Coronavirus wave this fall could infect 100 million, administration warns

Authors: Yasmeen Abutaleb, Joel Achenbach May 6, 2022 The Washington Post

The Biden administration is warning the United States could see 100 million coronavirus infections and a potentially significant wave of deaths this fall and winter, driven by new omicron subvariants that have shown a remarkable ability to escape immunity.

The projection, made Friday by a senior administration official during a background briefing as the nation approaches a covid death toll of 1 million, is part of a broader push to boost the nation’s readiness and persuade lawmakers to appropriate billions of dollars to purchase a new tranche of vaccines, tests and therapeutics.

In forecasting 100 million potential infections during a cold-weather wave later this year and early next, the official did not present new data or make a formal projection. Instead, he described the fall and winter wave as a scenario based on a range of outside models of the pandemic. Those projections assume that omicron and its subvariants will continue to dominate community spread, and there will not be a dramatically different strain of the virus, the official said, acknowledging the pandemic’s course could be altered by many factors.

Several experts agreed that a major wave this fall and winter is possible given waning immunity from vaccines and infections, loosened restrictions and the rise of variants better able to escape immune protections.

Many have warned that the return to more relaxed behaviors, from going maskless to participating in crowded indoor social gatherings, would lead to more infections. The seven-day national average of new infections more than doubled from 29,312 on March 30 to nearly 71,000 Friday, a little more than five weeks later.

“What they’re saying seems reasonable — it’s on the pessimistic side of what we projected in the covid-19 scenario modeling run,” said Justin Lessler, an epidemiologist at University of North Carolina Gillings School of Global Public Health. “It’s always hard to predict the future when it comes to covid, but I think we’re at a point now where it’s even harder than normal. Because there’s so much sensitivity, in terms of these long-term trends, to things we don’t understand exactly about the virus and about [human] behavior,” Lessler said.

Another modeler, epidemiologist Ali Mokdad of the University of Washington’s Institute for Health Metrics and Evaluation, said in an email Friday that a winter surge is likely. His organization, which has made long-term forecasts despite the many uncertainties, just produced a new forecast that shows a modest bump in cases through the end of May and then a decline until the arrival of winter.

New Omicron BA.4 and BA.5 Sublineages May Evade Vaccines, Natural Immunity. What Experts Say

Authors: Mint Newsletters April 29, 2022

  • The BA.4 and BA.5 sublineages appear to be more infectious than the earlier BA.2 lineage
  • The sub-lineages have been detected in seven of South Africa’s nine provinces and 20 countries worldwide

New omicron sublineages, discovered by South African scientists this month, are likely able to evade vaccines and natural immunity from prior infections, the head of gene sequencing units that produced a study on the strains said, according to Bloomberg report.

It is important to note that the BA.4 and BA.5 sublineages appear to be more infectious than the earlier BA.2 lineage, which itself was more infectious than the original omicron variant, Tulio de Oliveira, the head of the institutes, said.

Omicron sublineages  mutated to evade immunity

  • As almost all South Africans either having been vaccinated against the coronavirus or having had a prior infection the current surge in cases means that the strains are more likely to be capable of evading the body’s defenses rather than simply being more transmissible, de Oliveira said.
  • There are “mutations in the lineages that allow the virus to evade immunity,” he said in a response to queries. “We expect that it can cause reinfections and it can break through some vaccines, because that’s the only way something can grow in South Africa where we estimate that more than 90% of the population has a level of immune protection.”
  • South Africa is seen as a key harbinger of how the omicron variant and its sublineages are likely to play out in the rest of the world. South African and Botswanan scientists discovered omicron in November and South Africa was the first country to experience a major surge of infections as a result of the variant.
  • The new sublineages account for about 70% of new coronavirus cases in South Africa, de Oliveira said in a series of Twitter postings. 
  • “Our main scenario for Omicron BA.4 and BA.5 is that it increases infections but that does not translate into large hospitalizations and deaths,” he said.
  • So far, the sublineages have been detected in seven of South Africa’s nine provinces and 20 countries worldwide. 

