reached out to investigators across Fred Hutch and the University of Washington, inviting them to join a long COVID-19 working group to share challenges and solutions, and find collaborators to help investigate specific questions.

As medical director of the Hutch’s COVID-19 Clinical Research Center, or CCRC, Bender Ignacio had a good sense of who at both institutions were treating or studying the syndrome. She was also hearing from CCRC trial participants who had transitioned from acute to long COVID-19 and wanted to know how scientists were addressing it. “I have my ear to the ground,” she said.

Bender Ignacio felt that progress required stronger connections between clinicians and laboratory and translational scientists. Physicians needed a better understanding of the biological mechanisms driving long COVID-19 before they could move proposed treatments into clinical trials, and basic scientists could reveal those mechanisms but needed tissue samples and clinical insights from the people providing patient care.

“Bringing everyone together was the least I could do,” Bender Ignacio said.

The working group she put together is an example of international and multidisciplinary efforts to tackle the challenges that vex investigators studying long COVID-19, including how to best classify and diagnose the syndrome, what’s causing it, and how to treat it. The recently launched National Institutes of Health RECOVER initiative, aimed at understanding PASC, is giving the investigators in the field hope that standards may be forthcoming, said Dr. Eric Chow, a working group member and UW infectious diseases fellow who studies the damage that respiratory viruses can do outside the lungs.

The researchers who joined Bender Ignacio’s collective span disciplines and body systems, including the brain, heart and lungs. They include researchers and clinicians at UW and Harborview Medical Center, which opened one of the nation’s earliest clinics devoted to helping long COVID-19 patients. The working group members bring expertise in long-term complications from viral infections like HIV and influenza, and know how viruses or the immune reaction to them can damage the body. SARS-CoV-2 may be wreaking the most havoc right now, but it’s not the only virus that can upend sufferers’ lives: Many, including Bender Ignacio, have spent their careers studying the long-term effects of HIV.

Now the team is bringing their wide-ranging expertise to bear on the many questions of long-haul COVID-19, hoping to surmount its challenges and help patients.

Learning on the fly

Studying a little-understood problem in a rapidly shifting pandemic is incredibly challenging. At the beginning, scientists had no knowledge base to inform their data collection or study design. Every week or month brought new information that forced them to reassess the data they had already collected — and adjust their data-collection methods to incorporate new understanding.

“It’s like building a boat while you’re sailing it,” said working group and CCRC member Dr. James Andrews, a University of Washington rheumatologist who studies how sepsis, particularly severe cases requiring hospitalization, can lead to long-term disability.

The first challenge was realizing that a problem existed. Many of the long-haulers Czartoski interviewed for the Seattle COVID Cohort Study struggled to find help and even recognition of their symptoms, she said.

“In the beginning, a big part of my job was just listening,” Czartoski recalled.

Study participants wept as they described to her their crushing fatigue and debilitating symptoms, and the struggle to get health care providers to understand that their vague-seeming complaints posed a real problem. Macnofsky, too, found it difficult to get help for her constant fever, headaches, fatigue and brain fog.

In the beginning, no one knew what information would be important to understand why these patients were suffering and how to help.

A snapshot of data “is one piece of the whole puzzle,” said Hutch statistician Dr. Zoe Moodie, who helps design and analyze HIV vaccine trials and develops statistical methods to analyze immunological data. “Generally, the more pieces the better, and as time goes go on we learn which are the important pieces.”

Czartoski tackled the problem by collecting everything she could: “Sometimes [a symptom] didn’t seem important, then a week later I’d have five people reporting it.”

And sometimes the information that most impacts a patient’s life can seem negligible when committed to paper, she said. One person’s loss of smell or taste may seem like small potatoes compared to others’ chronic exhaustion and continual fevers. But such seemingly small symptoms can make life and some careers difficult: Firefighters smell phantom burning and parents who can no longer smell a dirty diaper. Once-favorite food now repells.

“And [those symptoms] are really tough on quality of life,” Czartoski noted. Depression can set in, straining a person’s long-term relationships, affecting quality of life and for some, the ability to hold down a job.

Initially, she had a limited systematized questionnaire, and took notes longhand while patients noted every symptom they could think of — whether they knew it related to their COVID-19 or not. As time passed, Czartoski and her colleagues were able to spot common symptoms that they added to an ever-expanding checklist. (Then, they had to get the checklist built into the study records system.)

