BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: SARS-CoV-2

Genetic Variation the Savior

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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.

Microorganisms-08-01259-g001

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?

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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.

SARS-CoV-2 without background

 

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.

Healthy Human T Cell
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

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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.

SARS-CoV-2 without background

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

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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.

Coronavirus. SARS-CoV-2

SARS-CoV-2 Spike Protein

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

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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.

Fphar-11-00937-g001

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

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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.

Remdesivir

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. 

SARS-CoV-2 without background

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

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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. 

Asthma attack-airway (bronchiole) constriction-animated

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.

Protein IL13 PDB 1ga3

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 Bronchiolar epithelium 3 - SEMup 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?

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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!

Structural model of SARS-CoV-2 infection - Oo 422117

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.

Healthy Human T Cell

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!

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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.

CanSino Convidecia

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.

 

CanSino Biologics logo

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?

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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

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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.

Fimmu-11-579250-g001

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?

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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.

Ginglymostoma cirratum bluffs

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?

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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

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

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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.

Memory B cell response

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.  

 

 

 

Changing Course: How Scientists Can Update Vaccines With Emerging Variants

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On December 20, 2021

In Student Post

SARS-CoV-2 , the virus which causes COVID-19, is changing rapidly, which in turn warrants changes to the vaccines created to slow its spread. This virus is mutating fast, with a new mutation establishing about every 11 days. These mutations may not be different enough to cause an immediate difference, but each and every person who catches SARS-CoV-2 opens more possibilities for mutations.

Spike omicron mutations top

Omicron Mutation Spike Protein

The most recent large variant to be identified was B.1.1.529 Omicron originating in South Africa. The Omicron variant has more than half the amount of mutations as the Delta variant, raising concern among health officials, who fear that the virus may differ just enough from the original for vaccines to be less effective. This fear stems from the idea that the vaccine-created antibodies will no longer be able to recognize the mutated virus’ spike proteins, resulting in an ineffective vaccine.

The current mRNA SARS-CoV-2 vaccines work in a fascinating way. Scientists utilize harmless lab-grown mRNA that contain coded instructions on how to create the SARS-CoV-2 spike protein, and place that technology into a vaccine.

Then, once the mRNA vaccine is injected into the patient, the patient’s cells will create the identical spike proteins, prompting an immune response. As we have learned in AP Bio, the adaptive immune system would eventually churn out antibodies tailored to the spike protein, so any future SARS-CoV-2 virus that enters the body will be neutralized and destroyed, even before it has the chance to infect someone.

Solo-Viral Vector-vaccine-27

SARS-CoV-2 Vaccine Vial

Because of this technology, scientists are readily able to create an updated version of the SARS-CoV-2 vaccine within a matter of days, for distribution in around three months. How do they “update” the vaccine? First, the Omicron spike protein is sequenced into their nitrogen bases (A, T, G, and C’s). Once that is complete, scientists use this sequence to create a DNA template. They then mix in enzymes which build an mRNA copy of the DNA template through a process known as transcription.

This process unfolds in a matter of days… so why does it take three months? Creating the physical mRNA for the vaccine takes only three days, but then the vaccine makers need to produce enough mRNA for doses, which would be used the next six weeks in pre-clinical testing on human cells. Once pre-clinical testing is complete and proves the vaccine works as expected, then the manufacturing of the vaccine can begin. The vaccine wouldn’t be released just yet — the next five weeks would be clinical trials and testing, and after that, the updated vaccine can begin rolling out to the public.

Even though SARS-CoV-2 is evolving faster than vaccines can keep up with, past technology was no where near as quick as today’s. In my eyes, being able to produce an updated vaccine in a matter of months is nonetheless a scientific feat. Comment what you feel was a gigantic scientific leap during this pandemic below!