Two COVID Variants Just Combined Into a ‘Frankenstein’ Virus

Authors: David Axe Published  Apr. 07, 2022 4:49AM ET 

The first subvariant of Omicron, the latest major variant of the novel coronavirus, was bad. BA.1 drove record cases and hospitalizations in many countries starting last fall.

The second subvariant, BA.2, was worse in some countries—setting new records for daily cases across China and parts of Europe.

Now BA.1 and BA.2 have combined to create a third subvariant. XE, as it’s known, is a “recombinant”—the product of two viruses interacting “Frankenstein”-style in a single host.

With its long list of mutations, XE could be the most contagious form of the coronavirus yet. “From the WHO reports, it does appear to have a bit more of an edge in terms of transmissibility,” Stephanie James, the head of a COVID testing lab at Regis University in Colorado, told The Daily Beast.

But don’t panic just yet. The same mix of subvariants that producedXE might also protectus from it. Coming so quickly after the surge of BA.1 and BA.2 cases, XE is on track to hit a wall of natural immunity—the antibodies left over from past infection in hundreds of millions of people.

Those natural antibodies, plus the additional protection afforded by the various COVID vaccines, could blunt XE’s impact. For that reason, many experts worry less about XE and more about whatever variant or subvariant might come after XE.

And rest assured, that future subvariant is coming. “COVID-19 continues,” Eric Bortz, a University of Alaska-Anchorage virologist and public health expert, told The Daily Beast.

Testers first detected XE in the United Kingdom back in mid-January. Six weeks later U.K. authorities had identified 600 XE infections. Those cases are a proverbial drop in the bucket in light of the millions of BA.1 and BA.2 cases the U.K. has tallied in the past three months. But XE stood out.

According to the World Health Organization, XE is 10 percent more contagious than BA.2, which itself is up to 80 percent more contagious than BA.1, a subvariant epidemiologists described as the most transmissible respiratory virus they’d ever seen when it first appeared in South Africa back in November.

There’s a lot of uncertainty about XE. The WHO stressed that its own finding about the subvariant “requires further confirmation.” But given what we think we know, it seems XE evolved in someone with overlapping BA.1 and BA.2 infections, when two separate but related viruses swapped genetic material.

“We don’t have a roadmap.”

XE isn’t the first COVID recombinant—there have been at least two others, including the so-called “Deltacron” subvariant that sprang from simultaneous Delta and BA.1 infections. But with two highly contagious parent viruses, XE stands a chance of being the fastest-spreading recombinant. Health officials have also detected XE in Thailand.

The subvariant hasn’t shown up in U.S. tests yet. But that doesn’t mean it hasn’t reached U.S. shores. “It might not be detected by the standard analysis pipeline,” Rob Knight, the head of a genetic-computation lab at the University of California, San Diego, told The Daily Beast. Major new forms of SARS-CoV-2 can require tweaks to testing methods.

XE is a nasty bug, owing to potentially dozens of mutations to its spike protein, the part of the virus that helps it grab onto and infect our cells. And it’s a strong reminder that the pandemic isn’t over. Even with widespread natural immunity and highly effective and safe vaccines, SARS-CoV-2 keeps finding pockets of unprotected people—and opportunities to evolve.

But it’s not 2020 anymore. The novel coronavirus has changed, but so have we. Each successive wave of infections—Alpha then Delta then both major forms of Omicron—has seeded the population with natural antibodies that offer strong, albeit temporary, protection against the worst effects of future infection by a related form of the virus.

The leading vaccines, meanwhile, have stood up to each new variant and subvariant, especially when you add one or two booster doses.

Even as more and more countries fully reopen schools, businesses and borders, the peak death rate from a COVID wave keeps dropping in a lot of countries. Cases might go up as some new subvariant outcompetes an earlier subvariant and becomes dominant. But deaths don’t necessarily increase in the same proportion—a phenomenon epidemiologists call “decoupling.”

Decoupling is partially a function of the time between waves. Natural antibodies from past infection can begin fading after three months. But if two variants or subvariants strike within a few months of each other, the second strain collides with the immunity left over from the firs strain—especially if the strains are related. Meanwhile, the second strain produces antibodies that could mitigate the worst outcomes of the next strain, assuming it arrives fast enough.

