SARS-CoV-2 – BioQuakes

Tag: SARS-CoV-2 (Page 1 of 2)

“Globally, there has been a slow but steady increase in the proportion of BA.2.86 reported, with its global prevalence at 8.9% in epidemiological week 44” (WHO)

Another variant? Since the beginning of the epidemic, we have seen a few strains of COVID-19 arise, notably the Omicron, Delta, and Alpha variants. You may ask, how do these mutations keep on materializing?

Like all viruses, SARS-CoV-2 — the virus responsible for COVID-19 — goes under, and will continue to go under, several mutations.

As a coronavirus, SARS-CoV-2 uses protein spikes (visualization on right) that fit into cellular receptors, in order to infiltrate our cells. Upon entry of the virus, the invaded cell begins to translate the viral RNA into viral proteins, which leads to the production of new viral genomes. According to Akiko Awasaki, PhD, this is where mutations often arise, stating that, “When viruses enter the host cells and replicate and make copies of their genomes, they inevitably introduce some errors into the code.” While these introduced errors may be inconsequential, they can also be of benefit to the virus, increasing contagiousness. These successful mutations may change how the virus behaves in the future, becoming the foundations of new evolutionary steps.

As we learned in AP Bio, the sequence of amino acids plays a heavy role in the primary structure of the spike protein. When the sequence is altered, hydrogen bonds will be corrupted or created, affecting the stability of the secondary structures like alpha helices and beta pleated sheets. This changes will in turn affect the tertiary structure, ultimately morphing the three-dimensional shape of the spike protein.

Given this knowledge of how SARS-CoV-2 invades cells, and how it may lead to evolution and mutation, what is the significance of this newest variant, and how can it be fought?

BA.2.86 was discovered over the summer with cases from Denmark, Israel, the United Kingdom, and the United States. Later on, it spread to various countries all over the globe, being discovered in wastewater in countries such as Spain and Thailand. As weeks passed, the new strain did not seem to pose a threat compared to its predecessors. However, months later, BA.2.86 on the rise. On November 11th, the CDC estimated that 3.0% of cases came from BA.2.86. November 28th’s estimate, 8.9%, is shockingly almost triple of the earlier estimate just two weeks prior. This is apparently garnering the strain some sort of reputation, now being labelled a “variant of interest” by the World Health Organization.

While the percentage may seem scary, the rise of the strain has not brought a disproportionate growth in infections or hospitalizations. Rather than posing new or threatening danger, it seems to be much better adept to escaping our bodies’ defense systems. The improved ability to slip past antibodies, compared to previous variants, likely comes from its large number of mutations, 30, on its spike protein. Antibodies, which serve to fight these invaders, may find difficulty recognizing and defeating the new strain.

Due to the strain only taking the notice of researchers recently, there are still many things to be uncovered. Some researchers have affirmed their support in newer vaccines against BA.2.86 and future variants. As always, it is best to wear masks when necessary, wash your hands, quarantine if you are experiencing symptoms, and receive the latest vaccine.

Astronomy tools used to detect COVID-19 !?

By sandovalosome

On December 15, 2023

In Student Post

Would you ever expect a laser designed for outer space to analyze your health? If you answered yes, get ready to learn why! If not, pay close attention because what you’re about to learn is incredible! This laser is called an “optical frequency comb.” These lasers emit light waves, initially for researching outer space and accurate timekeeping. Because of the COVID outbreak, researchers have found a more promising use of this frequency mechanism.

The Optical Frequency Comb received its name from the way it functions. These
rapid bursts happen in a specific order across different colors of light, ranging from infrared to ultraviolet. When these frequencies are on a graph, it creates peaks that are said to look like the “teeth” of a comb. Now, researchers are exploring the possibility of utilizing this tool to identify specific molecules associated with COVID, and the comb can potentially identify these molecules by recognizing the absorbed colors. It would make most sense that the laser seeks out particular proteins on the virus. As evaluated in our AP Biology class, we know proteins are extremely important in terms of viruses. Proteins in viruses play a vital role by building the virus’s structure and helping it interact with the host’s cells. They enable the virus to enter cells, replicate, and avoid the host’s immune response. Viral proteins also manipulate the host’s cellular functions/processes, ensuring the virus’s survival and spread in the host organism.

Because specific molecules absorb distinct colors of light. The comb can recognize certain molecules in an air sample by identifying the absorbed colors. Because of the severe global pandemic, scientists have found a way to utilize this tool to diagnose patients with COVID in a less “nosy” technique (literally)! Rather than sticking a swab up your nose, all you have to do is exhale. Easy!

Researcher Qizhong Liang mentions that it is best to take the typical PCR test for a more precise result. Because this new COVID testing method is new and still under evaluation, it is best to double-check the test results. Nevertheless, this research offers a promising future for detecting diseases, such as COVID-19, in a quicker, less effortless way! I find it incredibly fascinating how a group of scientists could take an astronomy tool and use it medically to help diagnose patients. Would you trust this method to diagnose you?

Cracking Down on Long COVID

By fishgi

On December 15, 2023

In Student Post

In a study funded by the National Institutes of Health (NIH), nearly 10,000 Americans, including COVID-19 survivors, became the researcher’s focus, attempting to figure out the complexities of “Long COVID-19”. This condition leaves individuals fighting with lingering symptoms even after the virus has been vanquished, which presents various challenges, ranging from persistent fatigue to cognitive fog and prolonged dizziness. Nature Reviews Microbiology further examines the ongoing challenges in “long COVID” symptoms, emphasizing the necessity for consistent research efforts. This exploration acknowledges the need for continued studies to understand and address the complexities of the condition. It urges a proactive approach, encouraging the scientific community to stay observant and work together to enhance our understanding of long COVID. By prioritizing continuous research, strategies for diagnosis and management can adapt to the evolving nature of this condition. As part of the NIH’s 1.15 billion dollar “recover initiative,” the study revealed vital insights, showing that the severity of “Long COVID” is higher in individuals infected before the emergence of the 2021 Omicron variant.

