AP Biology class blog for discussing current research in Biology

Tag: #COVID (Page 1 of 2)

Subvariant EG.5 is on the rise and dominating the U.S!

Since COVID’s peak in 2020, what has been going on? Is it still on the rise? According to a recent article from LiveScience, the omicron subvariant of Eris, or EG.5.1, has been the leading cause of new COVID-19 cases in the U.S. In this research article, the data from a model of the Centers for Disease Control and Prevention (CDC) , from July 23 to August 5 of 2023, EG.5 was 17.3%  of the new cases of COVID-19, which had previously only been 11.9% two weeks prior. Personally, seeing that jump in percentage within two weeks worries me about what harm this subvariant could cause. Additionally, more recently, EG.5 had a higher percentage of infection than any other omicron subvariant in the XBB lineage!

Map of countries with confirmed SARS-CoV-2 Omicron variant cases

But the real question is, what is EG.5? How is it a subvariant, and why is it dominating the U.S.? Well, EG.5 was derived from a branch of omicron, an XBB variant. Yet, how it differs from omicron is what makes it EG.5 and what is allowing it to become so prevalent. EG.5 has a mutation in its spike protein that helps evade the body’s immune system. This spike protein called S:F456L may not only be able to escape our immune system, but the mutation in its subvariant Eris, EG.5.1, has an additional spike change, S:Q52H, that can be beneficial for the virus itself. To further the idea that the virus is harmful, the World Health Organization currently lists the variant as “under monitoring.” The article says that the genetics of the virus, EG.5, can theoretically boost its transmissibility, meaning that this virus is more easily spread than past variants. This article, to some relief, does not have enough evidence of it yet. Still, according to Johns Hopkins, the mutation is known to avoid the immunity you get after infection or vaccination. I think the idea that the virus is benefiting itself while infecting millions of people is, to say the least, cause for worry. Knowing that this immune system-bypassing virus could infect my grandparents or fellow students is unthinkable.

Spike omicron mutations top

After hearing that, I wanted to know what that means. Is there going to be another outbreak? But there is no need to worry. In this article, using the Washington Post, it is displayed that EG.5 is only different because it has more ability to enter the cells and does not seem to be more lethal than other variants. Dr.K Srinath Reddy proposed that it had the same effect on the human body. As of July 2023, a variant XBB.1.16 was still more prevalent globally than EG.5, and the subvariant only accounted for 11.6%, previously 6.2% in June 2023, of the sampled SARS-CoV-2 sequences. Even though EG.5 is only 11.6%, it is still on the rise and will still infect more people in every country, so it is essential to know your options. According to YaleMedicine, updated vaccines such as Pfizer and Moderna are not a perfect match for eradicating this subvariant and that the vaccine was aimed for a close relative called XBB.1.5. But, the CDC states that the updated vaccines, since XBB.1.5 and EG.5 are so similar, should give a reasonable degree of protection and that the genetic code among omicron subvariants allows for cross-protection.

COVID-19 Vaccine vial and syringe - US Census

Now, as an AP Bio student, this change of structure in COVID is something we have talked about a lot recently. We discussed how the SARS-CoV0-2 virus comprises five main parts: spike proteins, membrane proteins, viral genome, nucleocapsid protein, and envelope protein. To explain these briefly, the spike proteins, membrane proteins, and envelope proteins are on the virus’s surface. The nucleocapsid protein protects the RNA, the viral genome. For this particular variant, I want to speak about the spike proteins and how, in AP Biology, we learned that these spike proteins recognize membrane-bound proteins of human cells and bind to them. Since this is an omicron variant, it follows a Receptor-Mediated Endocytosis pathway, a form in which receptor proteins on the surface capture and encapsulate specific molecules. This makes it more infectious. Once the omicron virus senses the membrane-bound protein of ACE2, it can enter the cell. This works because the omicron variant uses the ACE2 protein to become an endosome, enter the cell by endocytosis, and then break through Receptor-Mediated Endocytosis.

Contrary to the more extended version for SARS-CoV-2, how a transmembrane protease serine 2 cuts the spike protein in a specific location to which the protein will then undergo changes to insert itself into the cell membrane, the omicron version skips these steps to be able to go straight into the cell. The ability to skip these steps also connects to my article because it says the EG.5 subvariant can enter cells even more quickly. At this faster rate, this process can be hazardous and can spread much more quickly, causing more death and destruction. Therefore, learning this in AP Biology and how this process works allowed me to realize how bad this variant can be if the cross-protection is insufficient! But, please, if you are an AP Bio student like me, let me know what you think. Do you think this is more dangerous than portrayed? What do you think we should be doing!?

The Revolutionary mRNA COVID Vaccines

Biochemists Katalin Kariko and Drew Weissman have won the 2023 Nobel Prize in medicine/physiology. Why? Because they were the people behind the vaccines that just allowed us to control the worldwide COVID pandemic.

Usually, vaccine development takes about 5 to 10 years. However, more resources were put into the urgent battle of fighting the rapidly spreading COVID-19 than ever before: in record time, after the genetic sequence of the SARS-CoV-2 virus was discovered, several pharmaceutical companies, namely Moderna and Pfizer, created messenger RNA vaccines. Then, for the first time ever, the FDA approved mRNA vaccines.