That’s why Omicron has infected more people than the previous variant, Delta, but has killed fewer. And why many experts consider XE less frightening than BA.2 or BA.1. “Immune responses to XE should be similar to that of Omicron,” Bortz said. “Those with prior Omicron infection and vaccination are going to be mostly immune.”

By the same token, a big gap between separate variants—that is, a long reprieve from COVID—might actually be more dangerous to a population than back-to-back-to-back waves of related strains.

There’s another risk. We were lucky with the major variants and subvariants before XE, in that the leading vaccines worked really well against all of them. Experts are cautiously optimistic that the jabs hold up against XE, too. “XE is, as you say, supposed to be more contagious than BA.2 [or] BA.1,” Edwin Michael, an epidemiologist at the Center for Global Health Infectious Disease Research at the University of South Florida, told The Daily Beast, “but it seems not to be more severe or immune-evasive.”

But if some new variant, perhaps even a recombinant of XE and some other strain, eventually mutates in a way that helps it evade the vaccines and arrives three months or longer after the previous surge in cases, we could be in trouble.

“While thus far mutants that are more transmissible have emerged and spread, there is also the possibility of one that is both more transmissible and immune-evasive to emerge,” Michael said. In that case, neither of our approaches to building population-level immunity–vaccines and natural antibodies—would be able to prevent a devastating spike in deaths.

New Mutant “XE” Omicron Variant May Be The Most Transmissible Version Of Covid Yet, According To WHO

Authors:  Tom Tapp March 31, 2022 4:46pm Deadline Breaking News Alerts

The CDC announced this week that the BA.2 Omicron variant, which is reportedly 30% more transmissible than the original BA.1 Omicron strain — has become dominant among new cases sequenced in the United States. That’s a startling rise for a variant that was less than 1% of all sequences as recently as January. But, just as Americans are hearing about BA.2, there’s already a newer, even more transmissible variant on the rise.

There are actually three new variants that have been given designations. According to a recently-released report from the UK Health Services Agency, the two being called XD and XF are combinations of Delta and BA.1, or so-called “Deltacron” strains, which have been talked about for months but made no significant inroads in any country.

XD is present in several European countries, but has not been detected in the UK, according to the report. XF caused a small cluster in the UK but has not been detected there since February 15. The variant of greater concern, it seems, is the one dubbed XE.

Like the other two new arrivals, XE is a recombinant strain, meaning it is made up of two previously-distinct variants. But it is not a Deltacron mix. XE is actually made up of the original Omicron (BA.1) and the newer Omicron (BA.2) which has taken over in the U.S.

Omicron BA.2 Variant Now Dominant In U.S.; Hitting Northeast Hard

The World Health Organization issued a report yesterday with some preliminary findings about XE.

“The XE recombinant was first detected in the United Kingdom on 19 January and >600 sequences have been reported and confirmed since,” reads the WHO document. “Early-day estimates indicate a community growth rate advantage of ~10% as compared to BA.2, however this finding requires further confirmation.”

Further confirmation is getting more difficult by the day, according to WHO, which registered concern this week at what it calls “the recent significant reduction in SARS-CoV-2 testing by several Member States. Data are becoming progressively less representative, less timely, and less robust. This inhibits our collective ability to track where the virus is, how it is spreading and how it is evolving: information and analyses that remain critical to effectively end the acute phase of the pandemic.”

Covid BA.2 Omicron Variant Likely Now Accounts For Majority Of New Cases In Los Angeles

Last week’s briefing from the UK Health Services Agency reinforces some of the WHO report’s assertions and urges caution about jumping to conclusions. One difference between the two documents is that the WHO data and analysis seems to be more recent.

From the UK HSA briefing:

XE shows evidence of community transmission within England, although it is currently less >1% of total sequenced cases. Early growth rates for XE were not significantly different from BA.2, but using the most recent data up to 16 March 2022, XE has a growth rate 9.8% above that of BA.2. As this estimate has not remained consistent as new data have been added, it cannot yet be interpreted as an estimate of growth advantage for the recombinant. Numbers were too small for the XE recombinant to be analysed by region.