The research identified 12 key symptoms, establishing a comprehensive scoring system that not only aids in diagnosis but also classifies patients into distinct subgroups, hence refining our understanding of the condition. Health Affairs jumps into the global impact of long COVID, stressing the significance of collaborative international efforts in research and treatment. Furthermore, the study described the influence of vaccination status and the timing of infection, compared with unvaccinated individuals and those infected pre-2021, demonstrating a higher susceptibility to severe forms of long COVID-19.
In the context of our AP Biology class, this study aligns with our exploration of infectious diseases and the biological responses to pathogens. The study advances our scientific understanding of the complexities between our immune system and the evolving nature of viral threats. B and T memory cells are formed during vaccination when specific immune cells are activated in response to antigens present in the vaccine. These memory cells, produced by both B and T cells, retain a “memory” of the encountered antigens. Upon exposure to the same pathogen, these memory cells enable a quicker and more effective immune response, contributing to long-term protection through vaccines. Throughout the year, we have learned the biology behind vaccines, and this study reinforces our learning by demonstrating that vaccines play a crucial role in preventing individuals from experiencing ‘Long Covid’ symptoms. The reason behind this is the vaccine’s ability to prime the immune system, effectively fighting the virus and reducing the risk of prolonged symptoms. Decoding the mysteries of “long COVID” through collaborative initiatives like NIH’s “RECOVER” not only fuels my scientific curiosity but also emphasizes the real-world impact of scientific research on global health.

(Post includes edits made through Grammarly)

Unlocking Omicron’s Secrets: Breakthrough in COVID-19 Research Reveals NSP6 Protein’s Key Role

By corroninvirus

On December 15, 2023

In Student Post

While in a global battle against an invisible enemy, a team of spirited scientists have found a remarkable discovery that could change the course of the pandemic and challenge everything we thought we knew about the elusive Omicron variant! The study, led by Boston University and involving international researchers, investigates the Omicron variant of the SARS-CoV-2 virus. SARS-CoV-2, short for Severe Acute Respiratory Syndrome Coronavirus 2, is an RNA virus belonging to the Coronaviridae family, known for its distinctive spike proteins that facilitate entry into host cells. This virus, causing the COVID-19 disease, primarily targets the respiratory system and spreads via aerosolized droplets, leading to symptoms ranging from mild flu-like manifestations to severe respiratory distress.

It identifies mutations that enable Omicron to evade prior immunity and introduces a new protein, NSP6, as a key factor in its reduced disease-causing potential. This study refutes earlier misconceptions about its findings and offers new insights for vaccine and therapeutic development. Hopefully, we can create a vaccine that will finally rid us of COVID for good.

Mohsan Saeed, the study’s senior author, highlights the minimal role of the spike protein in Omicron’s lower pathogenicity. We learned in AP Biology this year that a spike protein is a surface protein found on certain viruses, including the coronavirus, that facilitates their entry into host cells. These cells recognize foreign proteins, including viral spike proteins, and help orchestrate the body’s defense by binding to these proteins and signaling other immune cells to respond. This knowledge enhances our understanding of viral mechanisms and immune responses, highlighting the significance of proteins other than the spike protein in viral pathogenicity. It binds to receptors on the host cell’s surface, triggering a process that allows the viral genome to enter and infect the cell. Instead, mutations in the NSP6 protein are crucial in Omicron’s pathogenicity. This discovery opens new possibilities for future vaccines and treatments. The research, which will also be published in print, is a collaborative effort between various universities and research centers, emphasizing the need to explore non-spike regions of the viral genome.

The study began when researchers noticed the fast spread but reduced severity of Omicron. The initial focus was on the spike protein, as it was the primary differentiator between Omicron and the original virus. However, experiments showed that while the spike protein contributed to Omicron’s characteristics, it was not the sole factor. The National Institute of Health says that another reason for quick spread is several mutations of Omicron, which promote its ability to diffuse worldwide and its capability in immune evasion. It always amazes me how something so microscopic can have so many different factors at play!

Researchers adhered to strict protocols to avoid enhancing the virus’s strength, a concern known as “gain of function.” Comparing the chimeric virus (combining Omicron’s spike with the original virus) with the original strain revealed that the chimeric virus was weaker but not as weak as Omicron, indicating other factors at play.

Further research led to the discovery of the role of the NSP6 protein. This protein, previously understudied, was found to significantly reduce viral replication and infection severity. This finding shifted the focus from the spike protein to NSP6, revealing its importance in the virus’s ability to cause disease.

Understanding the role of NSP6 opens new avenues for combating COVID-19. It highlights the importance of examining genetic differences between variants to develop new treatments and vaccines. The research team plans to further investigate NSP6, potentially leading to more effective pandemic control strategies. Now that you’ve got the scoop on what’s happening with COVID-19 if you were hesitant about the vaccine, did this blog make you think differently? If it did, how so?

What Impact Can Covid-19 Have on You? How Long Will It Last?

By charbonknioxide

On December 11, 2023

In Student Post

The University of Melbourne conducted a study, from January 2020 to October 2022 that involved over 12,000 participants. The study examined long COVID’s ability to last, and its correlation with different SARS-CoV-2 variants. The results showed a clear trend, where nearly 40% of individuals who had contracted COVID-19 had reported persisting symptoms associated with long COVID. The study observed a lessoning likelihood of COVID-19 causing lasting symptoms as the pandemic advanced. It was also revealed that individuals infected by the more recent Omicron variant were less prone to developing long COVID, with only 12% reporting persisting symptoms.

The study also revealed some demographic factors that influenced long COVID risk. Notably, women, individuals aged 40-49, and those with a history of chronic illness, anxiety, depression, or severe COVID-19 were identified as being at a higher risk for long COVID. In addition, the decrease in long COVID with newer strains did not appear to be solely attributed to vaccination rates, suggesting the involvement of other contributing factors. This new understanding of long COVID could pave the way for further exploration, offering insights into immunological and autoimmune mechanisms, and potentially shaping broader health research. Furthermore, the impact of long COVID, has caused 36 million people to still feel unwell up to weeks, months, and even years after contracting COVID-19.

Overall, the study underscores the widespread impact of long COVID, emphasizing the need for refined strategies in prevention, treatment, and support for individuals grappling with lasting symptoms after a COVID-19 infection. The evolving nature of the virus and its varying impact on different demographic groups highlight the importance of ongoing research to enhance our understanding and response to the long-term effects of COVID-19.

In AP Bio, we recently learned about the body’s immune system. The immune system is a complex network of cells that work together to protect the body from harmful pathogens. When a virus enters the body, phagocytic cells, like macrophages and dendritic cells, engulf the virus particles through phagocytosis.
Then, the virus is broken down into small peices. These pieces are presented on the cell surface as antigens. Those viral antigens are then presented to the helper T cells and once the helper T cells bind to the viral antigen, they become activated. Then the activated helper T cells release cytokines which starts the immune response and activated the other cells. The newly activated cells are helper B cells, cytotoxic T cells, and Memory B and T cells. The helper B cells have receptors that are specific to the viral antigens so they can directly recognize the virus. These cells begin to multiply. The cytotoxic T cells are able to directly kill the already infected cells, stopping the spread of the virus. They do this by releasing perforin into the cell, which tells the cell’s lysosomes to burst so the cell gets destroyed from the inside out. In addition there are plasma B cells which prevent the virus from infecting anymore cells. Then the memory cells remember the virus’ specific antigens so if the same virus infects again in the future, a faster response can be launched.