Covid Vaccine

Typical vaccines consist of weakened viruses or bacteria that provoke the immune system to make antibodies to protect against future infections:

As I learned in AP Bio class, once those weakened pathogens are allowed to get through the body’s innate defenses (skin, mucus, tears, saliva, etc.), macrophages and dendritic cells engulf the antigens of the foreign pathogens (the spike protein for coronavirus) through phagocytosis, which the phagocytes can display on the outside of their plasma membranes on MHC proteins, while simultaneously releasing chemical messengers called cytokines. Activated by the cytokines, certain T-helper cells then recognize the antigens displayed on certain MHC proteins and call for an appropriate response. If this process is in a cell, T-helper cells activate cytotoxic T cells and T-memory cells. However, if it is in the blood, T-helper cells activate B-plasma cells and B-memory cells. B-plasma cells are the cells that create antibodies, which effectively neutralize pathogens and B-memory cells remember how to create those antibodies significantly more effectively for better future protection.

However, it is a very costly and tedious process for scientists to get loads of the coronavirus and weaken it for vaccines. The way Pfizer and Moderna created working COVID vaccines so quickly, based on the research that Kariko and Weissman began in 2006, is by creating vaccines with mRNA that tells cells how to create weakened coronavirus proteins; this process is instead of scientists manually putting weakened proteins into vaccines and is significantly more efficient since our bodies are already good at making proteins based on DNA/RNA code.

The reason why mRNA vaccines have never been FDA approved before the COVID vaccines is because pumping mRNA into the body releases cytokines itself. As mentioned previously, in AP Bio we learned that cytokines trigger helper-T cells. If helper-T cells are triggered when they shouldn’t be, that could create many problems. So, to fix this problem, Kariko and Weissman slightly altered the structure of the RNA to lessen cytokine triggering. Additionally, they encased mRNA in bubbles of lipids. As I learned in AP Bio class, lipids are nonpolar, meaning they can travel through cell plasma membranes. This lipid bubble, therefore, allows the mRNA to travel directly to and inside the nuclei of cells without causing harm elsewhere. Then, the mRNA can tell ribosomes to create the certain weakened coronavirus proteins that trigger the immune response of creating antibodies as previously described.

With the help of the research of the very deserving 2023 medicine/physiology Nobel Prize winners, Weissman and Kariko, the problems with mRNA technologies have finally been resolved (for now). Thus, this more efficient and may we call it, revolutionary mRNA technology is now being looked at to potentially defend other viruses and even cancers. The opportunities for this technology seem extraordinary, but what other challenges will scientists and researchers face when trying to explore these opportunities?

I would argue it is time for them to explore and find out.

Clot Chronicles: Decoding the Intricacies of Proteins and Vaccines in COVID-19 Immunity

Are you vaccinated for COVID-19? Well, the article titled, Protein interaction causing rare but deadly vaccine-related clotting found, discusses a mechanism that has led people to deadly clots. These scientists identified that some individuals developed these clots after receiving certain COVID-19 vaccines. The research explains  Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT) which is a condition where the body produces blood clots. When a patient has this condition antibodies attach to a protein called Platelet Factor 4 (PF4), forming immune complexes. 

Protein PF4 PDB 1f9q(PF4)

Additionally, Platelet Factor 4 is a small cytokine in the CXC Chemokine family. Cytokines are small proteins that are released by macrophages to attack a virus.  Platelet Factor 4’s most prominent function is to promote blood coagulation; but, it is also involved in innate and adaptive immunity

The Immune System, as discussed in depth in my AP Biology class,  protects the body against pathogens such as bacteria and viruses. COVID-19 is an example of one of these viruses that infects the body through its various openings, most generally, the nose and mouth. Innate and Adaptive response are the two parts of the immune system. The innate response is something everyone is born with, works immediately upon infection, and is nonspecific which contrasts the adaptive immune response which is slower and more targeted. 

Returning to the vaccines, these complexes activate platelets and immune cells and lead to clotting and inflammation. Inflammatory responses are a result of the mast cells locating the “invader” and releasing histamine as an “alarm” to the body. Histamine causes inflammation in the body and an inflammatory response which is typically painful. When I had COVID I remember taking anti-inflammatory medications to reduce the pain I felt from the inflammatory response I was experiencing such as my high fever.

In summary, the ongoing research wants to find people who might be more likely to get VITT with future vaccines, so we can understand and manage the risks better, making vaccines more effective. 

After reading this article and doing outside research I believe this study to be highly important because researchers understand how to make vaccines safer for the future. As someone who has not been vaccinated it is valuable for me to know the risks and rewards of the vaccine. So … COVID-19 vax worth it or not? Let me know what you think in the comments!

COVID-19 Vaccine Going Retro?

Bottle with Coronavirus Vaccine and syringe with Novavax logo on white background
Have you ever wondered why the world started to use mRNA vaccines all of a sudden ever since the COVID-19 pandemic? Where did the traditional methods of vaccination go? This sudden shift in vaccine technology didn’t just happen by chance but was a result of years of scientific research and experiments. As the world faced an unprecedented pandemic, the traditional method of vaccination, while reliable, was slower and less effective to adapt to mutating virus than the mRNA vaccines, which is faster and more flexible when combating COVID-19 viruses. However, the traditional methods have returned! The new Novavax COVID-19 vaccine is an old-fashioned, protein-based approach to vaccination, a contrast to the mRNA technology used in Pfizer and Moderna vaccines. The Novavax vaccine especially targets the SARS-CoV-2 variant XBB.1.5, which is a descendent of Omicron. 

Novavax’s Differences: A Protein-Based Approach
Unlike the mRNA vaccines, which use modified viral genetic materials to cause an immune response, Novavax relies on a more traditional approach which injects proteins that resemble SARS-CoV-2 directly into the body. This method has over 30 years of application in vaccines such as the Hepatitis B Vaccine. The Novavax Company also uses insect cells, such as moth cells, to produce SARS-CoV-2’s unique spike proteins. The reason why Novavax researchers use moth cells is because of its efficiency in producing spike proteins. They first select the desired genes that create the spike proteins, and then they put these kinds of genes into a baculovirus, which is basically an insect virus. The baculovirus will then infect moth cells and replicate rapidly inside them creating lots of spike proteins. Finally, the researchers will extract and use the spike proteins for vaccines. Additionally, Novavax’s formula also includes Matrix-M, a compound from Chilean Soapbark Trees, which will further enhance our immune system’s response to the spike protein.