An Antidepressant Is The Next “Weapon” Against COVID-19

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On December 17, 2021

In Student Post

Is the COVID-19 vaccine the only way to lower death rates and hospitalization rates? While more individuals are becoming vaccinated against COVID-19, researchers have looked at how a low-cost antidepressant prescription could potentially tackle the virus. Fluvoxamine (Luvox), an antidepressant medication, has the capacity to reduce hospitalization and morality rates after patients receive COVID-19 within a few days. Although fluvoxamine is licensed by the FDA for the treatment of obsessive-compulsive disorder (OCD) and other disorders such as depression, it is not approved for the treatment of COVID-19. In a study, conducted in Brazil, 1,500 newly diagnosed COVID-19 patients were assessed. 741 of the participants received a 100 mg pill of fluvoxamine twice a day for 10 days and the remaining 756 participants received a placebo twice a day. 16 percent of those who took the placebo twice a day got ill enough to necessitate a lengthy hospital stay compared to 11 percent of those who took fluvoxamine. Researchers discovered that participants who took at least 80% of the fluvoxamine administered to them had a two-thirds lower chance of hospitalization! Furthermore, there was only one fatality among individuals that took fluvoxamine, compared to 12 fatalities in the placebo group. According to The Lancet Global Health, this research has shown that the drug has reduced morality rates by roughly 91 percent. The antidepressant drug can be easily prescribed by doctors for COVID-19 using their clinical judgement.

Diagnostics-10-00453-g001

When the COVID-19 virus enters the body through the eyes, nose, or mouth and travels to the lungs, the immune system strives to protect itself from the invading pathogens by producing antibodies that, on occasion, eliminate invading infections. If the invading pathogen is unfamiliar to the body, B-memory cells will be unable to detect it, and B-plasma cells (antibody secreting cells) will be unable to manufacture antibodies, allowing the virus to enter the cell and flourish in the body.

Fluvoxamine

Fluvoxamine is a 2-aminoethyl oxime ether of aralkylketones. The antidepressant medication, if taken promptly after receiving COVID-19, may be an additional method of minimizing viral transmission and accompanying medical concerns. Fluvoxamine is easy to get and inexpensive to manufacture, particularly as a generic drug. COVID-19 treatments, in general, serve as both a cure for severe sickness and a treatment for the beginning of illness. Fluvoxamine, as an SSRI (selective serotonin reuptake inhibitor), attaches to a cell’s receptor that governs cellular stress response and the generation of cytokines, proteins that alert the body of a problem and lead to extreme inflammation. Nevertheless, fluvoxamine has been shown to minimize inflammation. When people get COVID-19, it’s theorized that the damaged cells produce a slew of cytokines that generate inflammation in the lungs, making it difficult to breathe. Patients would be able to breathe better and require fewer hospitalizations if fluvoxamine was taken to help decrease inflammation.

Fimmu-11-01648-g002

Who knew that an antidepressant that inhibits the serotonin reuptake pump at the presynaptic neuronal membrane might reduce inflammation and allow you to breathe? Because fluvoxamine works by boosting serotonin levels between nerve cells in the brain, it is impressive that the medicine might be used for purposes other than treating depression or OCD. The lingering question is whether someone with COVID-19 who has been taking these antidepressants for a previous disorder has an edge.

Are Genes Inherited from Neanderthals Protecting People Against COVID-19?

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On October 31, 2021

In Student Post

Neanderthals, from roughly 40,000 years ago, have had an impact on protecting people, that contain a specific haplotype on chromosome 12, from having severe symptoms due to the Sars-COV-2 virus. Researchers conducted a study that showed a ~22% decrease in severe illness connected to a gene inherited from Neanderthals.   

Neanderthals evolved in western Eurasia -the largest continental area consisting of Europe and Asia- about half a million years ago, living mostly separated from early modern humans in Africa. Neanderthals likely developed certain genes allowing them to fight off infectious diseases during the time of their existence. Due to natural selection, which is when animals with the most favorable traits for survival will survive to reproduce and pass on their genes, these neanderthals were able to evolve and pass on the favorable gene allowing modern humans today to fight off Sars-Cov-2. Through natural selection, the haplotype, on chromosome 12, linked to protection against certain viruses has been passed on. This specific haplotype has helped people during the current pandemic to stay out of the hoHuman male karyotpe high resolution - Chromosome 12spital. 