The immune system’s ability to recognise, combat, and remember viruses is what allows us to survive.

I chose this topic because one of my math teachers said he had long COVID and it was absolutely miserable so I wanted to learn more about it.

What is changing in the immune system that allows COVID-19 systems to persist in some and not others?

COVID-19: Multiple Doors and Multiple Species

By atomicmass

On December 11, 2023

In Student Post

An article published in August of this year identifies how the Coronavirus is able to jump from one species to another. Since the discovery of the COVID-19, the disease caused by the virus SARS-CoV-2, in 2019, many scientists have wondered how SARS-CoV-2 infiltrates cells by hijacking a protein called ACE2 which is found on human cells. At first, many believed that the ACE2 protein was required for infection, but recent discovery from the Virginia School of Medicine reveals that SARS-CoV-2 can use multiple pathways to enter cells. A good example to describe this discovery is a house. To the virus, ACE2 is the front door, but if the front door is blocked, the virus can use other proteins to enter the cells which can serve as a back door or windows in the “house.” This is concerning as SARS-CoV-2 is able to adapt to different proteins that serve as the doors into cells of other species.

After discovering that SARS-CoV-2 has the ability to enter cells using proteins other than ACE2, scientists conducted further research to determine the necessity of ACE2 in the infiltration fo healthy cells. As a result, it was revealed that SARS-CoV-2 can bind to and infect cells without ACE2 being present at all. You may be wondering what proteins besides ACE2 COVID-19 and SARS-CoV-2 use to enter and infect cells. Here is one example.

An article published in the same month identifies TMPRSS2 as an endothelial cell surface protein that allows the spread of COVID-19 and SARS-CoV-2. The definition is similar to that of ACE2 as TMPRSS2 is simply another door or window that SARS-CoV-2 can use to enter healthy cells and infect them. TMPRSS2 is commonly found in the respiratory and digestive tracts which is a supporting factor to why the Coronavirus may encounter this protein. For example, someone infected with COVID-19 may sneeze near you resulting in you breathing the virus into your respiratory tract.

In addition, an article published in the summer of 2022 explains an experiment done in order to determine the structure of the TMPRSS2 protein. The results section of the article confirms that TMPRSS2 is composed of three domains and three subdomains. An image of the protein shows tertiary protein structure surrounding the protein which is integrated into the membrane. The experiment allows us to see how similar TMPRSS2 is to ACE2 and how an antigen is able to bind to either protein and enter the membrane, but, how can this be prevented?

Although SARS-CoV-2 can enter cells in our body and infect them by entering protein channels such as ACE2 on the cell membrane, cells can create antibodies that attach to their cell membranes. In AP Bio class, we learned that in adaptive immunity, B-cell antibodies bind to foreign antigens while also inhibiting B cells to divide. B cells are then able to create B Memory Cells which recognize a foreign disease such as COVID-19 if it enters the body multiple times. B cells which are activated by B-Cell antigens, can protect our cells and prevent SARS-CoV-2 from infecting our cells by entering through ACE2 channels.

I agree that these new findings have helped us understand how SARS-CoV-2 enter healthy cells allowing them to jump species, but I also believe there is more to discover about both of these diseases such as the question of whether or not a variant of SARS-CoV-2 can be created that is able to bi pass antibodies and enter cells at the same rate it would before vaccination or first infection. ACE2 and TMPRSS2 have been around for a while but we are just now discovering how proteins like them allow diseases to jump species. What do you think?

Genetic Variation the Savior

By ellectron

On April 30, 2023

In Student Post

In the article “Genetic variation in the SARS-CoV-2 receptor ACE2 among different populations and its implications for COVID-19,” published in Nature Communications, the authors explore the genetic variation in the ACE2 receptor across different populations and its potential impact on COVID-19 susceptibility and severity. The ACE2 receptor is a key entry point for the SARS-CoV-2 virus into human cells. Its expression level and genetic variants may affect the virus’s ability to infect and replicate within the host. Therefore, understanding the genetic variation in ACE2 among different populations can provide insights into the different susceptibilities and severity of COVID-19 seen across the world. The authors analyzed genetic data from various global populations and found that there is significant genetic variation in ACE2 between populations. Specifically, they identified several ACE2 variants that are more prevalent in certain populations, including a “variant that is more common in East Asian populations” and may affect the receptor’s expression level.

The authors also conducted in vitro experiments – medical procedures, tests, and experiments that researchers perform outside of a living organism – to investigate the impact of these ACE2 variants on SARS-CoV-2 infection. They found that some variants, such as the one more prevalent in East Asian populations, led to reduced viral entry and replication, while others did not significantly affect viral infection. These findings suggest that genetic variation in ACE2 may contribute to the different COVID-19 outcomes observed across different populations. For instance, the higher prevalence of the ACE2 variant in East Asian populations may explain why these populations had a lower incidence of severe COVID-19 despite being initially hit hard by the pandemic. Furthermore, the author highlights the importance of considering genetic variation when developing COVID-19 treatments and vaccines. For instance, vaccines that were designed based on the original strain of SARS-CoV-2 may be less effective against strains that have evolved to better utilize ACE2 variants prevalent in certain populations. Overall, the article sheds light on the genetic variation in ACE2 among different populations and its implications for COVID-19 susceptibility and severity. The authors’ findings show the importance of taking genetic diversity into account when studying diseases and developing treatments and vaccines, particularly in the context of a global pandemic. In our recent DNA unit in class genetic variation was one of the topics of discussion, genetic variation is extremely important for the survival of a population as there is an easier chance that the species will be able to adapt and survive in different situations. Without genetic variation, many species can die out and therefore including the topic of genetic variation in viruses like covid-19 is extremely detrimental to the survival of humans when fighting this illness.

Why are some people’s sense of smell unable to recover after COVID-19?

By nescleus

On January 16, 2023

In Student Post

A recent finding published on December 21, 2022, in Science Daily, regarding the topic on why COVID-19 affects our ability to smell in the long run, was uncovered by the Duke University Medical Center. The biological mechanisms that are behind the loss of smell many people face who have had COVID-19, may also be the reason for some of the other symptoms of COVID-19 such as fatigue, shortness of breath, and brain fog.