Targeted Variants and Efficiency:                                                                    Novavax vaccines are developed specifically for the XBB.1.5 variant, and they are not optimized for the newer Eris and Pirola variants. However, vaccinologist Gregory Poland notes that all vaccinations, including Pfizer and Moderna, have all been “chasing the tail” of the emerging variants all over the pandemic, so Novavax is not alone in this situation. Additionally, all of the vaccine boosters seem to be able to provide some protection against new variants, but protein vaccinations are way slower to adapt to the new variants than mRNA vaccines. In terms of efficiency, according to infectious disease researcher Kirsten Lyke, Novavax stands on par with other mRNA vaccines. It is 55% effective in preventing COVID-19 symptoms and 31% effective at preventing infections, and this is very similar to the mRNA vaccines.

Protein Synthesis Elongation.png (mRNA coding protein)

Side Effects and Availability:
When it comes to side effects, the Novavax booster demonstrates a lower risk of myocarditis(inflammation of heart muscle) or pericarditis(inflammation of the outer lining of the heart) compared to mRNA vaccines, but of course, it is not entirely risk-free. It also tends to have fewer side effects like muscle fatigue and nausea post-vaccination. A huge advantage of the Novavax vaccine is its availability, it can be stored in a typical refrigerator, making it considerably more accessible than mRNA vaccines, which require subfreezing storage. The Novavax booster is now available in pharmacies across the country, with the CDC recommending having two doses that are eight weeks apart for unvaccinated people.

Which one should I get?
Both the protein vaccines and the mRNA vaccines can help you fight against the SARS-CoV-2 virus, and neither is better than the other. The mRNA vaccine has a faster efficiency in preventing COVID and has a higher adaptability to new variants, while the Novavax vaccine uses a more familiar technology, has a more accessible storage requirement, and has a lower risk of side effects post-vaccination. But no matter which kind of vaccine you think is better, Lyke suggests that the most important thing is to “pick one and get it.”

Novel Coronavirus SARS-CoV-2 (SARS-CoV-2)

Connecting to AP Biology:
In AP Biology, we’ve learned about how our bodies fight bacterial and viral infections and specifically talked about how the spike proteins on SARS-CoV-2 work to attack our bodies. When our body first recognizes the SARS-CoV-2 virus, white blood cells like Macrophages and Dendritic cells will engulf the virus, breaking it down into small pieces and displaying it to Helper T cells on their MHC proteins. The Helper T cells will then release Cytokines which will trigger both the Cell-mediated response and the Humoral response of your immune system. These responses will ultimately kill most of the bacteria/viruses in your body. Additionally, your immune system will then remember the SARS-CoV-2 virus, and if you ever get affected again, your immune system will immediately respond to it. Understanding how vaccines help your body defend against real viruses links directly to our studies on the human body’s defense mechanisms against foreign pathogens.

Leave a Comment!
COVID-19 is a years-long pandemic that still hasn’t ended today, I think it is really important for everyone to know how they can protect themselves through modern technologies and minimize the impact of the virus. I am also intrigued by how fast different vaccine technologies have evolved to help mankind to combat the virus. How do you feel about the re-introduction of protein-based vaccines like Novavax? Do you think this will change the public’s preferences on COVID-19 vaccines? Feel free to leave a comment below and we can discuss more about this topic! For more information on this post, go to for the latest research and updates.

Unlocking Our Ancient Past: Exploring the Genetic Legacy of Extinct Cousins DNA

Have you ever wondered where we came from? Who we were? What genes truly lie within us, our mothers, fathers? According to a recent research article from ScienceDaily, Neanderthal genetics is one of them, and the genes still affect human life today. In this research article, the researchers from multi-institution teams, including Cornell University, have shown that Neanderthal genes comprise about 1 to 4% of the genome of present-day humans, mostly of those whose ancestors migrated out of Africa. These genomes are not surprising to the scientific community, but their effect on today’s society in human bodies is remarkable. Through a new plethora of computational genetic tools, researchers found the genetic effects of interbreeding between humans of non-African ancestry and Neanderthals that took place 50,000 years ago, as well as the effects on present-day human life. 

Close up of a Neanderthal in a museum

 In a study published in eLife, researchers reported that some Neanderthal genes are essential for specific traits in modern humans. Using an extensive dataset from the UK Biobank consisting of hereditary and trait information of nearly 300,000 Brits, the researchers examined more than 235,000 genetic variants likely to have originated from Neanderthals. They found that 4,303 of those differences in DNA play a vital role in modern humans and influence 47 distinct genetic traits. These genetic traits can include how fast someone can burn calories or a person’s natural immune resistance to certain diseases. Isn’t that unbelievable? How did something from so many years ago affect such a critical part of our lives? Even though they lived thousands of years ago, we all have a part of the Neanderthals in our genetics.

In another article by U.S.News, the idea of immune resistance through our body’s fight against COVID-19 is displayed. The results show that some people who have increased genes from their Neanderthal ancestors may have an increased likelihood of suffering severe forms of COVID-19. These genes, haplotype, increase the risks of hospitalization and not recovering from the virus, showing that having these traits while being able to burn calories fast may cause harm to us as well. As appealing as it might sound, I know it does to me that Neanderthal genes can help in various ways; it is also quite scary. The risk factors of diabetes, heart problems, and obesity can lead to death when mixed with the virus and the gene itself lingering within us. Since these genes are a part of our fundamental hereditary units and will continue to pass down from generation to generation, with all of these effects, this investigation commenced and evolved into an important and crucial step toward understanding where we came from and who we are. Therefore, these traits affect the lives of humans every day in COVID as well as provide multiple factors of traits that we live with every day, not even knowing where they came from.

