COVID-19 Variants – BioQuakes

In the United States, there are currently more than 10,374 patients hospitalized per week who tested positive for COVID-19. 15% of these patients are in the ICU (Intensive Care Unit). As of November 4, the test positivity rate is 8.5%. When the test positivity is above 5%, this indicates that transmission is considered uncontrolled.

Due to the fact that many people are using home tests that are not reported through public health or are not testing at all, the official case counts underestimate the actual prevalence of COVID-19.

The dominant variant nationwide currently is HV.1, with 29% of cases, followed by EG.5, with 21.7% of cases and FL.1.5.1, with 9.3% of cases. HV.1 was documented by the Centers for Disease Control and Prevention (CDC) in low numbers during the summer. However, now that the strain has the highest prevalence of any, it claims responsibility for more than a quarter of new coronavirus cases in the U.S. as of late October.

This strain is still a sub-variant of omicron, as is every strain that is in circulation. This strain is a descendant of EG.5, which is the second most common variant in the U.S.

HV.1 is highly infections. The emergence of HV.1 shows how the SARS-CoV-2 virus, which causes COVID-19, is able to mutate and cause new, highly transmissible variants. The symptoms of HV.1 are very similar to those caused by recent variants of omicron.

Omicron S exhibits a heightened dependence on a significantly elevated level of host receptor ACE2 for effective membrane fusion compared to other variants. This characteristic may elucidate its unanticipated cellular tropism. The mutations not only reshape the antigenic configuration of the N-terminal domain of the S protein but also modify the surface of the receptor-binding domain in a manner distinct from other variants. This alteration aligns with its notable resilience against neutralizing antibodies. These findings imply that Omicron S has developed an exceptional capacity to elude host immunity through an abundance of mutations, albeit at the cost of compromising its fusogenic ability.

The Omicron variant of the SARS-CoV-2 virus introduces a distinctive challenge to the immune response system, primarily through mutations in the spike protein. These alterations in the antigenic configuration of the spike protein have raised concerns about the potential impact on the effectiveness of the immune response, particularly with regards to neutralizing antibodies generated from prior infections or vaccinations. The unique genetic makeup of Omicron may allow the virus to partially evade recognition by existing antibodies, potentially leading to breakthrough infections. Moreover, the variant’s influence on cellular immunity, mediated by T cells, is still under investigation, but T cell responses may play a crucial role in controlling infections even if antibody responses are compromised. The evolving nature of the virus underscores the importance of public health measures, including vaccination campaigns and booster shots, to adapt to the changing landscape of the pandemic and reinforce the immune system’s ability to respond to new variants like Omicron. Ongoing research is essential to comprehensively understand the implications of Omicron on the immune response and to inform effective strategies for mitigating its impact on public health.

Omicron stands out with approximately 50 mutations, surpassing the mutation count of any prior SARS-CoV-2 variant. Among these, 32 alterations are within the spike protein, the primary target for most vaccines aiming to neutralize the virus. As of December 2021, numerous mutations in Omicron were novel and distinct from those observed in earlier variants. By April 2022, the variant exhibited 30 amino acid changes, three small deletions, and one small insertion in the spike protein when compared to the original virus. Notably, 15 of these changes were situated in the receptor-binding domain (residues 319–541). As of December 2022, the virus featured additional modifications and deletions in various genomic regions. For instance, three mutations at the furin cleavage site, crucial for its transmission, were identified.

Health officials are not concerned with the latest variant. This is because it appears that HV.1 is very similar to EG.5, also known as “eris.” They are so similar that the World Health Organization (WHO) does not separate the two in its estimates. Globally, Eris is the most prominent strain, accounting for 46% of global cases as of late October, according to the WHO. This estimate also includes cases from HV.1 and another similar strain, HK.5.

HV.1 does not appear to cause more severe illnesses. However, it is expected that it brings the same high transmissibility that eris has. More cases will cause more variants with more mutations to occur.

Dr. Perry N. Halkitis, the dean of Rutgers School of Public Health, says that “the concern about the multitude of mutations is that it is likely and possible that there are versions of the virus that will be more evasive to the immunity that people have.”

However, the fact that HV.1 is so similar to EG.5, the updated coronavirus vaccines are expected to work on the new strain.