The working group members brainstorm statistical and analytical strategies that could help, and which take into account the fact that not everyone’s data has been collected in the same way at the same time points during the course of their disease.

Even now, their efforts to untangle long COVID-19 are hampered by what they didn’t know six, 12, 18 months ago, Czartoski said.

“Researchers will ask about blood drawn a year and a half ago: Were they taking Tylenol?” she said. “It could change the immune response, but I don’t know!”

Fred Hutch HIV researchers Dr. Julie McElrath (left) and Dr. Rachel Bender Ignacio (right) are parlaying their expertise in viral infections and clinical trials to help patients suffering from long COVID-19. McElrath gathered a cohort of long-haulers who are helping researchers dig into the immune drivers of PASC. As the CCRC’s medical director, Bender Ignacio helps make crucial connections between basic and translational scientists working in the field.

Photos by Robert Hood / Hutch News Service

Finding the right box

Another major challenge that long COVID-19 researchers face is classification. Many studies are producing data on the syndrome, but if symptoms aren’t collected and classified similarly, trying to compare different studies will be like comparing apples and oranges.

Decisions about how to classify symptoms also affect how patients are grouped together and how the data is analyzed. One big concern: Should patients be grouped by symptom, or should symptoms be grouped by the organs they affect?

It’s a bit of a chicken-and-egg issue, but it gets into the problem of what’s behind long COVID-19 to begin with, said Chow, who began treating Macnofsky after her hospital stay. (The two teamed up to tell Macnofsky’s story in a dual first-person essay published in the scientific journal Open Forum Infectious Diseases.)

“For example, what about fatigue? Do you group everyone with fatigue together? But what if one person’s fatigue is caused by damage to the nervous system, another’s by damage to their heart, and someone else’s by lung damage,” said Chow, who at the start of the pandemic was part of the Centers for Disease Control and Prevention team that went to New York state to confirm COVID-19-associated multisystem inflammatory syndrome in children.

Even in cases where it’s clear the immune system is at fault, fatigue may not have a single cause. Energy-sucking immune activation could explain one person’s fatigue, but post-infection autoimmunity, in which their own tissues are under attack, could be the reason behind another’s, Andrews said.

Trying to find the biological similarities in data taken from these patients would be like trying to compare pages of text written in different languages: more likely to result in gibberish than to identify a helpful pattern.

And sometimes, symptoms may not even be the result of a person’s coronavirus infection. Part of the problem is the often-vague, widely varying collection of symptoms, many of which long COVID-19 shares with other chronic health problems, such as autoimmune diseases or chronic fatigue syndrome. Autoimmune diseases often strike in young adulthood. For some people, SARS-CoV-2 infection and an autoimmune diagnosis are just two pieces of unrelated bad luck.

“In a longitudinal cohort like this, nothing is ever completely clean,” Czartoski said.

Working group members share questions and strategies. Should they classify symptoms by severity score, or follow the CDC’s recommendations to classify symptoms by outcome measures in different areas? Members often draw on their or other members’ expertise in different disciplines, such as adapting questionnaires used by neurologists to assess cognitive difficulties. Czartoski recommended a severity scale long used by HIV researchers to assess how symptoms impact patients’ daily living.

The team also grapples with the challenges of classifying symptoms that may seem focused on a specific organ system, but are actually emblematic of a body-wide problem. Researchers noted that some simplification needs to occur to make it possible to analyze the reams of data that can be collected.

But sometimes it’s unclear what’s causing someone’s symptom — so researchers can’t classify symptoms by underlying cause. What then?

Members also keep an eye on trends in the wider scientific community to see if they can align with areas of growing consensus, the better to compare their results with other studies.

Who’s at risk for symptoms, and how long will they last?

But sorting out the logistical challenges of classification is just the first step. Long COVID-19 researchers want to understand why symptoms develop and who’s at risk. Why do some symptoms affect some patients but not others? Who will have a mild course, and who will suffer greatly? A deeper understanding, they hope, will shed light on why symptoms linger so long for some people, and how to predict how a patient’s experience will unfold.

UW neurologist Dr. Payal Patel is focusing on the cognitive symptoms of PASC.

“I want to know, what is the cause of the symptoms we see in PASC,” said Patel, who studies the continuing effects of infections of the central nervous system, including HIV. “We know PASC affects different organ systems. I’m trying to get a better clinical understanding of how it affects the brain.”