Hospital HallwayNovel Coronavirus SARS-CoV-2

As an AP Bio student, in Unit 1, we talked about the parts of the cell along with the DNA that is within the cell. These cells are deeply related to what this topic is about, as the process in which genes work revolves around the cell that it is in. First, it starts with transcription, which is the process in which the genetic material is stored in DNA and replicated into a molecule of messenger RNA. The information goes from the DNA in the nucleus to the cytoplasm to carry out protein synthesis. In the cytoplasm, ribosomes make the proteins that create these specific effects mentioned above. Each gene carries instructions for the proteins that determine your features, such as eye color, hair color, height, and, in this case, immune resistance. These two must connect with each other to fully understand how these genes are still here thousands of years later. The answer is that the genetic material has been carried down for this time through each and every ancestor we have had. It’s pretty scary, if you ask me.

Diagram of a gene on a chromosome CRUK 020

I am not the only one who believes that these causes of our ancestral genes are threatening. If you are like me and want to continue learning about this, reach out! As well as anyone with first-hand knowledge of the research or possible medical intervention, please comment! Share your knowledge with me. The custom software discussed in the ScienceDaily link from UCLA is available for free download and use by anyone interested in further research. So, if you are an AP Bio student like I am or just interested in the genes defining us, even though they are from thousands of years ago, join the conversation. These traits and genes are just being figured out, as most of the work started in September 2023. No matter what fears you may have, to leave you with a sense of comfort after a long list of possible effects, modern human genes are prevailing over successive generations. Therefore, this research, although evolving with us, must continue.

Genetic Variation the Savior

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.

Can Your Lungs Work Against COVID-19?

Within the last two to three years there has been an immense focus in the field of science, COVID-19. This pandemic has sparked a myriad of research opportunities as well as brought up questions we didn’t even know we needed answered.

With this, recent research at the University of Sydney shows that our lungs contain a protein that blocks the COVID-19 infection and works to create a protective barrier within our body. The way it works is that a protein receptor found in our lungs sticks to the virus, and then pulls it away from the targeted cells. The protein is known as the Leucine-Rich Repeat-Containing Protein 15 or in short, LRRC15. For context, leucine is an essential amino acid for protein synthesis as well as many other biological functions. The protein is a built-in receptor inside of our bodies that binds to the COVID-19 virus and doesn’t pass on the infection.

Lungs diagram detailed

Initially, the research was published on February 9, 2023, in the PLOS Biology Journal. Led by Professor Greg Neely and his team members, the findings serve to open a new sect of immunology and COVID research, specifically around the protein, LRRC15. Moreover, it creates a path to develop new drugs and treatments to prevent infections such as COVID-19. Greely states that ” This new receptor acts by binding to the virus and sequestering it which reduces infection,” essentially the receptor is able to attach to the virus and “squish” it before it moves to infection. He also pushes the idea that the new receptor can be used to “design broad-acting drugs that can block viral infection or even suppress lung fibrosis.” Continually Dr. Lipin Loo, one of Greely’s team members, mentions, “We think it acts a bit like Velcro, molecular Velcro, in that it sticks to the spike of the virus and then pulls it away from the target cell types,” here he outlines the stickiness of both the receptor and the virus as well as the receptor’s nature to latch onto the virus and “hold” it. In addition, Loo states, “When we stain the lungs of healthy tissue, we don’t see much of LRRC15, but then in COVID-19 lungs, we see much more of the protein,” here he fronts the idea that COVID-19 lungs are far richer in the LRRC15 protein than normal lungs, this may be due to a result of the protein’s ability to immobilize the virus.

To outline COVID-19 infects us by using a spike protein to attach to a specific receptor in our cells. It mainly uses the ACE2 receptor to enter human cells. Moreover, our lung cells have high levels of ACE2 receptors, which is why being infected can often cause severe problems in our lungs. Similar to ACE2, LRRC15 is a receptor for COVID. But, LRRC15 does not support infection, instead, it sticks to the virus and immobilizes it. This prevents other cells from becoming infected. LRRC15 attaches to the spike of the virus and pulls it away from certain target cell types. The LRRC15 protein is widely present throughout our body, it is in the: lungs, skin, tongue, fibroblasts, placenta, and lymph nodes. However, the researchers observe that the lungs “light up” with LRRC15 after infection. They think the new protein is a part of our body’s natural response to combatting the COVID-19 infection. It creates a barrier that separates the virus from our lung cells most susceptible to COVID-19 infection


To connect to our AP Bio Class, we learned about adaptive immunity where we develop an acquired immunity after being exposed to pathogens, a specific response. I see some similarity here in that the LRRC15 protein is specific to immobilizing the COVID-19 infection. Additionally, in our Cell Signalling Chapter, we focused on signal transduction and its stages, reception, transduction, and response. Specifically in the reception stage, we focused on intracellular and transmembrane receptors. I think that LRRC15 would be transmembrane in order for it to efficiently bind to the COVID-19 Spike. With this, however, I would like to see more about the transduction component of the LRRC15 receptor. Lastly in our Enzyme Unit, we learned about how different factors can affect enzymatic activity; heat, pH, and even general surroundings. I wonder which factors work to hinder and work to stimulate the purpose of the LRRC15. I invite any and all comments with additional info relevant to the topics discussed.

COVID-19 Puts the AGE in TeenAGEr

A new study from Stanford UnBrain 090407iversity suggests that stress from the COVID-19 pandemic may have changed the brains of teenagers, resulting in their brains appearing years older than the brains of pre-pandemic teenagers. The pandemic resulted in increased anxiety and depression among teenagers, but this new research indicates that the effects may not just stop there.