This study discovered that this specific haplotype on chromosome 12 contains three helpful genes: OAS1, OAS2, and OAS3. These genes encode for a specific enzyme called oligoadenylate synthetase. As we learned in AP Biology, enzymes are created by free ribosomes in the cytosol; the ribosomes manufacture proteins(a chain of amino acids), such as enzymes for cellular reactions. The oligoadenylate chain triggers ribonuclease L. The ribonuclease L, also known as RNase L, is only activated when a viral infection enters the body; it breaks down the viral RNA molecules, leading to autophagy. This enzyme breaks down the viral Sars-Cov-2 RNA and slows/stops the spread of the virus in the body. 

Many people have been trying to find ways to move forward from this pandemic and return to our previous form of normal life. Scientists may be able to use this information about this specific haplotype on chromosome 12 with gene editing technologies, such as CRISPR, to help individuals slow and later stop the spread of COVID-19. Research like this may be one way to be able to return to a normal life-style and keep people out of hospitals from COVID-19. As we continue on in AP Biology this year, I look forward to learning about the idea of genes and gene editing as I will have more knowledge to touch back on this research study. Do you think that this is a possible solution to the COVID-19 pandemic?

 

 

Comparing Saliva Tests to Nasopharyngeal Swabs

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On January 10, 2021

In Student Post

Although many college campuses have closed within the past couple of weeks, for the few months they were in session, the general public was introduced to a new procedure for COVID-19 testing: Saliva tests. There are multiple reasons why a saliva test would be more ideal for campuses to use, and it’s not just because the nasopharyngeal swab testing is extremely uncomfortable.

A nasopharyngeal swab is basically a biological term for the COVID-19 test that goes all the way up your nose. News-Medical actually came out with an article going through the testing procedure, and how the SARS-CoV-2 is detected. The purpose of the swab test is to reach the nasopharynx, which is where nonpathogenic and pathogenic bacteria and viruses lie. It’s also used to test the flu and pneumonia. In fact, UC Davis published that they have just come up with a rapid test that could detect both the flu and COVID-19 in one nasopharyngeal test. This makes it the most convenient method, but it’s more expensive; making this harder to upscale for mass testing). It also requires more supplies, and puts health care workers in close contact with infected individuals. Saliva tests would be a lower cost, but there was uncertainty in its accuracy. The Scientist highlights three main experiments that help better our understanding of saliva testing.

The first experiment was led by Yale epidemiologist, Anne Wylie. Wylie and her colleagues tested the accuracy of swab testing using 70 suspected COVID-19 patients admitted to the Yale-New Haven Hospital. They found that saliva samples contained more copies of the SARS-CoV-2 than swabs. The group concluded by saying that they see potential in the saliva swab; however, this was only tested in one controlled area, and the patients at this point were showing symptoms.

The second experiment, led by Mathieu Natcher, took place throughout the French Guiana. There were 776 participants ranging from (wealthier) villages, forests, and more poor neighborhoods. Natcher discovered that the SARS-CoV-2 virus was still present within saliva for a long period of time, despite climbing temperatures, which makes this idea for situations where testing needs to happen in areas where temperature can’t be regulated. The one downside noticed during this experiment was that saliva testing was less sensitive than nasopharyngeal swabs, which means that it can be harder to pick up the bacteria, if there is less in their system. Therefore, saliva testing may not always be as efficient for asymptomatic carriers or people who just became infected.

Pharmacologist at the University of South Carolina helped develop the school’s saliva test, and reported her findings after school came back in session. She noticed that although saliva may be less sensitive, the repetition of testing these students makes it more possible to catch the infection shortly after it comes. She also ran an experiment on two students living together: one of which had a confirmed COVID-19 diagnosis, and the other was at risk. Both students got tested daily using the nasopharyngeal and saliva swabs for the two weeks. She found that the amount of the virus detected in both tests for the positive patient were the same, leading her to conclude that saliva and nasopharyngeal tests both have the same sensitivity. Banister also explained that not the lower sensitivity coming from the saliva test in comparison to the nasopharyngeal test could be due to the fact that saliva turns over quickly in the mouth, while the nasal cavity and lungs hold the virus for longer. Banister also said because of this saliva tests might be a more accurate depiction of who is actually infectious, because the virus stays in the lungs even after the patient is no longer infectious.

We have come a long way since this article was initially posted, and saliva tests have been released to more of the public for a longer period of time. It is interesting to see how these preliminary tests played a role in whether or not to further release saliva tests.

So we beat SARS and MERS… Why haven’t we beat COVID-19?