However, the shots’ advantages are limited by low uptake so far. Only about 7% of U.S. adults and 2% of children got the new COVID-19 vaccines during the first month it was available, according to national surveys. Despite the rollout being hampered by availability and insurance issues, U.S. health officials say those problems have been mostly resolved.

Surveys also found that almost 38% of adults and parents said that they probably or definitely will not get the shot for themselves or their children.

Hesitancy and vaccine fatigue are surely large parts of the uptake problem. When it comes to COVID-19, there is a general lack of urgency now that vaccines and treatment are widely available.

Halkitis says, “we’ve opened a window of opportunity for people who are resistant to vaccination to begin with to say, ‘Well, it doesn’t look so bad anymore, so I’m just going to bypass it.’ Just like how they react to the flu.”

According to CDC data, COVID-19 weekly hospital admissions have been decreasing or stagnant for nearly two months. However, these numbers remain elevated at more than 15,700 new admissions for the last full week in October, more than double summer’s low of about 6,300 in June.

With the upcoming cold winter months approaching, scientists are anticipating more COVID-19 infections as cold temperatures push people indoors.

Halkitis says that, “I expect there to be more rapid spread as is the case with any respiratory virus in the winter months.”

The CDC is predicting that a moderate COVID-19 wave will sweep over the U.S. according to its respiratory disease season outlook.

The CDC said in an update to its respiratory disease season outlook published last month that, “COVID-19 variants continue to emerge but have not resulted in rapid disease surges. We continue to anticipate a moderate COVID-19 wave, causing around as many hospitalizations at the peak as occurred at last winter’s peak.”

Scientists anticipate that the variants circulating in the U.S. will continue to change as the virus spreads and adapts to its environment.

Halkitis says, “The more we spread it to each other, the more it’s going to keep replicating in people’s bodies, the more likely it will be that mutations are going to occur.”

Based on these findings, I am not very concerned about COVID-19 mutations and variants. Having recently received the COVID-19 booster, I feel great and confident in the effectiveness of the vaccination. In my view, the pandemic no longer appears to be a national emergency. What are your thoughts on this? Do you believe the government should continue to declare the U.S. in a state of emergency due to COVID-19?

Personally, I commend the government for its handling of the pandemic. The implementation of vaccination campaigns, testing protocols, and treatment plans has been commendable. The availability of booster shots is a testament to the ongoing efforts to curb the spread of the virus and protect public health. I believe these measures have played a crucial role in mitigating the impact of the virus.

While I acknowledge that COVID-19 mutations and variants are still a consideration, the fact that I feel well after receiving the booster is reassuring. I think it’s essential to strike a balance between vigilance and a sense of normalcy. What’s your perspective on the current state of the pandemic and the government’s response?

Sticky Viruses – How Strengths of Adhesion Influence the Transmission of COVID-19

By henribosome

On December 7, 2023

In Student Post

Keeping track of each new SARS-CoV-2 strain and variant may feel like learning a new language. The myriad of Greek letters used to designate each one quickly turns science into classics, so it’s understandable how one may get lost in the confusing terms. But keep calm, these identifiers are crucial for understanding how COVID-19 evolves. They help scientists organize the virus’ different traits and open a window into understanding its behavior at the molecular level. A recent experimental study has just discovered how one of the determining factors that contribute to virulence could be the strength with which the virus binds to the host cell. In a joint effort between the University of Auburn, University of Munich, and Utrecht University, scientists analyzed the virus’ atomic structure.

The team observed how the different variants’ spike proteins interacted with the human ACE-2 protein and found that Alpha’s docking sequence is much stronger than those of Beta and Gamma. However, these latter variants appeared equally virulent as Alpha, leading researchers to conclude that it was their ability to evade immune responses that compensated for their relatively weak adhesion. The lead experimental scientist, Dr. Bauer, took an innovative approach by using force stability – essentially the net force with which the virus binds to the protein receptor of the host cell – as a means of determining the strength of adhesion.