Scientists know that traumatic childhood experiences can accelerate changes in brain structure. Research conducted by Katie McLaughlin, associate professor of Psychology at Harvard University, and her team led to the conclusion that adversity was connected with reduced cortical thickness. This is a sign of brain aging because as people age, their cortices naturally thin. 

Marjorie Mhoon Fair Professor of Psychology Ian Gotlib originally designed a long-term study to research the effects of depression during puberty. He had been conducting brain scans on 220 children, ages 9-13, but he was not able to continue due to COVID-19. After the pandemic, Gotlib resumed his study, and the results were shocking. Researchers discovered that the deveDiversity of youth in Oslo Norwaylopmental process of cortical thinning had been accelerated for the teenagers compared to normal brain development. According to Gotlib, “Compared to adolescents assessed before the pandemic, adolescents assessed after the pandemic shutdowns not only had more severe internalizing mental health problems, but also had reduced cortical thickness, larger hippocampal and amygdala volume, and more advanced brain age.” It remains unclear to scientists whether or not the teenager’s brain age will eventually catch up to its chronological age.

Scientists speculate that the increased anxiety, depression, and overall mental health issues teenagers are experiencing following the pandemic may be linked to cortical thinning. Researchers speculate that cortical thinning may be linked to the expression of certain patterns of genes associated with different psychiatric disorders. Additionally, from studying children who suffered childhood trauma prior to the pandemic, researchers already know that negative childhood experiences can increase the risk of depression, anxiety, addiction, and other mental illnesses. The risk of physical conditions, such as cancer, diabetes, and heart disease, increases as well. 

Jason Chein, professor of psychology and neuroscience and the director of the Temple University Brain Research & Imaging Center, found the research intriguing, but he cautioned against accepting the conclusion that children’s brains definitely aged faster. “It’s pretty interesting that they observed this change,” he said. “But I’m reluctant to then jump to the conclusion that what it signals to us is that somehow we’ve advanced the maturation of the brains of kids.”


AP Bio Connection 🙂

I chose this topic because I was interested in the effects of the pandemic on people in my age group. This topic connects to AP Bio because brain aging has been linked to increase stress hormones. The stress hormone corticosteroid activates an intracellular receptor which results in the changed gene expression. Due to the fact that corticosteroids activate intracellular receptors, they must be nonpolar molecules in order to enter the cell membrane. Feel free to comment down below if you enjoyed the article!!

SARS-CoV-2 Is Making My Heart Ache??

New research from the University of Maryland School of Medicine’s (UMSOM) Center for Precision Disease Modeling identifies the specific protein in SARS-CoV-2, the virus responsible for COVID-19, that causes damage to heart tissue.

Protein Structure Gif

Some experiments they did were performed on fruit fly hearts. When Nsp6 is present in a fruit fly heart, the heart shows structural defects compared to a normal heart without the viral protein. However, when fruit fly hearts with the viral Nsp6 protein are treated with the drug 2DG, the hearts begin to resemble normal hearts more closely.

In their latest study, researchers found that the Nsp6 protein is the most toxic SARS-CoV-2 protein in the fruit fly heart. They also discovered that the Nsp6 protein hijacks the fruit fly’s heart cells, activating the glycolysis process and disrupting the mitochondria, which produce energy from sugar metabolism. When they blocked sugar metabolism in fruit fly and mouse heart cells using the drug 2DG, they found that it reduced the heart and mitochondria damage caused by the Nsp6 viral protein.

Dr. Han, the lead researcher, says this about the protein : “We know that some viruses hijack the infected animal’s cell machinery to change its metabolism to steal the cell’s energy source, so we suspect SARS-CoV-2 does something similar. The viruses can also use the byproducts of sugar metabolism as building blocks to make more viruses,”


Drosophila melanogaster under microscope

Thus, the University of Maryland School of Medicine’s research identified the specific protein in SARS-CoV-2 that causes damage to heart tissue and has found a potential treatment for it. The protein, called Nsp6, activates the glycolysis process in heart cells and disrupts the mitochondria, which are responsible for producing energy through glycolysis and oxidative phosphorylation. By blocking the processes  with the drug 2DG, the researchers were able to reduce the heart and mitochondria damage caused by Nsp6. This discovery aligns with the topic of glycolysis and ATP generation in AP Biology as it highlights the importance of proper metabolism in the functioning of cells and the potential consequences of disruptions to this process.


COVID-19 and Its History Through The Variants

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

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?

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!

The Covid Complacency Craze!

In the pandemic’s early days, countries reported their COVID-19 levels daily. However, that isn’t the case now. In 2022, countries most often report their COVID-19 infection and vaccination levels only five days a week. Despite this, there are still outbreaks of the virus. China, however, has a strict zero COVID-19 policy which results in lockdowns when too many cases are reported. This means that Chinese citizens often find daily life disrupted by the presence of COVID, an experience that we Americans have left more or less in the past.SARS-CoV-2 without background

This begs the question, which course of action should be adopted by countries worldwide? Of course, a middle ground would be ideal, however, that may be unrealistic as governments are trying to find a “new normal” (as the UK put it). Despite this hope to live with COVID, many people are outraged at what seems to be complacency coming from international governments, as citizens say that more needs to be done. What more is there to be done, though? Besides going back to the early ways of the pandemic, reporting cases and deaths daily, governments worldwide are doing everything possible to keep people informed on both COVID and its effects.