Without this, it’s difficult to give worried patients a clear picture of what they can expect from long COVID. Patel wants to better understand how long such symptoms last, who’s most at risk, and what’s causing them. Is brain fog caused primarily by immune dysfunction? Or could the clotting problems associated with COVID-19 have damaged the cells lining blood vessels in the brain? Patel and a team of scientists have studies underway to answer these questions.

This type of location-specific question can be very difficult to address, Chow noted. It’s relatively easy to take blood samples and look at general patterns of immune cells or antibodies floating through the blood. But what about problems that are occurring at a hard-to-reach spot, like tiny blood vessels in the brain or lungs?

Some working group members focus their research questions on specific areas of the body. With Patel, Andrews is trying to understand who’s most at risk for cognitive and physical impairments after COVID. Some patients’ fatigue is related to muscle wasting, known medically as sarcopenia, and Andrews wants to know what’s behind that and who’s at risk.

Role of the immune system in long COVID-19

Since it became understood that an overactive immune response (known as a “cytokine storm”) lurks behind some of COVID-19’s most dire complications, scientists have begun digging deeper into how the immune system responds to SARS-CoV-2. Macnofsky herself participated in a Benaroya Research Institute study looking at the immune response to the novel coronavirus.

Bender Ignacio’s working group is drawing on the Hutch’s longstanding expertise in immunology and infectious diseases and looking to the immune system for answers.

“We’re studying what natural infection looks like over time,” said Fred Hutch immunologist Dr. Maria Lemos, who studies immune responses in mucosal tissue like vaginal and nasal surfaces, where we first encounter many viruses. “People could have cold symptoms for nine days, then four moths later they’re diagnosed with a lung condition or a heart condition.”

To understand why, she and others on McElrath’s team are mapping the immune response to SARS-CoV-2 infection as it unfolds over months. With collaborators at Emory University in Atlanta, they’re charting the rise and fall of antibodies against the virus and how different immune-cell populations grow, shrink and morph over time.

By describing how these responses differ between people who did and did not develop long COVID-19, the researchers hope to identify key biomarkers, like specific inflammatory proteins, that help predict which patients will have persistent problems. Such biological predictors could help doctors intervene early, either to help connect patients with the right services to help them deal with symptoms, or (once scientists crack this problem) stave it off entirely.

McElrath’s team, with collaborators at Emory University and the Seattle-based Allen Institute for Immunology, has revealed some tantalizing immunological patterns, Lemos said, which the group posted on the preprint server The immune trajectory in many long-haulers looks startlingly unlike that seen in people who recover quickly and permanently.

“The alarm system of the immune system doesn’t get turned on as quickly in these people — but surprisingly it seems to remain on for way longer,” Lemos said. They’re currently putting together a paper for peer review at a scientific journal.

On top of this project, Moodie is working with investigators the Allen Institute to identify immunological signatures, including cellular features like proteins and gene expression, that distinguish long COVID-19 from acute COVID-19. Some patients — including Macnofsky — report improvement of symptoms after vaccination for COVID-19, and Moodie and her collaborators want to understand how vaccination may help their bodies resolve their chronic, damaging immune responses.

(Whether prior COVID-19 vaccination helps protect against developing long COVID-19 is still being explored. A recent study in The Lancet suggests that vaccinated people are less likely to have long-lasting symptoms after SARS-CoV-2 infection.)

Treatments for long-haulers?

Macnofsky said she’s recently been helped by six months of weekly pulmonary rehab sessions. It’s possible that early access to rehabilitative therapies could help prevent or alleviate severe long COVID-19 in others.

It is taking time for scientists at the Hutch and elsewhere to get a clear enough picture of what’s driving long COVID-19 to open clinical studies to address patients’ problems, but a few have begun.

The Seattle arm of a multi-center, Phase 2 trial of a drug called RSLV 132, is administered through the CCRC and headed by Andrews. (People interested in participating can contact the CCRC.) Developed by biotech company Resolve Therapeutics, the drug has already shown promise against fatigue in people with autoimmune diseases like Sjögren syndrome, and scientists hope long COVID-19 patients will also benefit.

“One of the exciting things about this study is that it’s taking a targeted therapy approach to treating symptoms,” Andrews said. “It’s targeting the mechanism behind fatigue — chronic inflammation — to see if it helps.”