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On December 15, 2020

In Student Post

Many people, especially those who were alive during the SARS and MERS outbreak, may be wondering why we haven’t beat the Coronavirus yet if we beat the SARS and MERS outbreaks, two very similar viruses to COVID-19 or Sars-CoV2. This is a question many people have been facing everyday as the Coronavirus disease has caused a shift in the entire globe’s day to day life unlike SARS and MERS. 

SARS, MERS, and COVID-19 are all part of the coronavirus family. “Coronaviruses are a large family of enveloped RNA viruses” that can be found in a variety of bat and bird species. While this makes the three viruses similar, they all have specific differences causing unique results in terms of outbreaks and how the specific viruses have spread. What is so powerful or different about the coronavirus causing COVID? 

First of all, let’s talk about how viruses hijack our bodies. Viruses are microscopic parasites, much smaller than bacteria, that contain key elements that make up all living things such as nucleic acids and DNA or RNA, but are unable to replicate and access this information encoded in their nucleic acids, meaning they cannot self replicate. In order to reproduce, they rely on the genetic material of host cells (our own cells). As we talked about in class, viruses are able to bind to our cell surface receptors and trick our cells to “let them in”. The viruses are then able to hijack our cells by releasing their genomes, or that information they couldn’t previously access, resulting in our cell making millions of copies of that genome to spread throughout the body in order to infect other cells and / or other human hosts. This is how all three of the coronaviruses hijacked our bodies and communities. Let’s hear what happened once this step occured.

SARS stands for Severe Acute Respiratory Syndrome. The SARS outbreak began in the Guangdong province in China in 2002. The coronavirus that caused SARS, called SARS-CoV, was likely spread to humans, in the China wet markets, from civets or other animals who acquired the virus from horseshoe bats. The World Health Organization (WHO) issued a global alert after identifying an atypical pneumonia spreading amongst hospital staff and later names the virus SARS based on the symptoms people began to express. The epidemic was controlled on July 5th 2003 and only four cases have been reported since, 3 of which being in a lab setting dealing with the specific coronavirus. The reason why SARS was able to be contained so quickly was due to the fact that one could only spread the virus if he/she had symptoms and if one expressed symptoms it was easy to self isolate, therefore not spreading the virus to others. In addition, SARS has a fatality rate of 9.6% meaning a good number of people who contracted SARS were likely to pass on and therefore not pass on the virus to others. 

MERS stands for Middle Eastern Respiratory Syndrome. As we learned in class, viruses are no longer named by their place of origin, but this was not the case in 2012 during the outbreak of MERS. Similar to SARS, MERS is a zoonotic virus, meaning MERS was passed from an animal, in this case a camel who contracted the virus from bat once again, to humans in Saudi Arabia. Although 27 countries have reported cases of MERS since 2012, transmission among people is rare and MERS has a fatality rate of 34.3%, making it even more deadly than SARS and therefore making it even harder to spread. 

The first case of COVID-19 or SARS-CoV-2 was reported in Wuhan China in December 2019. By the end of January 2020 the WHO had declared a public health emergency of international concern and by the beginning of February the WHO had declared a pandemic. So what makes the coronavirus disease so much worse than the other ones? How did COVID-19 spread so quickly and to the entire globe? And why are our daily lives changed forever or at least until we can get a handle on the virus?

First of all, the COVID-19 causing coronavirus SARS-CoV-2 is very similar to SARS-CoV, but with very unique and important differences. What we have all learned about SARS-CoV-2 is that you don’t need to be experiencing symptoms to transmit the virus. This is very different from SARS-CoV where you needed to have symptoms in order to transmit the virus. Also, while the transmission rates are lower for MERS and SARS because the fatality rates are higher, in the case of COVID-19, the fatality rate is approximately 1-3%, meaning more people are surviving COVID-19 making it easier for this virus to survive and pass on to other people that it has yet to infect. In addition, as we talked about in class, we have evidence that “viruses can naturally mutate to mimic host biology so as to ensure successful viral propagation” and as a result “a host of high frequency mutations have resulted in a least 5 differentiated SARS-CoV-2 strains to date” making it even harder to develop a successful vaccine to target and eliminate the coronavirus disease.   