Although many people recover from the side effects of being infected with SARS-CoV2 within a few weeks, there are many cases where some people’s smell is still altered for several months after. An experiment at Duke University conducted by Bradley Goldstein, M.D., Ph.D., associate professor in Duke’s Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology, collected 24 biopsies and examined the olfactory epithelial in each one. Using a single- cell analysis to examine the biopsies, it was discovered that multiple T-cells were heavily inflamed in the olfactory epithelium and that there was a loss of multiple olfactory sensory neurons. This is why many people have had a loss of smell even in the absence of SARS-CoV-2.

In biology class when learning about the immune system and can fight and prevent viruses, such as SARS-CoV-2. We also learned about the importance of T-cells, which are a large group of lymphocytes that play an important role in the immune response. We also specifically touch upon the central roles of T- cells and how “helper T- cells” recognize antigens and stimulate humoral and cell mediated immunity by releasing cytokines. We have discussed how vital T- cells are to our bodies while fighting off viruses because they protect us from infection and Without T cells, every exposure of pathogens that we face daily could be life-threatening to us. This relates to why our smell could be altered for so long after being infected with SARS-CoV-2 virus because our T-cells aren’t able to properly function since they are inflamed in the olfactory epithelium.

According to Goldstien, other COVID-19 symptoms might be caused by a similar inflammation that affected people’s loss of smell.

COVID-19 and Its History Through The Variants

By ellectron

On January 5, 2023

In Student Post

Since 2019 SARS-CoV-2, a positive-sense single-stranded RNA virus has impacted and changed human life. A Johns Hopkins article titled “What is Coronavirus,” states: “A coronavirus identified in 2019, SARS-CoV-2, has caused a pandemic of respiratory illness, called COVID-19.” Coronaviruses cause highly infectious disease, with variants known as SARS-CoV-2, SARS, and MERS. Although COVID-19 only recently sparked conversation – due to the pandemic – Coronaviruses were identified in the mid-1960s, and even so, it has most likely been around for much longer than that. The first recorded case of COVID-19 spreading in the United States was on January 30th, 2020, and continues to apply to the current day: with 305,082 reported COVID-19 cases in the US this week alone (Day of writing December 1, 2022). Evidently, heavy research has gone into the post-COVID effects it has on adults aged 18 to 64 (although there has been less research done on the younger age groups). But, in current times with the Omicron and Delta variants researchers have begun testing to see if its post-COVID effects are the same or different than the original COVID-19 strand.

In the original COVID-19 strand there were many different side effects that people encountered: difficulty thinking or concentrating – referred to as brain fog -, headaches, sleep problems, dizziness – when standing up – pins-and-needles feelings, change in smell or taste, and depression or anxiety. In Omicron, individuals had similar post covid complaints – regarding fatigue, cough, heart palpitations, shortness of breath, anxiety/depression. While individuals infected with Delta from 14 to 126 days found that even in acute (14-29 days), sub-acute (30-89 days), and chronic (90 -126 days) found that they were at a lower risk of having post-COVID complaints. The main difference between the original COVID-19 variant and the Delta variant is that the spike proteins have different structures, with the Delta variant infecting lungs more easily – making it the most contagious version of covid. As stated on the government’s site: “SARS-CoV-2 uses its viral membrane fusion protein, known as a spike protein, to bind to angiotensin-converting enzyme 2 (ACE2) as a ‘receptor’…causing severe pneumonia and acute respiratory distress syndrome.” In the immune system, our body’s ability to react and destroy antigens sufficiently depends on a few things. One of them is if the human body has experienced this antigen in the body before it would have made B Memory cells and would be able to fight it off more efficiently. The adaptive immune system response goes through B Cells, Helper T cells, and Cytotoxic T cells which are in charge of encountering, activating, attacking, and remembering this antigen for the potential next time the body faces this virus. Overall, not only do the viruses change but the way they affect the human body changes as well due to the humoral immune response.

Why Nearly Every Human on the Planet Has Contracted Covid-19

By almoschetto

On December 8, 2022

In Student Post

While some have only heard the term ‘Coronavirus’ starting in 2020, the drama around this type of infectious disease is not new. This type of virus brings on illnesses that you have most likely contracted long before the start of the pandemic in March of 2020. For example, the common cold. But of course, Coronavirus is not responsible for just that– they also bring on SARS (severe acute respiratory syndrome) and MERS (middle eastern respiratory syndrome). With SARS-CoV-2 being the virus that causes COVID-19, this extremely contagious disease is, in fact, a strain of SARS.

But if the Coronavirus has been around long before now and there are so many types of it, what makes SARS-CoV-2 special? The answer to this is its relationship with a particular enzyme, ACE-2, whose shape, function and location opens doors right up for COVID-19 to enter and infect our healthy cells.

While other types of SARS also attached to this enzyme, the ingenious design of the SARS-Cov-2 protruding spike protein is what makes this virus particularly contagious; Throughout the evolution of this virus from other versions of SARS, the shape of their spike protein has become more refined and specific through compaction of its structure to better mimic the shape of the receptor dock of a naturally-occurring enzyme called ACE-2. This mutation allows the virus to strengthen the grip that they can have on human’s cells, making their infection rate much more high and effective.

The function and location of ACE-2 also practically facilitates the infection of SARS-CoV-2 within us. These enzymes play a critical role in the renin-angiotensin system (infection-fighting system), and while this virus utilizes them as an entrance to the body as a means to infect, it is reducing the function of the very cells that are supposed to be fighting it. Additionally, this suppresses the rest of the functions of our immune system.

In the human body, one way in which our immune system works is by the release of T lymphocytes, or T-cells, along with macrophages and monocytes to fight off infections. However, with SARS-CoV-2 having already hijacked ACE-2 at the time when T-cell release is activated, the immune system becomes dysfunctional; the three aforementioned immunity cells are released via a positive feedback loop in a much greater magnitude than usual/ than with other illnesses. Lastly, ACE-2 positive cells are present in over 70 types of our bodily cells, and are especially abundant in oral, nasal, and nasopharynx tissues, which are hot spot entrances for this virus (and many others).

With the involvement of just one enzyme within our bodies, SARS-CoV-2 throws all aspects of our immune system into a disarray. With the many adaptations and evolutions of SARS viruses, infectious diseases such as these are just getting smarter and smarter each time they sweep through the human population.

SARS-CoV-2 Spike Protein

NMT5: A New Enemy To SARS-CoV-2?

By Allisteric Site

On December 8, 2022

In Student Post

In the past few months, scientists in the United States have developed a potential new antiviral to SARS-CoV-2. The drug, called NMT5, is effective against several variants of SARS-CoV-2, the virus that sent the planet into lockdown only a few years ago.