In addition to testing whether RSLV 132 outperforms a placebo when it comes to alleviating fatigue in long COVID-19 patients, researchers will collect tissue samples that they’ll study to get a better picture of how it might be working (if it does), he said. If it turns out that some patients respond and some don’t, such samples could also help investigators figure out why.

And, if there’s a similar biological process underpinning the fatigue seen in long COVID and other diseases and syndromes, the study could benefit a wide array of patients, Andrews said.

That’s a hope that other members of the working group also harbor. One of the big questions, said Chow, is whether long COVID-19 patients are suffering from the same immunologic problems as patients with chronic fatigue syndrome, autoimmune diseases, or other virus-associated chronic damage. Or is there something unique about the biology behind long COVID-19?

Bender Ignacio sees potential for the close ties between the CCRC and the long COVID-19 working group to help fast-track promising treatments or treatment strategies that emerge from group members’ projects.  

Working toward a more certain future

One thing Chow hopes come from the studies is more predictability. Right now, clinicians struggle to determine whose symptoms will last, and whose will resolve. A better understanding of long COVID-19 subgroups will help clinicians guide patients toward the best therapies for them. Improving doctors’ ability to diagnose and clinically characterize long COVID-19 will also help improve insurance reimbursement, he said. Right now, he stressed the need to recognize and validate what patients with long COVID-19 face.

Macnofsky, who at one point couldn’t take a phone call from a friend without falling back into a zombie sleep, feels fortunate. She joined Facebook groups organized by long COVID-19 sufferers, where many reported not just horrible symptoms but job loss and crushing debt. Macnofsky’s leave of absence from her career was fully supported — emotionally and financially — by her husband. She’s recovered enough now to step back into some job duties, though not at her previous level. But she knows other patients who continue to suffer, with no idea when — or if — their symptoms will ever improve.

On top of everything else, her uncertain future is one of the biggest challenges Macnofsky faces Luckily, she said, her “keep calm and carry on” attitude (and compassionate family) are helping her ride her waves of symptoms.

“There’s a mental health component to being so ill,” Czartoski said. She still encourages patients to treat themselves gently and take it one day at a time. While most will improve with time, a few will worsen — and she still can’t tell someone which patient they’ll be. The answer will only come with more data.

“I’m still collecting everything I can,” Czartoski said.

Natural Immunity From Omicron Strong Against Virus Subvariants: Study

Authors: Zachary Stieber via The Epoch Times, UL 18, 2022

The protection afforded by surviving COVID-19 was strong against the latest virus subvariants, including the one currently dominant in the United States, scientists in Qatar found.

People who were infected with Omicron, a variant of SARS-CoV-2, had 76.1 percent protection against symptomatic reinfection from BA.4 and BA.5 and 80 percent shielding from any reinfection, regardless of symptoms, according to the preprint study.

SARS-CoV-2, also known as the CCP (Chinese Communist Party) virus, causes COVID-19.

Omicron became the dominant virus strain in many countries in late 2021. Since then, a number of subvariants have taken hold. BA.5 is the strain currently dominant in the United States.

While protection from an Omicron infection provided robust shielding against reinfection, those who contracted a pre-Omicron strain had little protection, according to the Qatari scientists, who were led by Dr. Laith Abu-Raddad with Weill Cornell Medicine-Qatar.

Pre-Omicron infection provided just 15.1 percent effectiveness against symptomatic BA.4 and BA.5 reinfection and just 28 percent infection against any reinfection.

The scientists analyzed data from national COVID-19 databases.

Infections before Omicron were those that occurred before Dec. 19, 2021, when the variant wave started in Qatar.

Protection ‘Strong’

“Protection of a previous infection against BA.4/BA.5 reinfection was modest when the previous infection involved a pre-Omicron variant, but strong when the previous infection involved the Omicron BA.1 or BA.2 subvariant,” the scientists wrote.

Natural immunity has long been found to be superior to the protection from COVID-19 vaccines, and the new study is no exception. Vaccines provide little protection against Omicron infection and perform worse against infection and severe illness from the BA.4 and BA. 5 subvariants, studies have shown.

Natural immunity also waned against BA.4 and BA.5, highlighting how the subvariants are better at evading protection, the Qatari researchers found.