To be clear, XE only accounts for a tiny fraction of cases worldwide. That may change, given that XE is thought to be about 10% more transmissible than the already more-transmissible BA.2. That means it may be roughly 43% more transmissible than the original Omicron that savaged the globe last winter.

But a new wave of infections from the now-dominant BA.2 has not materialized, even as restrictions have been eased. So hopefully the trend with XE, should it out-compete BA.2, will be similar. Only time — and good surveillance — will tell.

Study evaluates mutation-induced SARS-CoV-2 spike protein fold stability

Authors: Tarun Sai Lomte Mar 24 2022 BioRxiv

In a recent study posted to the bioRxiv* preprint server, researchers evaluated the stability and expression of mutations in the spike (S) protein of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2).

Study: Stability and expression of SARS-CoV-2 spike-protein mutations. Image Credit: Design_Cells/Shutterstock
Study: Stability and expression of SARS-CoV-2 spike-protein mutations. Image Credit: Design_Cells/Shutterstock

Background

The coronavirus disease 2019 (COVID-19) pandemic caused by SARS-CoV-2 has resulted in extensive research into S protein. Its evolution introduces several variations in the protein surface that negatively affect the efficiency of antibodies elicited by vaccines. The virus requires the S protein for host cell entry, and vaccines against SARS-CoV-2 are designed with S protein as the target. The prominent presence of anti-S antibodies in a population might induce selection pressure in the virus to modify its S protein structure to evade vaccine- or infection-induced antibodies. Such antigenic drifts drive the emergence of novel variants with persistent challenges. Moreover, understanding the effects of evolution requires knowledge of the protein’s structure.

The study

The present study assessed whether protein expression levels might serve as a proxy for fold stability. The principal objective was to examine whether expression and ACE2- receptor-binding domain (RBD) binding measured experimentally could relate to the thermodynamic stability of the RBD mutants.

Expression data on the effect of RBD point mutations on ACE2 binding and yeast expression were previously reported. The impact of mutations on expression levels was calculated as the log mean fluorescence intensity difference relative to wildtype. The effect on ACE2 binding was determined from the apparent dissociation constants difference relative to the wildtype.

The free energy change of protein folding (ΔΔG­) was computed using three in silico methods: Deep DDG, SimBa-IB, and mutation cutoff scanning matrix (mCSM) protein stability. In its apostate determined by cryo-electron microscopy, eight experimental structures of S protein were obtained from the protein data bank (PDB). SimBa-IB program calculated the mutated sites’ relative solvent accessible surface area (RSA), and the ΔΔG­ and RSA values were reported as average values.

Results

The authors observed that the effect of mutations on ACE2 binding and expression was strongly correlated. Moreover, the expression levels could affect binding constants even at the same level of ACE2 affinity. The free energy or stability changes were predicted and later compared with binding and expression changes observed experimentally using the three computational methods. The stability effects, as computed, observed that mutations in the 388 – 390 stretch had an impact on the stability of the protein.

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The effect of the mutation at each site was calculated as the mean absolute effect of 19 mutations as a surrogate of tolerance at each mutant site. Expression-affecting mutations were mainly inside the core RBD subdomain, particularly the central beta-sheet with the alpha-helices flanking it. The mutations affecting ACE2 binding were primarily observed in the ACE2 binding subdomain or the central beta-sheet.

The mutations affecting the stability of the protein were observed in the structured core of the RBD. RBD mutations affected its expression, binding, and stability differentially, although some overlap between protein expression and stability was observed. Next, the authors quantified the relationship by plotting predicted ΔΔG­ values against the changes observed in the expression and ACE2 binding of RBD for all mutations and each experimental structure with three methods.

RBD expression and ΔΔG­ for individual structures were correlated with varying magnitudes based on the type of prediction. Similarly, ACE2 binding and ΔΔG­ were associated to varying degrees based on the prediction method; nonetheless, the correlations (for binding) were weaker than that for expression, and the observed correlations were statistically significant.