As stated in the journal Nature Chemical Biology, NMT5 coats SARS-CoV-2 particles as they travel through the body. Thus, when the virus attempts to attach to the ACE2 receptor proteins of the cell, NMT5 attaches first. The drug changes the shape of the cell’s receptor upon attachment, which makes it harder for SARS-CoV-2 to infect the cell, and on a larger scale, the organism’s body.

In order to ensure that the drug isn’t toxic, researchers tested NMT5 on healthy cells. According to the National Institute Of Health, it was “found that NMT5 was non-toxic and only changed receptors that were being targeted by the virus. These effects lasted for only about 12 hours, meaning the receptors functioned normally before and after treatment”. In fact, in an experiment that used hamsters as models for the human immune system, NMT5 reduced SARS-CoV-2’s ability to bond to ACE2 receptors by 95%!

A significant reason NMT5 is so effective is that it not only limits one particle of SARS-CoV-2, but the effectiveness of the virus as a whole, when present. When a SARS-CoV-2 particle with NMT5 attaches to an ACE2 receptor, it adds a nitro group to the receptor, which limits the ability of the particle to attach to the receptor for 12 hours by changing the receptor’s shape. Thus, no COVID-19 particle can attach to the ACE2 receptor – even ones that haven’t been surrounded by NMT5. Stuart Lipton, a professor at The Scripps Research Institute, states that “what’s so neat about [NMT5] is that we’re actually turning [SARS-CoV-2} against itself”, as particles surrounded by NMT5 serve to limit the ability of other SARS-CoV-2 particles. The drug has excited scientists studying SARS-CoV-2 around the world, as they have “realized [NMT5] could turn the virus into a delivery vehicle for its own demise” (PTI, The Tribune India).

Cell reception and signaling are incredibly important to both viruses and the human immune system. A virus works by infiltrating a cell through cell receptors that line the outside of the desired cell’s phospholipid bilayer. Viruses attach to these receptors and infect the cell as a result. SARS-CoV-2’s process is depicted below, as it attaches to the ACE2 receptors described earlier. The immune system works by recognizing the virus at hand and signaling B-Lymphocytes and T-Lymphocytes to destroy the virus and infected cells. B-Plasma cells surround the virus, as shown below, which neutralize it and allow it to be engulfed and destroyed by macrophages. Cytotoxic T-cells kill cells already infected by the virus. Both B and T Lymphocytes are activated as a result of T-Helper cells, as T-Helper recognize the virus when a piece of it is displayed at the end of a macrophage, and signal the Lymphcytes by releasing cytokines (another example of cell reception and signaling). This process is all shown in the image below, with the specific virus depicted being SARS-CoV-2.

However, NMT5 prevents the initial infection from happening when SARS-CoV-2 enters the human body by bonding with SARs-CoV-2 particles before they attach to cells, which allows for the immune system to quickly destroy the virus. By blocking SARS-CoV-2’s access to receptors, the drug stops the particle before it can infect a cell and do any damage. Since cell receptors are specifically shaped, and any change in form results in a loss of normal function, the ensuing change in shape of a receptor limits any SARS-CoV-2 particle from attaching to said receptor, further limiting the virus’s damage by blocking cell reception from occurring. Thus, the immune system kills the virus without major symptoms.

All in all, the development of NMT5 is exciting for scientists all around the globe. If it is as effective as studies show, it could play a major role in limiting the effects of SARS-CoV-2. Hopefully, all goes well, and you should be hearing a lot more about the drug sometime soon.

If you have any updates or questions on NMT5, I invite you to share them in the comments below. Thank you for reading my blog post, and stay curious!

New mutation of COVID-19 discovered

By hypotheoni

On December 8, 2022

In Student Post

A new version of COVID-19 that is resistant to remdesivir was discovered in organ transplant recipients. “What is remdesivir?” you may ask. Well, remdesivir is one of the very few medications approved to treat SARS-CoV-2. This medication is extremely important for the treatment of COVID-19 within transplant patients because the other medication, Paxlovid, has been found to interfere with immunosuppressants. Remdesivir works by stopping the spreading of SARS-CoV-2 by stopping the virus from copying itself. The virus replicates itself using the enzyme polymerase, which replicates strands of DNA using 2 strands.

It was reported that two COVID-19 vaccinated liver transplant patients of NYU Langone were infected with SARS-CoV-2, and then that the remdesivir had no effect on them. To investigate, the patients were swabbed before their release from the hospital. Although they had already been vaccinated from the disease before their surgeries, the two patients began showing symptoms of SARS-CoV-2, such as lingering fatigue, cough, and fever. Both patients were readmitted to the hospital when their symptoms got worse.

Researchers found that the patients were both infected with the non-mutated form of SARS-CoV-2 (the one non-resistant to remdesivir), and the mutation happened sometime after the infection. It was discovered that the virus developed a different form of their polymerase, and that that form of polymerase was more resistant to the remdisivir. The researchers stated that this mutation could have been created because of “the antiviral treatment itself, combined with the patients’ weakened immune systems”. This weakened immune system could make cells such as natural killer cells have a harder time fighting off against the virus, because of the immune systems’ inability to fight off everything coming at it.

The discovery of this mutation is important to the study of COVID-19, as we are now more aware of the fact that we have to continue to monitor the disease. This study also opens a door of investigations towards the mutations the virus might make in resistance to the vaccines. Now that we know the things that the virus can mutate against, we have a precedent to how it might mutate in the future.

How Having Allergic Asthma Can Protect an Individual From COVID-19

By DNAva

On December 8, 2022

In Student Post

Scientists have found that individuals with asthma are, in fact, less susceptible to COVID-19. One could question how a pre-existing health condition could actually aid in fighting off a virus? It is accurate to assume that an individual with allergy asthma would be at more risk than a perfectly healthy individual.

Allergic asthma occurs when your airways tighten when an allergen is inhaled. The same immune system proteins that are involved with excess mucus production and the tightening of airways are used to form barriers around exposed airway cells (immune system mechanism for people with allergy asthma). This information is the basis behind the studies that explains the reasoning behind why people with asthma are less susceptible to COVID-19.

When a patient has asthma, usually the development viruses such as the Flu and Strep Throat are more dangerous for them, and still these patients with asthma are at more risk when they are infected with COVID-19. The difference lies between asthma and allergic asthma. Researchers were able to identify that people with allergic asthma were not showing major symptoms to COVID-19, which was not what one would expect. Why is that?