The group has been studying natural immunity for years and recently discovered that the protection from prior infection against severe disease showed no signs of waning, regardless of what strain infected the person.

Among the listed limitations for the new study was the young population of Qatar, where just 9 percent of residents are 50 years of age or older. That means the findings “may not be generalizable to other countries where elderly citizens constitute a larger proportion of the total population,” researchers wrote.

Some experts, including Abu-Raddad and U.S. Centers for Disease Control and Prevention Director Dr. Rochelle Walensky, continue recommending vaccination for people with natural immunity, pointing to studies that indicate one or more doses increase protection, but others say vaccination isn’t needed for people who survive COVID-19, since some research suggests the elevated protection is minimal and that the naturally immune are at higher risk of vaccine side effects.

New England Journal of Medicine: “Conspiracy Theory” confirmed

The America First Report breaks the story: July 12, 2022

Several recent studies have indicated the Covid-19 vaccines actually increase the risk of contracting the disease over time, but these studies have been ignored or even debunked by corporate media and Big Pharma for months. Now, they’ll have to contend with a new study published in the highly respected New England Journal of Medicine.

This study was huge in scale, sifting through data collected from over 100,000 people infected by the Omicron variant. It lends credibility to the statistical significance of the findings, which are absolutely startling. Here are the key points:

  • Those who have been “fully vaccinated” with two shots from Moderna or Pfizer are more likely to contract Covid-19 than those who have not been vaccinated at all
  • Booster shots offer protection approximately equal to natural immunity, but the benefits wane after 2-5 months
  • Natural immunity lasts for at least 300-days, which is the length of the study; it likely lasts much longer

This jibes with the current narrative coming from Big Pharma and their minions in government and corporate media that the jabs are supposed to mitigate the effects. But even that claim has been called into question as recent studies indicate the vaccinated may be dying even more than the unvaccinated. According to The Exposé:

The Government of Canada has confirmed that the vaccinated population account for 4 in every 5 Covid-19 deaths to have occurred across the country since the middle of February 2022, and 70% of those deaths have been among the triple vaccinated population.

Despite the scope of the study and the credibility of the source, it will not receive any attention from corporate media. It is imperative that our readers get the word out because this is an absolute narrative-buster for Big Pharma. Now more than ever, we must alert the people of the truth because we are on the verge of seeing millions of children under the age of five-years-old injected.

Children do not readily acquire this pathogen, spread to other children, spread to adults, take it home, get severely ill, or die from it. It is that simple. We know children tend not to transmit Covid-19 virus and that the concept of asymptomatic spread has been questioned severely, particularly for children.

Children, if infected, just do not spread Covid-19 to others readily, either to other children, other adults in their families or otherwise, nor to their teachers. This was demonstrated elegantly in a study performed in the French Alps. The pediatric literature is clear science on this. Overwhelming data shows that the SARS-CoV-2-associated burden of severe disease or death in children and adolescents is very low (statistically zero).

Swedish data by Ludvigsson reported on the 1,951,905 children in Sweden (as of December 31, 2020) who were 1 to 16 years of age who attended school with largely no lockdowns or masks. They found zero (0) deaths. “Despite Sweden’s having kept schools and preschools open, we found a low incidence of severe Covid-19 among schoolchildren and children of preschool age during the SARS-CoV-2 pandemic.”

recent German study (collating evidence from three sources 1) a national seroprevalence study (the SARSCoV-2 KIDS study), 2) the German statutory notification system and 3) a nationwide registry on children and adolescents hospitalized with either SARS-CoV-2 or Pediatric Inflammatory Multisystem Syndrome (PIMS-TS)) reported that there were zero (0) deaths in children 5 to 18 years old across the period of study.

Governments and public health officials have driven this pandemic of fear and propaganda. But parents willing to assess this purely from a benefit versus risk position might ask themselves: ‘If my child has little if any risk, near zero risk of severe sequelae or death, and thus no benefit from the vaccine, yet there could be potential harms and as yet unknown harms from the vaccine (as already reported in adults who have received the vaccines), then why would I subject my child to such a vaccine?

Because the life of your child (or yourself) is a price the purveyors of this genocide are entirely willing to pay in exchange for a nice, fat paycheck.

Comport yourselves accordingly.