So, will we ever be able to put a stop to the spread of the coronavirus disease and therefore the pandemic? The answer is yes, but we first need to figure out how to stop the spread of the virus. The truth about COVID-19 is that unfortunately, as stated above, it is much easier to transmit than SARS and MERS, and COVID-19 has been able to get on planes and travel the world unlike the previous coronaviruses. While it is easier to transmit it is also more survivable than the other coronaviruses that have impacted our communities thus far.

Can your common cold help you beat vicious COVID-19?

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On October 25, 2020

In Student Post

Season colds are quite common, and while they are inconvenient and make us feel icky, they may be our advantage for our battle with COVID-19. 

To start off, when reading this article, I noticed that the author used the term “coronavirus” more casually. He referred to a “coronavirus” as a common cold, which of course left me confused. So I dug a little deeper…

Here’s a fun fact that I learned from this:

Many of us having been thinking that COVID-19 is the same as what we call the “coronavirus.” After reading an article differentiating the difference between the terms, I found that the term coronavirus is actually the broad term to describe a whole range of viruses. SARS-CoV-2 is the specific virus that causes only COVID-19 and is causes what doctors call a respiratory tract infection.

Basic biology tells us that while there are many cells that make up our body, they are all interconnected. A pathogen, like the SARS-CoV-2 virus, is an enemy to the cell. We learned about how things enter the cell in biology: the pathogen enters the cell, travels through the cytoplasm, and enters the nucleus. Because the virus has genes, it is able to rapidly produce copies of itself to infect the other cells. And of course, we know how scary these infected cells are when they start spreading to the lives around us given our situation with a global pandemic.

What we now know is that the SARS-CoV-2 virus, our “bad guy,” can actually induce memory B cells. These memory B cells survive for quite a long time; they are important in identifying pathogens, and creating antibodies to destroy such pathogens. So when we got sick during the winter last year, chances are these memory B cells fought them off. The key part of the memory B cell in our fight against COVID-19 is the cell’s ability to remember the antibodies it created from past illness for the future.

What does this mean?

The belief is that anyone infected by COVID-19 already has the memory B cells from past common colds to fight the virus off.  Taking a further step, it is believed that since everyone already has the memory B cells, anyone who has had COVID-19 in the past is unlikely to get it a second time. If the SARS-CoV-2 virus were to enter your body a second time (which is likely considering the virus has not gone away and is literally all around us), our bodies would be prepared with former knowledge of the antibodies used to fight and win this time.

A study performed at the University of Rochester Medical Center is the first to demonstrate how this may be so.

Mark Sangters, Ph.D., is a research professor of Microbiology and Immunology at URMC; he has backed up his findings by comparing different blood samples. When looking at 26 blood samples of recovering moderate COVID- 19 patients (people who have had it for their first time now), it seems that many of them had a pre-existing pool of memory B cells that could recognize the SARS-CoV-2 virus and rapidly produce antibodies to destroy it. He also studied 21 blood samples of healthy donors, collected years before COVID-10 existed. What he found was that these B cells and antibodies were also already present.

When we are sick with a common cold, our antibodies are created by memory B cells to attack the Spike protein. This protein is what helps viruses infect our cells. What Sangters noticed, is that although each Spike protein is different for each illness, the S2 portion of the Spike protein is the same throughout all sickness. Our antigens can not differentiate the parts of the S2 subunit, so they attack the Spike protein regardless. This was his final piece in his conclusion that our common colds that caused our memory B cells to make antibodies, could be used to fight against COVID-19.

The Long Road Ahead:

My concern with this article is that this is the biggest issue we face with COVID-19 is patient outcome. As of right now, there is no way to fully prevent everyone from COVID-19 because it is still all around us. The issue the world is facing, is how to treat those who have already contracted the virus. This information just simply is not enough to help. How will these memory B cells help those who are currently sick? The answer: Scientists are unsure. There is still the uncertainty of the future vaccine and study of these memory B cells for a possibility of milder symptoms or shorter length of illness from COVID-19.

 

Despite all of this concern, this is still a step in the right direction. Any information about this terrorizing virus is still helpful given how little we know about COVID-19. If we were to expand more on this information, we could save the lives of those around the world!

 

 

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