People's Republic of China (no claimed territories)

China’s lockdowns, while effective, are very extreme by international standards. There is a call from citizens in China asking for the COVID-19 protocols to be lessened, as the lockdowns are affecting people’s livelihoods. There are small wins, as the Chinese government has slightly repealed COVID-19 protocols, as citizens no longer need to show a negative covid test to use public transport. A study showed that when intrusive protocols are introduced, people overall show “non-compliance in applying health protocols” meaning that while China’s health practices may be effective for now, they may mean trouble in the long run as people stop following them. This supports the idea of a happy middle ground between the United States’ and China’s current protocols.

Fears of a Winter COVID-19 Surge

         In March 2020, our planet was invaded, as we were threatened by the very initial strain of the SARS-CoV-2 virus. This event was commonly referred to as the Coronavirus pandemic. Little did we know then that there would also be several increasingly virulent variants facing us in the immediate future. This highly infectious and adaptive virus forced virtually everyone on Earth to quarantine and patiently wait for a worldwide team of multi-disciplined scientists and medical practitioners to develop an approvable and effective vaccine. For at least a year, we sat before our TV sets and awaited the daily numbers of the newly infected, hospitalized, and deaths. Populations throughout the world were being sent to hospitals in an effort to survive this dangerous virus. The hospitals and healthcare workers across the globe were stretched way beyond capacity, and the untold emotional effects on care providers, in itself, reached epidemic proportions.

SARS-CoV-2 without background
The SARS-CoV-2 virus enters and attacks our lungs through our normal respiratory process. The virus causes our lungs to become inflamed, making it challenging for us to breathe. This can lead to pneumonia, an infection of the tiny air sacs inside your lungs where your blood exchanges oxygen and carbon dioxide. These viral effects made it difficult for middle-aged and older adults to cope and often left them vulnerable to the disease. Once the vaccines were advancing to a stage of government approval and being administered to the general population, we began to see statistically significant improvements in the overall ability of our immune systems to “take on” the virus and win the battle. As people were receiving the vaccine, most people were choosing the mRNA vaccines. These vaccines teach your cells to produce a harmless piece of the coronavirus spike protein that triggers an immune response to build antibodies. A spike protein is a specialized combination of amino acids designed to help the immune system know how to respond to the spike protein. In this way, one begins to build immunity to COVID-19, which results in mitigating the adverse effects of the virus or, in some cases, not succumbing to the effects of the virus. Once it does its job, the mRNA quickly breaks down, and the body clears it away in a few days.
All vaccines leave the body with a supply of T-lymphocytes and B-lymphocytes that will remember how to fight that virus in the future. Since COVID-19 is highly adaptive, as evidenced by the emergence of its numerous variants, biomedical researchers have to quickly produce a new vaccine to prevent a new SARS-CoV-2 virus variant from spreading.

Janssen COVID-19 vaccine (2021) F (cropped) 2
New concerns are now arising in the medical community with the threat of yet another new variant strand of SARS-CoV-2 emerging onto the scene as winter approaches. According to the Centers for Disease Control and Prevention, we could be looking at two new omicron subvariants becoming increasingly more dominant in the United States, raising fears that they could start another surge of COVID-19 infections. The new subvariants known as BQ.1 and BQ.1.1 are raising concerns because it appears to be proficient at evading the defenses of currently available vaccination formulations. According to the CDC, in recent weeks, BQ.1 and BQ.1.1 has quickly risen to 44% of all new infections nationwide and is approaching nearly 60% in some parts of the country, such as New York and New Jersey. Additionally, this viral landscape takes on even greater significance as we seem to be in a “viral trifecta” with the more common Influenza (flu) Virus and the Respiratory Syncytial Virus (RSV) taking the stage front and center this Fall and Winter season. Perhaps the best advice is to see your health care practitioner and see if a vaccination or booster shot is right for you!

Is Covid-19 Becoming Immune to Us?

The Coronavirus has been a focal point for each individual in the past three years. Regardless of your age, gender, ethnicity, or even location, COVID-19 has been the one commonality for everyone. Because of COVID-19’s immense reach and detriment, scientists have worked tirelessly to source treatments and provide them to the people. Although the initial treatments worked in the beginning, as the virus grew and adapted, scientists, doctors, and Coronavirus professionals were forced to follow suit. To this day professionals are still trying to keep up with the ever-changing nature of the virus.

New research shows that initial Coronavirus treatments are slowly becoming more and more ineffective as the virus continues to mutate. The initial treatments for COVID-19 mainly consisted of monoclonal antibodies. Simply put, these are antibodies targeted to a specific illness, Coronavirus in this case. Because the antibody is targeted to one specific disease, as the disease mutates the antibody can no longer be applied to the newly altered disease. For example, recently the US Food and Drug Administration issued information regarding one Coronavirus antibody, Evusheld. They essentially stated that there is an increased risk of COVID-19 as certain variants cannot be neutralized or treated by Evusheld, the current monoclonal antibody. These new changes are critical for those with weakened immune systems who are reliant on strong antibodies to protect them.

To continue, scientists are exploring new ways and attempting to find new treatments for mutated viruses. They do this by seeking out vulnerable parts of the virus and creating an antibody for it. A former Harvard Medical School Professor, William Halestine, hopes that these new treatments will soon be in clinical trials for research.

One example of these clinical trials is currently being administered in Brazil and South Africa by Immune Biosolutions, a biotechnology company. Here they have created a new mix of antibodies and administered them to patients with both mild and high-severity cases of COVID-19. Two of the antibodies in the mix aim at a region of a spike protein where the virus would attach to the human cell. They want these antibodies to block this region and prevent the virus from attaching.