Study: Natural Immunity Is 97 Percent Effective Against Severe COVID After 14 Months

Authors: Susan Berry, PhD | Star News Jul 15, 2022

A study has found that natural immunity following COVID infection provides protection against severe illness that is superior to that imparted by the COVID vaccines.

In a preprint article published at MedRxiv, Qatar researchers revealed they found people who survived COVID-19 infection, and were not vaccinated, had outstanding protection against severe COVID disease or death from COVID.

“Effectiveness of primary infection against severe, critical, or fatal COVID-19 reinfection was 97.3% … irrespective of the variant of primary infection or reinfection, and with no evidence for waning,” the researchers noted. “Similar results were found in sub-group analyses for those ≥50 years of age.”

The study, which was conducted on the total population of Qatar, set out to answer three questions:

  • 1) When infected with a pre-Omicron variant, how long does protection persist against reinfection with pre-Omicron variants?
  • 2) When infected with a pre-Omicron variant, how long does protection persist against reinfection with an Omicron subvariant?
  • 3) When infected with any variant, how long does protection persist against severe, critical, or fatal COVID-19?

“Despite waning protection against reinfection, strikingly, there was no evidence for waning of protection against severe COVID-19 at reinfection,” the researchers found. “This remained ∼100%, even 14 months after the primary infection, with no appreciable effect for Omicron immune evasion in reducing it.”

Just days after the release of the study, White House COVID-19 Advisor Dr. Anthony Fauci admitted it is “clear from the data” the COVID vaccines government health officials have been pushing do not actually work well in preventing the infection.

“One of the things that’s clear from the data,” Fauci told Fox News host Neil Cavuto of Your World Tuesdayis that the vaccines, “because of the high degree of transmissibility of this virus – don’t protect overly well, as it were, against infection.”

But Fauci then quickly moved on from his admission to assert the vaccines still “protect quite well against severe disease leading to hospitalization and death”:

And I believe that’s the reason, Neil, why at my age, being vaccinated and boosted, even though it didn’t protect me against infection, I feel confident that it made a major role in protecting me from progressing to severe disease. And that’s very likely why I had a relatively mild course.

“So, my message to people who seem confused because people who are vaccinated get infected – the answer is if you weren’t vaccinated, the likelihood [is] you would have had [a] more severe course than you did have when you were vaccinated,” he said.

Fauci insisted “we’re certainly not over” the pandemic, and asserted many Americans are not making use of the “available interventions,” namely, the COVID vaccines:

Let me give you an example. 67% of the people in this country are vaccinated. We rank very low among developed and developing nations in the proportion that are vaccinated of those who were vaccinated. Only about half of them have gotten their first boost. Again, we’ve got to do better than that. We’re giving the virus the opportunity to continue to spread in our community. And if we do simple things, which are not disruptive in any major way, vaccination, boosting, testing, for example, if you’re going to go to a function, you want to get tested to make sure you’re negative so that if you are infected and you have minimal symptoms, you don’t spread it.

“Those are relatively easy things to do, Neil, and yet we’re not doing enough of it,” Fauci complained.

The confusing narrative is addressed in a new soon-to-be-released film.

Vaccine Choice Canada provides links to several trailers to Uninformed Consent, a documentary that investigates the COVID-19 narrative people continue to hear from government officials in many countries.

The exclusive worldwide premiere of Uninformed Consent, will take place one night only on July 23. Viewers will also have the opportunity to participate in an interactive Q & A with the creators, producers, and doctors behind the documentary.

“This film explores our recent loss of human rights while weaving in the devastating impact of mandates and the deeply powerful story of one man’s loss,” Vaccine Choice Canada writes. “Hear the truth from doctors and scientists unafraid to stand up against Big Pharma and the Elite Class who profit from these mandates

New Study Contradicts ‘Experts’ – Shows Unvaccinated Adults Found “No increase in Myocarditis and Pericarditis” Following COVID Infection

Authors:  Jim Hoft July 8, 2022 Gateway Pundit

A new study from Israel reveals that there was “no increase in the incidence of myocarditis and pericarditis” in unvaccinated adults who had COVID-19 infection.

This contradicts the findings of earlier studies that suggested there may be a connection between cardiac inflammation and coronavirus infections.

In a study published in the Journal of Clinical Medicine, the researchers concluded that there is “no increase in the incidence of myocarditis and pericarditis in COVID-19 recovered patients compared to uninfected matched controls.”