The effects of mutations on protein stability correlated well with ACE2 binding and protein expression, better with the Deep DDG prediction. The expression and binding results were skewed, over-representing data points between 0 and -1. Therefore, the data were grouped into bins; each bin’s mean binding and expression effect and predicted stability energy values were calculated. The research team noted an increase of correlations upon binning, and it is noteworthy that the computational data correlated well with the binned experimental data.

Lastly, the study reported that mutations deeply buried in the protein core have a more significant effect on protein stability. Similar was the case observed for RBD, in which mutations in the core were less tolerated than those on or near the surface. A moderate correlation was observed when the effect of mutations on the binding and expression was studied regarding the surface exposure of RBD residues with a noticeable tolerance overall at sites with increased solvent exposure.

Conclusions

The current study’s findings demonstrated that the computed protein stability effects were significantly correlated with expression levels for all 48 comparative investigations, but to a certain extent with ACE2 binding. Further, there was a correlation between predicted stability changes and surface exposure.

Therefore, experimental mutational properties could be predicted, at least partly, and the phenotypes might correlate because of underlying correlators such as amino acid properties, site solvent exposure, and codon usage. Such correlations impact the S protein’s mutability, affecting phenotype tradeoffs and viral evolution.

STUDY: PFIZER VACCINE FUSES WITH HUMAN DNA IN THE LIVER: CAUTION

Authors: Jules Gomes  •  ChurchMilitant.com  •  March 2, 2022 

The mRNA from Pfizer’s COVID-19 vaccine converts into DNA within six hours of entering the body’s liver cells according to a groundbreaking study by Swedish researchers at Lund University. 

The explosive peer-reviewed research demolishes countless assertions by the “fact-checkers” and global health organizations.

Fact-Checkers Caught

UNICEF, for example, asserted that “mRNA vaccines are not live viral vaccines and do not interfere with human DNA.”

The Bill Gates–funded Global Alliance for Vaccines and Immunizations similarly claimed that “mRNA isn’t the same as DNA, and it can’t combine with our DNA to change our genetic code,” further stating that “there is no reason to think that they [COVID vaccines] will have a lasting effect on our biology.” 

“The genetic material delivered by mRNA vaccines never enters the nucleus of your cells — which is where your DNA is kept,” the U.S. Centers for Disease Control and Prevention categorically states on its webpage titled “Myths and Facts About COVID-19 Vaccines.”

UNICEF fact-checkers also quoted Prof. Jeffrey Almond of Oxford University, who said, “Injecting RNA into someone does nothing to human-cell DNA.” 

However, the new study, published Friday in the journal Current Issues in Molecular Biology, shows that the Pfizer COVID-19 mRNA vaccine “is able to enter the human liver cell line Huh7” and that “mRNA is reverse-transcribed intracellularly into DNA in as fast as six hours.”

The process of converting RNA to DNA is called “reverse transcription,” since it overturns the previous dogma of molecular biology — which held that such conversion was a one-way process (DNA into either DNA or RNA). 

If there is a viral genomic integration from these vaccines, there is the potential risk of subsequent autoimmune disease and cancer,” scientist Dr. Alan Moy, founder of the John Paul II Medical Research Institute, told Church Militant. 

“The implication of this data would suggest that the assertion that mRNA vaccines do not cause viral nucleic-acid integration is incorrect,” Moy emphasized, adding, “Did Pfizer and Moderna perform preclinical studies to evaluate this possibility? Did the FDA require these studies from Pfizer and Moderna in the first place?”

“This information is relevant from the recent revelation that the FDA and Pfizer have tried to delay the research findings to the public over 75 years,” Dr. Moy said, after consulting with peers on the paper titled “Intracellular Reverse Transcription of Pfizer BioNTech COVID-19 mRNA Vaccine BNT162b2 In Vitro in Human Liver Cell Line.”

Dr. Peter McCullough, the world’s leading expert on COVID-19, said that the discovery has “enormous implications of permanent chromosomal change and long-term constitutive spike synthesis driving the pathogenesis of a whole new genre of chronic disease.

“‘Injecting RNA does nothing to human-cell DNA.’