This process can connect to multiple concepts and ideas learned in our AP Biology Class. First, we learned about ligands and receptors, where each ligand is shaped specifically to its own receptor. In this scenario, the virus and antibody are both specific ligands for the spike protein and can only attach to specific spike proteins. This can be compared to our understanding of ligands docking with shape-specific receptors. Second, our understanding of antibodies can be paralleled with the company’s antibody mix. We learned that cells have a certain adaptive immunity to respond to new viruses. This can connect to the company creating new antibodies to adapt to the new virus. Furthermore, we learned that cells can have humoral or antibody-mediated responses, Immune Biosolutions antibody mix is exactly this, a humoral response.

I personally believe that there will be a point where the efforts of scientists and professionals surpass that of the virus. Where we can take control of the virus rather than working for it.  Hopefully, we as humans will eventually stop having to create newer and newer antibodies as the virus slows its mutations.

SARS-CoV-2 without background


Why does COVID-19 cause death in some people and no symptoms at all for others?

COVID-19 can have a variety of effects on the human body, ranging from no symptoms at all to death. Researchers have been investigating what factors such as demographics, pre-existing conditions, vaccination status, and genetics, may contribute to the severity of COVID-19 symptoms.

Researchers already know that older people and unvaccinated people are more likely to have complications. According to August data from the US Centers for Disease Control and Prevention, those unvaccinated and over the age of 50 were 12 times as likely to die than those who had received two or more booster shots.

Pre-existing conditions can have a significant impact on the symptoms COVID-19 can cause. For all ages, conditions like heart disease, kidney disease, chronic obstructive pulmonary disease, diabetes, and obesity can exacerbate COVID-19 symptoms. Cancer patients on immunosuppressants, however, are particularly vulnerable. Getting infected may cause a cytokine storm. In AP Bio, we learned that if a pathogen has managed to get past the barrier defenses, macrophages secrete cytokines as part of the innate cellular defense. Cytokines then attract other phagocytes called dendritic cells, as well as smaller phagocytes called neutrophils to digest pathogens and dead cell debris. A cytokine storm is harmful as it can trigger inflammation that damages organs and tissues. Fimmu-11-01648-g001

Scientists have also found that certain genes may predispose individuals to be more susceptible to COVID-19. Studies have shown that some genes from Neanderthals could protect against COVID-19, while other genes could raise the risk of developing severe symptoms. Additionally, scientists discovered that people with variations in the gene called toll-like receptor 7 (TLR7) are 5.3 times more likely to have severe symptoms from COVID-19. Proteins produced from this gene are involved with interferons to alert other cells to raise anti-viral defenses when a virus has invaded. Interferons essentially interfere with the virus. Conversely, having variations in another gene called TYK2 can protect against infection. TYK2 is involved with producing interferons. However, there is a genetic trade-off. Although having more interferons can help fight COVID-19, having more interferons when there is no infection may cause the immune system to attack its own body. Therefore, variations in TYK2 may also increase the chance of developing autoimmune diseases like lupus.

Even with all this research, scientists can not determine the risk that one individual has of having complications with COVID-19. The only factor we can control is our own habits. We should continue to wash our hands, wear masks in crowded spaces, and stay up-to-date with vaccinations. I thought this topic was very interesting because many of us at school do not perceive COVID-19 to be a serious disease anymore. However, we should remain vigilant in preventing the spread of SARS-CoV-2 and other viruses as there are others outside our community that are vulnerable.

How Bats Turned Themselves and the World Upside Down

In a research article written in early-mid November of 2022, Smriti Mallapaty conducts and evaluates the bat ancestry in SARS CoV-2. Over the few years of COVID research, scientists discovered that COVID shares ancestry with bats more recently than they believed. However, recent findings suggest that finding that ancestor is unlikely.
In a recent presentation at the 7th World One Health Congress in Singapore, scientists compared portions of the coronavirus set of genes, which led to the discovery that COVID and bats shared genes as recently as 2016. In addition, it narrowed down the time between SARS-CoV-2 jumping from bats to humans. According to the Bat Conservation Trust, the reason for the transmission of COVID from bats to humans is due to deforestation and livestock farming on the cleared land brought wildlife into much closer contact with humans providing the opportunity for a spillover event.
Bat 03
This study conducted by Mallapaty highlighted the difficulty of finding the direct ancestor of the coronavirus. However, this led to research efforts in Asia. Many southeastern Asian scientists have come together to test the sequencing of viruses in different tissues to identify the ancestor. But, due to their struggle to find their ancestors’ people began to believe that the virus came from a Wuhan Virology facility. In the Wuhan Virology facility, according to the United States Senate, researchers and their collaborators collected virus expeditions on large scales to Southern China and Southeast Asia, where bats naturally harbor SARS-related viruses, on an annual basis from 2004 onwards. Scientists collected samples of bat blood, urine, and saliva. The bats and or samples from the bats transmitted covid to humans beginning of the COVID-19 pandemic.
This passage relates to the AP Biology Curriculum, specifically the Immune system and Adaptive immunity. In adaptive immunity, the body uses Pathogen Specific Recognition to target infected cells through a cell-mediated response. The MHC protein on macrophages and dendritic cells displays the foreign antigen and releases cytokine. The cytokines activate the T helper cells to recognize the antigen and start the cell-mediated response. The T helper cells stimulate other T cells to divide into Killer T and T memory cells. The T-killer cells kill infected cells, and T-plasma cells block off and remember the antigen to cause a faster immune response if exposed again. In addition, one can be further protected by receiving the mRNA vaccine. The mRNAs vaccine blocks the spike protein surrounding COVID cells so it can bind to the receptor on human cells that would allow it in.
 Novel Coronavirus SARS-CoV-2 (51240985843)
Overall, from their rigorous research, these scientists were able to find that SARS-CoV-2’s closest known relative is a bat virus found in Laos called BANAL-52, whose genome is 96.8% identical to SARS-CoV-2. In addition, another virus = is called RaTG13, which is 96.1% identical. They did this using a method of isolating viruses from bats and comparing their genomes. All these percentages reveal that the virus has undergone between 40-70 years of evolution. On the other hand, some researchers say that comparing whole-genome sequences ignores the role of recombination in virus evolution. Recombination is a description of DNA made by combining genetic material from 2 different sources. In this process, pieces of RNA could be very different from SARS-CoV-2, suggesting they are more distantly related, whereas other fragments that are much more similar imply a closer relationship. Therefore to account for recombination, researchers compared bat and pangolin genes and split them into segments and smaller nucleotide segments. At that point, each segment was evaluated with a subset to estimate how recently SARS-CoV-2 shared a common ancestor with a bat or animal virus.
This topic grabbed my attention because I was reflecting on my interactions with animals. Besides domesticated animals, the only animals I have had true interactions with are bats and birds. In addition, since the pandemic, I heard about the role bats play in the spread of COVID but never took the time to understand their involvement. In short, I took this opportunity to educate myself on these creatures that hang upside down and turned our world upside down.