“Myocarditis and pericarditis are potential post-acute cardiac sequelae of COVID-19 infection, arising from adaptive immune responses,” the study stated. “We aimed to study the incidence of post-acute COVID-19 myocarditis and pericarditis.”

A total of 787,968 Clalit Health Services adult members were included in the study between March 2020 and January 2021. Out of that total, 196,992 adults were found to be infected with the COVID-19 virus (16,632 adults with previous vaccination were excluded from the group).

The control cohort of 590,976 adults with no Covid were age- and sex-matched, according to the study (5 adults with previous vaccination were excluded from the group).

“Nine post-COVID-19 patients developed myocarditis (0.0046%), and eleven patients were diagnosed with pericarditis (0.0056%). In the control cohort, 27 patients had myocarditis (0.0046%) and 52 had pericarditis (0.0088%),” the study stated.

“In the current large population study of subjects, who were not vaccinated against SARS-CoV-2, we observed no increase in the incidence of myocarditis or pericarditis from day 10 after positive SARS-CoV-2.”

The researchers went on and stated, “Multivariable analysis did show male sex as associated with a higher risk of developing myocarditis or pericarditis, regardless of previous COVID-19 infection.”

Delta reinfection risk low among unvaccinated children

But scientists warn that the findings do not mean that children should not be vaccinated against COVID-19.

Authors: Heidi Ledford July 4, 2022 NATURE

Children and adolescents who had not been vaccinated against COVID-19 mounted a long-lasting immune response to infection with the Delta variant of the coronavirus SARS-CoV-2, according to a large study of Israeli health records1. The study, which has been published as a preprint on medRxiv, has not yet been peer reviewed.

A year and a half after an infection, the resulting immune response was still about 80% effective at preventing reinfection, the study found. But it isn’t clear how the results will translate to infections by coronavirus variants of the Omicron lineage, which is now dominant in many countries. “There is a much less-robust immune response to Omicron among previously infected and/or vaccinated individuals,” says Yvonne Maldonado, chief of paediatric infectious diseases at Stanford School of Medicine in California. “Such immune responses are also significantly less durable.”

Even so, the study — which includes data from about 300,000 children and adolescents — is a welcome addition to the relatively small pool of knowledge about immune responses to SARS-CoV-2 in children, says paediatrician Nigel Crawford at the Murdoch Children’s Research Institute in Melbourne, Australia, who studies vaccinology. “They’re a group for which we haven’t seen a huge amount of data to date,” he says.

When Delta dominated

The study’s authors collected data on coronavirus infections from Maccabi Healthcare Services, an Israeli health-insurance plan. They focused on the risk of infection from 1 July to 13 December 2021, when the Delta variant was dominant in Israel.

The team found that unvaccinated children and adolescents were 89% less likely to be infected with SARS-CoV-2 3–6 months after their first infection than were children who had not previously been infected. For the 12–18 age group, this protection against reinfection dropped to 82.5% from 9 months to a year after infection and remained at around that level until up to 18 months post-infection.

Children aged 5–11, however, maintained the same level of protection. That, says Crawford, could fit with observations that young children often experience milder COVID-19 than do adolescents and adults.

The study authors are now working to collect data on Omicron infections, but that analysis will be more difficult because many people in Israel switched from PCR tests to at-home rapid antigen testing in December 2021. This means that fewer positive test results have since been reported in electronic health records.

Overall, the study design is robust, says clinical data scientist Hossein Estiri at Harvard Medical School in Boston, Massachusetts. He notes that some Twitter users have picked up on the preprint and are touting it as evidence that children who have had SARS-CoV-2 infections do not need to be vaccinated. But Estiri says it’s not clear from the study how well protection from natural infection stacks up to that from vaccines, because the researchers did not include a head-to-head comparison. “This study doesn’t say that those children don’t need to be vaccinated.”

Don’t discount vaccines

And because severe COVID-19 is rare in children, the study could not make strong conclusions about protection from serious illness and hospitalization. “We know that a lot of vaccine efficacy is against severe disease,” he says.

In addition, Crawford notes that people who have both been vaccinated and had a SARS-CoV-2 infection often experience a super-charged immune response compared with those who have had only a vaccine or infection. “You wouldn’t want to rely purely on infection alone for immunity,” he says. “We have no idea what the next wave will bring.”