Being a respiratory virus, the cells to which COVID-19 primarily binds are those along the path air takes from the nostrils to the lungs. After making contact with one of these cells, the virus begins a docking sequence that will allow it to assume control of the cell’s replicative mechanisms. In one of the universe’s most fascinating existential tricks, the virus is neither living nor dead: it is simply an envelope filled with genetic material. If it wants to replicate itself, it can’t do it alone. The virus binds to an ACE-2, a common receptor protein on the outside of the phospholipid bilayer. Once firmly connected, the host cell sends lysosomes to digest the envelope, revealing the virus’ genetic information, which enters the cell through a pinocytotic vacuole. Once inside, the virus then hijacks the existing cell structures to replicate itself. After assembling an army of fellow viruses, the host cell ruptures, releasing legions of viruses to neighboring cells in an attempt to repeat and amplify the process. This rupturing is often the source of the soar throats from which infected patients suffer.

As someone who has in the past gone toe-to-toe with COVID-19, I can say that it is a formidable opponent. It is clever, elusive, and stubborn. For a while I felt only the most bitter animosity towards this microscopic speck, but after developing an understanding of its behavior and anatomy, I can now respect its sophisticated biological processes that aid in its reproduction. I still view it as the most heinous and lowest “life” forms in the universe, but at least I understand its point of view. Let me know what you think about this groundbreaking research! Will it prove pivotal for engineering future vaccines for specific variants? How fascinating and haunting that the severity of the illness can be determined by how firmly the virus snatches at your cells!

Winter is Coming, and so is BQ.1 and BQ.1.1

By itsalive

On December 6, 2022

In Student Post

Winter is Coming

“The U.S. is going to see a winter surge in COVID infections,” predicts William Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health. “And I think that if nothing else changes BQ.1 and BQ.1.1 are likely to be very significant players”.

Two new omicron subvariants – BQ.1 and BQ.1.1 – are becoming dominant in the United States, causing fear of another COVID-19 surge as people prepare to gather for the winter holidays. These subvariants appear to be the most adept yet at evading immunity from vaccination and previous infection.

Mutations in Spike Proteins

New mutations in the virus’s spike protein appear to make BQ.1 and BQ.1.1 as much as seven times more ‘immune evasive’ than past variants. Spike proteins are the antigens on the surface of the COVID-19 virus. A mutation in the spike protein is an issue because the body’s immune system creates antibodies to fend off foreign invaders specific to that antigen. Memory helper T and B cells then keep these antibodies within the body in the case of a secondary exposure, which would then cause a faster, stronger, and longer immune response. Because the spike proteins are mutated, the body needs to reenact the process of producing antibodies, which could take a long time to have a noticeable effect on the body’s immune system, therefore increasing concern for the individual’s overall health.

A Closer Look at the Mutation (RBD)

The specific site of the mutation in the BQ.1 and BQ.1.1 variants is the receptor binding domain (RBD) which allows [the virus] to dock to body receptors to gain entry into cells and lead to infection; in other words, the RBD is the target of antibodies that deliver a potent immune response. Researcher Cao and his team believe that the RBD mutations allow the variant to evade infection-blocking ‘neutralizing’ antibodies that were a response to previous COVID-19 vaccines and exposure to earlier Omicron variants, such as BA.2 and BA.5. There seems to be a direct correlation between the RBD changes and the faster it spreads both within the body and the population. This is where BQ.1 and BQ.1.1 differ; variants, such as BQ.1, with five key RBD changes (relative to BA.2) seem to be growing in number at a slower rate than variants with six changes. A descendant of BQ.1 called BQ.1.1 has six such changes, and is rising rapidly across Europe, North America and other places.

Double Immunity?

Another variant of COVID-19, XBB, is predicted to “gain an edge” against BQ.1.1 because it has seven changes in its RBD, allowing it to grow at an even faster rate. Although there is currently no data to back up the theory that double immunity could be at play, researcher Cao and his team have a feeling that if you’re infected with BQ.1, you might have some protection against XBB.

How to Stay Safe

Although there is never a 100% guarantee that you won’t catch BQ.1, BQ.1.1, or XBB, there are preventative measures you can take to decrease your chances. As we have been advised since the start of COVID, one should continue to stay sanitary, wear a mask if in a susceptible/crowded place, and be updated on new vaccines. Winter is coming, and it is time to fortify and protect yourself against what lurks beyond your body’s walls.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: COVID-19 Variants

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