In February, McCullough, a widely published internist, cardiologist and epidemiologist, warned the Vatican to end its vaccine advocacy and mandates and “immediately apologize” for the “grievous error” of “violating a critical code of bioethics,” Church Militant reported.

Reminding Pope Francis that life is a gift, McCullough accused the pontiff of “giving a gift of the loss of life” and speculated that the Vatican “will have to account for potentially hundreds of thousands of lives lost due to the vaccine.”

The new study vindicates Church Militant’s publication of two academic articles by Dr. Massimo Citro Della Riva (with an introduction by Abp. Carlo Maria Viganò). The articles responded to the polemic against Viganò published in Corrispondenza Romana by pediatrician Gwyneth A. Spaeder. 

In her diatribe against Viganò, Spaeder, a senior Catholic doctor whose family profits from the pharmaceutical industry and has links to vaccine oligarchs, asserted:

Basic biology teaches us that messenger RNA (or mRNA) is a molecule that tells the body how to make proteins. Once the protein has been produced, the mRNA is broken down and exits the body with other waste products. This process occurs only in one direction. 

There is never a possibility of modification of the vaccine recipient’s genome, since the process that involves transcription and translation, by which proteins are produced, proceeds forward from DNA to RNA to protein. It can’t work the other way around.

Citing peer-reviewed research from 2020, Dr. Citro noted that “the reverse transcription of viral RNA [into DNA] is also possible (as occurs with other RNA viruses), which is then capable of triggering long-term chronic diseases.”

“The reverse transcription of the vaccine mRNA is, for now, only hypothetical — just as it is for the DNA of the adenovirus vector. It is, however, plausible due to the presence of retrotransposons,” Riva noted, adding “I would not be so sure that vaccine mRNA cannot reverse transcribe itself into our DNA. “‘There is no reason to think they will have a lasting effect on our biology.’

Riva’s hypothesis has now been confirmed by researchers — who have shown in vitro or inside a petri dish how the Pfizer mRNA vaccine is converted (on a liver cell line) into human DNA. 

Over the last year, fact-checkers and health regulators quoted pro-vaccination scientists to attack the claim of reverse transcription as a “conspiracy theory.” However, earlier studies did preempt the possibility of the risk of the Pfizer vaccine’s mRNA hacking into our DNA.

“A 2021 study by the Whitehead Institute, the National Cancer Center and MIT reported in the Proceedings of the National Academy of Sciences journal that the RNA from the COVID virus resulted in genetic integration in cultured human cells and in patients who were infected with COVID,” Dr. Moy told Church Militant.

“This background information led to the impetus for the more recent report to test whether the mRNA vaccine from Pfizer could similarly result in integration of the mRNA gene therapy into the human genome,” Moy explained.

COVID-19 Causes Genetic Changes that Create Long-Haul COVID-19 Symptoms, Researchers Find

Gene changes caused by SARS-CoV-2 spike proteins provide a potential answer for what causes long-haul COVID-19, Texas researchers find 

As COVID-19 vaccines become widely available and cases of COVID-19 in the United States begin to drop, the medical community is beginning to focus more on the long-term effects of COVID-19. Sometimes called “long-haul COVID-19,” the varied and long-term effects that a SARS-CoV-2 infection can create are just starting to be understood (See Long-Haul COVID-19 Emerges as a Concern, Potentially Increasing Need for More COVID-19 Antibody Testing).

New research out of Texas Tech University provides a possible explanation for why these symptoms occur. Led by Sharilyn Almodovar, PhD, at the Texas Tech University Health Sciences Center, researchers found that exposing airway cells to the spike protein of the SARS-CoV-2 virus caused genetic changes.

Potential Impact of Exposure to SARS-CoV-2 Spike Protein Alone

“We found that exposure to the SARS-CoV-2 spike protein alone was enough to change baseline gene expression in airway cells,” said Nicholas Evans, a master’s student at the Texas Tech University Health Sciences Center and one of the researchers involved in the study. “This suggests that symptoms seen in patients may initially result from the spike protein interacting with the cells directly.”