Protein Protection

The differentiating factor that sets allergic asthma from regular asthma is a specific protein called interleukin-13 (IL-13). The normal function of IL-13 is to help fight off parasites. Normally, specific T-Cells release this protein. In response to the release of IL-13, the body produces a sticky mucus substance and compacts airways. This traps the parasite until the immune system finishes the job by killing the parasite.

However, when an individual has allergic asthma, the body mistakes harmless matter such as pollen for a parasite, and uses IL-13 when it is not needed. The researchers now need to determine how, exactly, IL-13 is protecting patients from COVID-19.

No IL-13 Present Study

Researchers conducted a study in which they would compare how cells that haven’t been treated with the IL-13 protein react when healthy and when infected with coronavirus.

It was found that the healthy cells grew in lawns that nearly resembled grassland. This area is made up of a hair-like substance called cilium. The cilia move in waves which aids in mucus movement and the excretion of anything stuck in the mucus.

On the other hand, the cells that were infected with the coronavirus had a much different reaction. The cilia lawn was no longer clear. The cilia was covered with mucus and many bald spots that seemed as if infected cells died. The infected cells were compressed out of the lawn of the cilia, and in that process they become inflated. This inflation occurs due to vacuoles in the infected cells getting blocked up with viruses. Once the infected cell gets filled up with viruses past its capacity, it explodes and releases all of the viruses that had been in the cell.

Unfortunately, it is not as simple as this singular reaction, not all cells that were in the infected lawn were affected the same way. Researchers noticed that the cells that were attached to the cilia were infected with SARS-CoV-2, but the goblet cells, which are mucus producing cells, were barely affected. The researchers found that a protein called ACE2 is present on the surface of ciliated cells more commonly that goblet cells. With this finding, the researchers can assume that ACE2 is the protein receptor that allows SARS-CoV-2 to enter the cell.

IL-13 Present

Now the researchers conducted a second study in which they will coat the cell in the IL-13 protein and compare how the cell reacts when infected with coronavirus. The celia lawn surface with the IL-13 present has a lot less inflated dying cells on its surface and the movement of the cilia was much less rapid. This decrease in movement indicates that the mucus is present in the cilia for much longer than when IL-13 is not present. It was made clear that the IL-13 protein acted as a protectant towards the infection.

They later found out that untreated cells, once infected with SARS-CoV-2, release bursts of mucus. Whereas the IL-13 cells keep the mucus stored. Furthermore, it is known that IL-13 proteins produce a sticky mucus that has the ability to trap viruses before they get the chance to infect the cell. So, this excess mucus that is present in the treated cells can make sure the virus is out of the lungs before the damage has been done. Researchers also found A thick layer of keratan sulfate that was developed on the cell’s surface that was treated with IL-13, which protects them against SARS-CoV-2 from coming into contact with the cell.

In addition to protecting the cells, the IL-3 protein causes cells to produce less ACE2. And with less ACE2, not as many SARS-CoV-2 can come into the cell, since ACE2 is the SARS-CoV-2 receptor.

There is so much unknown about IL-3, and researchers are still trying to determine specific properties of this protein. Scientists are eager to find out more about IL-13 as they think this protein can lead to new treatment findings.

This new information about how people with allergy asthma react to COVID-19 can be looked at as a positive because it’s one thing about having allergy asthma that actually benefited the individual!

Why is SARS-CoV-2 able to evade our immune system?

By nescleus

On December 8, 2022

In Student Post

On December 1st, 2022, Nature Immunology published an article based on discoveries, founded by University of Birmingham researchers, regarding why SARS-CoV-2 still continues to invade our bodies and harm our immune systems!

In an experiment funded by the National Institute for Health and Care Researcher, CD4+ T cells (which are a necessity for our immune systems to protect from viruses) were tested at the beginning of the pandemic in healthcare workers that were infected with COVID- 19. This experiment determined that T-cells were successfully able to identify epitopes in the spike protein of SARS-CoV-2 but as SARS-CoV-2 continued to evolve and mutate, the T-cell recognition was impaired. Against certain variants of SARS-CoV-2 such as Omicron, it was shown through this experiment that the T-cell recognition was less effective against the Omicron variant. Due to SAR-CoV-2 constant mutation affecting the role of our T- cells, this causes a lack of protection from our immune system which effects our health. This relates to biology class where we have been learning about how our immune systems can fight and prevent viruses, such as SARS-CoV-2. We have discussed the central roles of T- cells and how “helper T- cells” recognize antigens and stimulate humoral and cell mediated immunity by releasing cytokines. Learning about how vital T- cells are to our bodies while fighting off viruses makes me understand why after 3 years we are still being affected by SARS-CoV-2 virus! This is also interesting to understand why certain variants of SARS-CoV-2 can be more detrimental to our health than other variants.

This study also makes it clear that while the current vaccines are still essential to protect us from COVID-19, researchers are continuing to develop new vaccines that are specific to other variants.

Afraid of needles? No Problem- inhale a covid vaccine!

By rysharifov

On December 8, 2022

In Student Post

Its been a few years now since the first COVID-19 vaccine became available to the public. And since then, there has been a multitude of people who have been hesitant to receive a vaccine. Some people don’t believe in the vaccine – or even in the virus itself, some are just anti-vaxxers, some however, are simply afraid of needles. A Chinese pharmaceutical company based in Tianjin, China, CanSino Biologics, has recently created a COVID-19 vaccine you can inhale – and hopefully with this introduction, people will be more likely to get vaccinated as the “fear of the needle” with disappear.

The vaccine is called, “Convidecia Air.” And while you may be skeptical about it since it’s not really a “real“ vaccine that is injected into your body, the nasal flu vaccine has been around for years now and it enters your body the same way as Convidecia Air. I have personally received both the nasal vaccine (the one you inhale), and the needle vaccine (injection) from the flu, and I feel that they have worked the same in the past- which is why I’m optimistic about Convidecia Air.

As we’ve talked about in AP Biology recently, a regular (via injection) COVID-19 vaccine enters your body, and T-lymphocytes and B-lymphocytes remain in the body as a result. These lymphocytes function as both a Cell-Mediated Response and a Humoral Response, respectively, to try to fight off invading pathogens and prevent re-infection. With this new vaccine that enters the body via inhaling, the same T-cells and B-cells remain in the body after it is introduced to you.

The introduction of this new type of COVID-19 vaccine seems promising to scientists, as by entering the body the same way as the actual SARS-CoV-2 Virus- through the lungs and mouth- scientists believe that an inhaled vaccine might be more effective in terms of preventing disease and stopping the spread since it is also enters the body via the lungs and mouth.