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

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.


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!  


Should EVERYONE Get Boosted? Young Men & COVID Vaccines

COVID-19 is perhaps the most politicized issue in medicine, yet the scientific community is generally in agreement that most, if not all, people should get vaccinated; however, recent studies have shown that for young people (specifically young men) the booster has some cardiac risks. These men are at risk for myocarditis, an inflammation of the heart muscle.

Scientists are concerned with the longHeart rotating.gif-term effects this has on young men, and they must weigh the risks of protecting people from COVID, and eliminating harmful long-term effects of the vaccine. Jane Newburger, a pediatric cardiologist at Boston Children’s Hospital has studied patients suffering from post-vaccine myocarditis. She says, “I am a vaccine advocate, I would still vaccinate the children.”

Conversely, Michael Portman, another doctor studying patients with myocarditis, is more skeptical. He said: “I don’t want to cause panic, but I crave more clarity on the risk-benefit ratio.” Although the rates of post-vaccine myocarditis are minimal, they are still concerning. The rate was 1 in 6700 for 12-15-year-old boys and 1 in 8000 for 16 and 17-year-old boys. For the vast majority of patients, short-term myocarditis resulting from the COVID vaccine was treatable. Scientists still don’t know why some people experience myocarditis after taking the vaccine, but they have some theories.

Jeremy Asnes, chief of pediatric cardiology at Yale Medicine and co-director of the Yale New Haven Children’s Hospital Heart Center gives insight on the topic: “Though rare, myocarditis can be caused by an immune response to a vaccine such as smallpox vaccine, which was the most successful vaccine in history.” The general consensus among scientists is that they don’t know the reason it’s happening, but the inflammatory reaction is concerning none the less.

Young boy receiving a vaccine (48545943301).jpgOverall, the medical community continues to recommend the coronavirus vaccine to people of all ages. A new study published in the American Heart Association journal indicates that the risk of myocarditis from COVID-19 is higher than the risk of myocarditis from the vaccine for the vast majority of people. Specifically, the risk from COVID is 11x higher than the risk from the vaccine.The exception in question is young men, but for now, scientists still believe that the safest choice for everyone is to take the vaccine; however, you should be aware of the rare side effects that can result from taking the vaccine so that you can stay vigilant after you take yours!! I encourage you to leave a comment on this post. I would love to read your feedback!

AP Bio side note 🙂

Myocarditis is related to AP Biology. Since Myocarditis is inflammation of the heart muscle, to determine the connection between AP Bio and this article, we can examine how myocarditis is resolved in patients. In order to fix inflammation, dying cells are engulfed in the coated by phagocytosis and later transOxford AstraZeneca and Pfizer BioNTech COVID-19 vaccine.jpgported by the vesicle to lysosomes that can digest them. This process is controlled by phagocytic receptors which signal to the cell that the particles can and should be engulfed.

I chose this topic to write about because I was interested in learning about the COVID vaccine. Coronavirus was such an integral part of my life experience, and the vaccine allowed my life to get closer to normal. I feel as if I owe the vaccine that changed my life and kept me safe the courtesy of learning about it.

Can Mouthwashes Suppress SARS-CoV-2?

Various Listerine Products

SARS-CoV-2, the COVID causing virus, could spread from the oral and nasal cavities (mouth and nose). Along with infecting the cells of the respiratory tract, the virus also also infects the cells of the lining of the mouth and salivary glands.

A recent study led by Professor Kyoko Hida at Hokkaido University suggests that a component found in mouthwashes could have an antiviral affect on SARS-CoV-2. Low concentrations of the chemical cetylpyridinium chloride, a component of some mouthwashes, has an antiviral affect on SARS-CoV-2.

Mouthwashes contain antibiotic and antiviral ingredients that fight oral bacteria. It has been demonstrated that cetylpyridinium chloride (CPC) reduces the viral load of SARS-CoV-2 by disturbing the lipid membrane surrounding the virus. While there are other chemicals with similar effects, CPC has the benefit of being tasteless and odorless.

In this study, researchers were interested in studying the effects of CPC in Japanese mouthwashes. Japanese mouthwashes typically contain a fraction of the CPC compared to previously tested mouthwashes. Researchers tested the effects of CPC on cell cultures that express trans-membrane protease serine 2 (TMPRSS2), which is required for SARS-CoV-2 entry into the cell.

During this study researchers found that within 10 minutes of treatment CPC decreased SARS-capacity CoV-2’s for cell entrance and infectivity. They also discovered that mouthwashes that contain CPC perform better than CPC alone.

This study relates to AP biology because the chemical found in mouthwash helps breakdown the lipid membrane surrounding the virus just like the cells on your tongue produce lipase which helps break triglycerides down.

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