This finding that changes in gene expression occur with exposure to the spike protein of SARS-CoV-2 provides a possible explanation of what causes the mysterious, unexplainable symptoms of long-haul COVID-19 that vary from patient to patient. Changes in gene expression can have different effects on different patients, depending on their genetic makeup and their exposure to the virus.

“Our work helps to elucidate changes occurring in patients on the genetic level, which could eventually provide insight into which treatments would work best for specific patients,” says Evans.

Research May Eventually Lead to Clues About Unexplained Illnesses

While the scientific community’s understanding of long-haul COVID-19 is still quite nascent, Almodovar’s team’s findings are one of the first findings in studying long-haul COVID-19 that provide a good explanation for what could potentially be the cause of these symptoms. This new research will undoubtedly lead to further research examining more in-depth which genes are affected and to what extent this impacts different individuals. These findings may also have implications for other previously unexplained illnesses, such as the long-term effects of Lyme disease.

One interesting result of the these findings is that they may explain why some people with long-haul COVID-19 symptoms have relief of their symptoms after getting vaccinated against COVID-19. Authorized COVID-19 vaccines are designed to use human cells to manufacture spike proteins and stimulate immunity. The finding that the spike protein of SARS-CoV-2 may cause long-haul COVID-19 symptoms could explain how vaccines that artificially create a form of the spike protein could cause these symptoms to change.

COVID-19 Vaccine Questions, Further Studies

Another question that this finding raises is if COVID-19 vaccines, which artificially create SARS-CoV-2 spike proteins, could also stimulate changes in gene expression, causing symptoms that mimic long-haul COVID-19 symptoms.

While Almodovar’s team’s research is only the beginning of study into the possibility of gene expression changes driving long-haul COVID-19 symptoms, it may become a foundational concept in this area of research.

Understanding the implications and effects of long-haul COVID-19 will be important for clinical laboratories that provide COVID-19 antibody testing. As the medical community’s understanding of long-haul COVID-19 increases, it may not only increase the demand for serology tests but may also create a demand for other related tests, particularly immunologically-related tests.

Clinical laboratories will benefit from keeping abreast of long-haul COVID-19 related research and being aware of developments that affect how testing will support clinical treatments and outcomes.

Gene changes and long-haul COVID

Authors: Nancy D. Lamontagne April 30, 2021

Airway cells exposed to SARS-CoV-2 spike protein exhibited persisting changes in gene expression

Results from a new cell study suggest that the SARS-CoV-2 spike protein can bring about long-term gene expression changes. The findings could help explain why some COVID-19 patients—referred to as COVID long-haulers—experience symptoms such as shortness of breath and dizziness long after clearing the infection.

SARS-CoV-2, the virus that causes COVID-19, is covered in tiny spike proteins. During infection, the spike proteins bind with receptors on cells in our body, starting a process that allows the virus to release its genetic material into the inside of the healthy cell. COURTESY OF JULIE A. FORREST Research team members included undergraduate student Ethan Salazar, principal investigator Sharilyn Almodovar and master’s student Nicholas Evans.

“We found that exposure to the SARS-CoV-2 spike protein alone was enough to change baseline gene expression in airway cells,” said Nicholas Evans, a master’s student in the laboratory of Sharilyn Almodovar, PhD, at the Texas Tech University Health Sciences Center. “This suggests that symptoms seen in patients may initially result from the spike protein interacting with the cells directly.”

Evans will present the research at the American Society for Biochemistry and Molecular Biology annual meeting during the virtual Experimental Biology 2021 meeting, to be held April 27–30.

Culturing human airway cells requires specific conditions that allow cells to mature into the differentiated cells that would be found in the airway. The researchers optimized a previously developed culturing approach known as the air–liquid interface technique so that it would more closely simulate the physiological conditions found in the lung airway. This involved exposing cells to air and then giving them time to mature into airway cells.

The researchers found that cultured human airway cells exposed to both low and high concentrations of purified spike protein showed differences in gene expression that remained even after the cells recovered from the exposure. The top genes included ones related to inflammatory response.

“Our work helps to elucidate changes occurring in patients on the genetic level, which could eventually provide insight into which treatments would work best for specific patients,” said Evans.