Overall, scientists are hopeful that with the introduction of this new type of “inhaled COVID-19 vaccine,” people will remain healthier, and the pace at which the world recovers during its post-pandemic state will increase.

Is the recently discovered hidden cavity on the SARS-CoV-2 protein a target for drugs?

By avacuole

On December 6, 2022

In Student Post

Many of us have been vaccinated against COVID-19 and have had the virus, leading us to become used to the virus being prevalent in our lives during the past few years. Even though a successful vaccine has been rolling out for a while now, new therapies have not yet been discovered for future strains. Finding new therapies for the virus remains a major priority in the field of science, even if many of us have been protected already. This issue remains a priority because new variants and strains have been continuing to emerge, and some resist present therapy mechanisms.

SARS-CoV-2

The most effective approach to attempting to combat the virus is addressing the proteins on the surface of therapeutic targets, known as spike proteins. The spike protein (S proteins) located on the surface of the virus leads to its spiky protrusions, and its mechanism to enter human cells. Like we learned in AP Biology class, the spike proteins of the virus latch to cells by matching with a specific receptor on a cell’s surface. The spike proteins of the virus have to latch on to the new cell to infect. Successful messenger RNA vaccines properly target this spike protein, which is the main goal when creating new therapies for viruses.

Spiky appearance of SARS CoV-2 virus

Luigi Gervasio, a chemistry and structural/molecular biology professor at University College London, and his team have been working towards addressing this issue. By partnering with the University of Barcelona’s research team, the two teams took the first steps to discover a possible mechanism for future drugs to detect and protect against the SARS CoV-2 Virus. Through thorough research and investigation, they uncovered a “hidden” cavity on the surface of a prominent infectious agent of the virus known as Nsp1. The team was able to make this discovery by testing small molecules that had the potential to bind to the Nsp1 cavity. The team identified one, 5 acetylaminoindane, which is essential for the development of new drugs against viruses. They concluded that this cavity permitted the calculation of the cavity’s atomically spatial arrangement, which will allow the development of these drugs.

The results of their breakthrough findings set the stage for developing new therapies that will be able to target the NSp1 protein against SARS-CoV-2 and present Nsp1 proteins in future coronavirus strains. Not only will this finding be impactful for targeting SARS-CoV-2 and future variants, but also new cavities on the surface of other proteins that have yet to be found by scientists. Finally, this research is monumental for both SARS-CoV-2 and virus treatment in years to come!

Novel Nanobody Treatment Could be Used to Treat Animals Infected with SARS-CoV-2

By rileybosome

On April 26, 2022

In Student Post

As we have learned in AP Biology class, the spike protein, or S protein, is located on the surface of SARS-CoV-2 is linked to transmissibility and cell entry. Located on the S protein is the receptor-binding domain (RBD) which is a key factor that allows the virus to dock to body receptors and invade host cells. Effective antibody therapeutics target S proteins.

Due to their small size and ability to penetrate into lung tissue, nanobodies have been speculated to be an excellent source for novel COVID-19 antibody therapeutics. A recent study measured these proposed capabilities for potential usage as a treatment. The proposed therapeutics would be used in veterinary medicine and aim to directly prevent SARS-CoV-2 pseudoviruses from compromising host cells.

The researchers screened and sequenced specific nanobodies, then, they were produced and amplified. The study validated the speculation by observing the carefully selected nanobodies bind to the SARS-CoV-2 S protein and RBD protein simultaneously. 85% of pseudoviruses were observed to be inhibited in a solution with 100mg of nanobody concentration.

What makes nanobodies even more attractive for usage in veterinary medicine is that its inexpensive to produce and can be made in large amounts. Given these beneficial qualities of nanobodies, they seem to be a plausible and favorable COVID-19 treatment.

Could Sharks be the Solution to Ineffective SARS-CoV-2 Antibody Treatments?

By rileybosome

On February 16, 2022

In Student Post

Sharks are often associated with gruesome stories of attacks and horror. However, lead researcher at the University of Wisconsin-Madison School of Medicine and Public Health, Dr. Aaron LeBeau believes sharks deserve to be recognized in a more positive light– due to their potential for creating advanced neutralizing antibodies (NAb) therapeutics for treating SARS-CoV-2.

Neutralizing antibodies have demonstrated efficacy in treating SARS-CoV-2 in previous trials. In the recent past, the FDA authorized two NAb therapeutics for emergency use for SARS-CoV-2. However, the effectiveness of these two treatments has been complicated by the development of new variants with highly mutated target antigens. These naturally occurring mutations in the target antigen result in insufficient neutralization of the virus when using those current therapeutics derived from classical human antibodies.

This is news for concern as genome sequencing exposed the virus to create two single-letter mutations each month.

As we learned in our AP Biology class, mutations to proteins such as SARS-CoV-2 antigens occur within the amino acid chains in the protein’s primary structure. These changes in chemicals could alter the kinds of covalent or ionic bonds in the protein’s tertiary structure. This, of course, changes the antigen’s three-dimensional shape. This is why the original NAbs have experienced diminished performance as new variants emerged. The antibodies from the treatments simply could no longer recognize the virus’ new antigen structure.

Therefore, there is a dire need for the development of new, more specialized NAbs, that can recognize the newly mutated epitopes that are currently incompatible with current neutralizing antibody therapeutics.

Dr. Aaron LeBeau believes that key findings for creating more efficient NAb treatments could be derived from the likes of nurse sharks! Within the immune systems of sharks, antibody-like proteins called Variable New Antigen Receptors (VNARs) were found to be highly effective at neutralizing coronaviruses, according to his recent publication in the Nature Communications journal.

Due to the small and highly specialized structure, VNARs are able to access and bind to epitopes that human antibodies normally couldn’t. This superior ability allows VNARs to reach deep into pockets and grooves within the target antigen, allowing for a better fit and neutralization. Dr. LeBeau’s research team concluded that their data suggests that VNARs would be effective therapeutic agents against emerging SARS-CoV-2 mutants, such as the Delta and Omnicron variants.

With the help from researchers from the University of Minnesota and the Scottish biotech company, Elasmogen, the team hopes to develop the shark antibodies for therapeutic use within 10 years.

Do you think this is promising news? How do you feel about using shark “antibodies” in place of our own for serious cases of SARS-CoV-2? Assuming it’s safe, effective, and accessible to you, would you accept this treatment if you contracted a serious case of SARS-CoV-2? Please leave your thoughts in the comments.

Could protein-based vaccines change the course of the pandemic?

By hydropherick

On January 17, 2022

In Student Post

Current mRNA vaccines provide sufficient protection against new SARS-CoV-2 variants, including Omicron, particularly for those who have received boosters. However, due to high manufacturing costs and the requirement for ultra-cold refrigeration, these vaccines are limited in low and middle-income countries. Protein-based vaccines have the potential to be much less expensive to manufacture on a large scale than mRNA vaccines and may not require ultra-cold storage. Protein vaccines would aid in delivering more vaccines to areas of the world where vaccination rates are currently extremely low, such as Africa to the lack of vaccines.

A research program in Cellular and Molecular Medicine (PCMM) is presenting a new strategy to build a better vaccine to directly target the antigen cells with a protein-based vaccine. This is not the first time we hear about protein vaccines; they have been around for decades now to protect others from hepatitis, shingles, and other infections. The protein-based vaccine will deliver proteins while also stimulating the immune system to respond to the vaccine more aggressively directed to the person’s cells. The protein-based vaccine will also enable a more efficient T cell response and high antibody production across variants while causing fewer side effects than other Covid-19 shots.

T regulatory cells (red) interact with antigen-presenting cells (blue) in a microscope image.

In connection to cell-to-cell communication, protein-based vaccines rely on the T cells to target the infected cells. The T-helper cells are able to divide and create two different types of cells. The T killer cell kills infected cells with the virus. Others, called T memory cells, stimulate the production of antibodies to prevent reinfection. In addition, the primary immune response will expose some of the antigens but the secondary immune response facilitates a faster, stronger, and longer response to the antigen produced due to the memory cells.

Could Protein-based vaccines be used instead of the mRNA-based vaccines that are currently approved to protect against Covid-19?

SARS-CoV-2 and Our Evolving Immune Systems

By anaplasia

On December 20, 2021

In Student Post

A scientific study analyzed in a recent article by Monique Brouillette brings hope with the emergence of possibly more infectious COVID-19 variants. The study looks at the blood of people who are vaccinated, and people who recently have had COVID-19, to learn more about the cells in our immune system. Studying and seeing these cells create their own way to counteract mutations could mean the evolution of our immune systems in response to the variants. So the study poses the question: Along with our cells ability to respond to the initial SARS-CoV-2 virus invasion, do our bodies adapt so that those same cells can recognize the new variants?

An Immunologist at the Rockefeller University, Michel Nussenzweig, conducted a study along with his colleagues by testing the blood of individuals both one month and seven months after they had COVID-19. The scientists noticed that individuals had lower levels of antibodies, and equal or higher levels of memory B cells, seven months after having COVID-19 than one month after. This was expected as the virus had been fully cleared by the seven month mark, and memory B cells were created in response to the initial invasion of SARS-CoV-2.

Memory B cells are created by the humoral response. This is when macrophages or dendritic cells recognize a forign antigen (in this case SARS-CoV-2), and stay in the body near its lymph nodes with the ability to recognize the virus.

If someone were to get infected for a second time, these memory B cells would activate to quickly produce antibodies and block the virus. This is called the secondary immune response (pictured on the right).

The scientists then did another test in the study. They tested reserve B cells and antibodies someone produced in response to SARS-CoV-2 against a version of SARS-CoV-2 they created to be more like a new variant. The replica new variant virus was made to be more like the new variants by having a mutation in the spike protein, which is the part of the virus that binds to our cells. When they tested this, they saw that some reserve B cells produced antibodies that went and attached to the mutated spike proteins, showing that the reserve B cells and antibodies from SARS-CoV-2 were able to adapt and recognize a different or mutated version of SARS-CoV-2.

New COVID19 mutant (SARS-CoV-2 VOC-20201-01)

Example of SARS-CoV-2 Mutation

The SARS-CoV-2 variants have many similar elements to the original SARS-CoV-2, but also contain mutations in their spike proteins and receptor binding domains (for the most part), which allow them to usually go undetected by our bodies. This is why those who are vaccinated or have SARS-CoV-2 antibodies are not fully immune to the variants.

Most recently, Nussenzweig and his team conducted the same experiment again, but with new and improved viruses that more closely resemble the COVID-19 variants. One of the replica variants is of B.1.351, which contains mutations K417N, E484K, and N501Y, was tested against cloned six month old (previously exposed to SARS-CoV-2) B cells. Although it has not yet been reviewed and confirmed, this test did show that some of the antibodies produced by these B cells had the ability to recognize and attach to these mutated variants engineered to be very similar to the viruses of the Covid variants.

What these scientists discovered with SARS-CoV-2 is a process called somatic hypermutation. This is when the immune system adapts to recognize and attack forign mutations or viruses it has not seen before when they have previously fought off a virus with some similar elements. The occurrence of this process with SARS-CoV-2 gives us hope that after getting the vaccine or having had COVID-19, our bodies will have a better defense against the new variants, which will, hopefully, in turn, lessen the fear and stress surrounding the emergence of new SARS-CoV-2 variants.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: SARS-CoV-2 (Page 1 of 2)

The “Slow but Steady” Increase of yet Another COVID-19 Variant: What are the Implications?

Another variant? Since the beginning of the epidemic, we have seen a few strains of COVID-19 arise, notably the Omicron, Delta, and Alpha variants. You may ask, how do these mutations keep on materializing?

Given this knowledge of how SARS-CoV-2 invades cells, and how it may lead to evolution and mutation, what is the significance of this newest variant, and how can it be fought?

Astronomy tools used to detect COVID-19 !?

Cracking Down on Long COVID

Unlocking Omicron’s Secrets: Breakthrough in COVID-19 Research Reveals NSP6 Protein’s Key Role

What Impact Can Covid-19 Have on You? How Long Will It Last?

COVID-19: Multiple Doors and Multiple Species

Genetic Variation the Savior

Why are some people’s sense of smell unable to recover after COVID-19?

COVID-19 and Its History Through The Variants

Why Nearly Every Human on the Planet Has Contracted Covid-19

NMT5: A New Enemy To SARS-CoV-2?

New mutation of COVID-19 discovered

How Having Allergic Asthma Can Protect an Individual From COVID-19

Why is SARS-CoV-2 able to evade our immune system?

Afraid of needles? No Problem- inhale a covid vaccine!

Is the recently discovered hidden cavity on the SARS-CoV-2 protein a target for drugs?

Novel Nanobody Treatment Could be Used to Treat Animals Infected with SARS-CoV-2

Could Sharks be the Solution to Ineffective SARS-CoV-2 Antibody Treatments?

Could protein-based vaccines change the course of the pandemic?

SARS-CoV-2 and Our Evolving Immune Systems

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