The researchers also compared their cultured human airway cells to studies from others where cells were collected from patients with COVID-19 infection. They were able to confirm that the optimized cell culture approach reflected what occurs in patients, making it useful for future translational studies. They plan to use the new approach to better understand how long the genetic changes last and the potential long-term consequences of these changes in relation to long-haul COVID-19 cases.

WHO monitoring new coronavirus variant named ‘Mu’

Issued on: 01/09/2021 – 07:25

The World Health Organization has said it is monitoring a new coronavirus variant known as “Mu”, which was first identified in Colombia in January 2021.

Mu, known scientifically as B.1.621, has been classified as a “variant of interest”, the global health body said Tuesday in its weekly pandemic bulletin.

The WHO said the variant has mutations that indicate a risk of resistance to vaccines and stressed that further studies were needed to better understand it.

“The Mu variant has a constellation of mutations that indicate potential properties of immune escape,” the bulletin said.

There is widespread concern over the emergence of new virus mutations as infection rates are ticking up globally again, with the highly transmissible Delta variant taking hold – especially among the unvaccinated – and in regions where anti-virus measures have been relaxed.

All viruses, including SARS-CoV-2 that causes Covid-19, mutate over time and most mutations have little or no effect on the properties of the virus.

But certain mutations can impact the properties of a virus and influence how easily it spreads, the severity of the disease it causes, and its resistance to vaccines, drugs and other countermeasures.

The WHO currently identifies four Covid-19 variants of concern, including Alpha, which is present in 193 countries, and Delta, present in 170 countries.

Five variants, including Mu, are to be monitored.

After being detected in Colombia, Mu has since been reported in other South American countries and in Europe.

The WHO said its global prevalence has declined to below 0.1 percent among sequenced cases. In Colombia, however, it is at 39 percent.

New South African COVID-19 strain is the most mutated one yet: report

Authors: By Yaron SteinbuchAugust 30, 2021 10:50am

COVID-19 variant first detected in South Africa could be more infectious than other mutations — and may have the potential of being resistant to vaccines, according to a report.

The C.1.2 strain has been linked to “increased transmissibility” and is said to have mutated the most from the original virus, which first emerged in the Chinese city of Wuhan, the Mirror reported.

The strain has a mutation rate of about 41.8 mutations per year, almost double the global mutation rate seen in any other existing variant of concern, according to experts at South Africa’s National Institute for Communicable Diseases and the KwaZulu-Natal Research Innovation and Sequencing Platform.

The number of C.1.2 genomes in South Africa has risen from 0.2 percent in May to 1.6 percent in June and 2 percent in July, according to scientists, who also have found 14 mutations in nearly 50 percent of the variants that had a C.1.2 sequence.

The C.1.2 strain also has been found in the UK, China, the Democratic Republic of the Congo, Mauritius, New Zealand, Portugal and Switzerland.

The latest South African variant could be capable of evading antibodies and immune systems, researchers said, while noting that additional research is needed.

“We describe and characterize a newly identified SARS-CoV-2 lineage with several spike mutations that is likely to have emerged in a major metropolitan area in South Africa after the first wave of the epidemic, and then to have spread to multiple locations within two neighboring provinces,” the researchers wrote in the report, which was published in the journal Nature.

 “We show that this lineage has rapidly expanded and become dominant in three provinces, at the same time as there has been a rapid resurgence in infections,” they added.

B.1.351, another South African strain found in April, had the potential to “break through” the Pfizer vaccine, scientists have found.

“We found a disproportionately higher rate of the South African variant among people vaccinated with a second dose, compared to the unvaccinated group,” said professor Adi Stern of Tel Aviv University in Israel, the Mirror reported. “This means that the South African variant is able, to some extent, to break through the vaccine’s protection.”

But still, he said the variant “has not spread widely through the population” — and that the UK variant may be “blocking” the spread of the South African strain.

News about the C.1.2 strain, which was discovered in May, comes as the US grapples with a resurgence caused by the Delta variant, which has complicated efforts to return to workplaces and schools.