BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: COVID-19 (Page 1 of 4)

Universal cure for all variants of Covid-19?

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On January 16, 2023

In Student Post

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The main issue with COVID-19 since the beginning of the pandemic has always been the various mutations. Someone could get COVID-19 and develop some sort of immunity, but then a new variant would come around and the immunity would be less effective. Scientists at the Pohang University of Science and Technology are working hard to develop a cure for all variants of COVID-19

COVID-19 is a disease caused by the SARS-CoV-2 virus, which is a member of the coronavirus family. In AP Biology, we learned about viruses and how they infect and replicate within host cells. We learned about how COVID-19 is a prime example of how a virus can cause disease in humans. The SARS-CoV-2 virus enters host cells by binding to a receptor called ACE2, which is found on the surface of cells in the respiratory tract and other organs. Once inside the host cell, the virus uses its own enzymes to replicate and produce more copies of itself. This can lead to the death of the host cell and the release of new virus particles, which can then go on to infect other cells. The immune system plays a crucial role in defending the body against viral infections such as COVID-19. When the body is infected with a virus, the immune system recognizes the virus as foreign and mounts an immune response to try to eliminate it. This can include the production of antibodies, the activation of immune cells such as T cells and B cells, and the release of inflammatory molecules.

The reason COVID-19 has been so infectious and is able to mutate so much is because of the ability of the virus to change structure. This structure change increases the strength of its interaction with hACE2 receptors. An hACE2 receptor is the human version of the Angiotensin-converting enzyme 2, the enzyme that serves as the entry point for SARS-CoV-2. As we learned in AP bio, in order for a virus to enter the body, the antigen must bind to a receptor and then travel into the cell. SARS-CoV-2 binds to hACE2. First, the presence of SARS-CoV-2 produces the protein called, IgG. IgG binds to the spike protein on the SARS-CoV-2 cell and that IgG protein binds with the hACE2 receptors in human cells. This binding of IgG is what allows coronavirus to enter human cells.

Understanding this binding process has been key to developing cures for the virus. Most recently, a research team at Pohang University of Science has developed a revolutionary SARS-CoV-2 neutralizer that can adapt to mutations in the virus. This discovery is groundbreaking in the disease prevention world because the type of technology that is used for this specific example can be spread out across the field and used for other viruses. As Professor Seung Soo Oh described: “It is significant that we have developed the world’s first self-evolving neutralizer-developing platform that shows increasingly better performance with the occurrence of viral mutations.” He added, “We plan to develop it into a core technology that can respond to the next-generation pandemic viruses, such as influenza and Hantavirus.”

This neutralizer works by mimicking the interaction between the virus and the receptor, and than once that reaction is mimicked, its protein fragment and nucleic acids can stick to virus, preventing further interaction with the receptor, which eventually prevents the virus from entering the cells.

In all, a neutralizer that adapts with the virus in order to prevent infection and sickness is a groundbreaking discovery that could potentially change the way COVIS-19 (and viruses as a whole) are looked at.

 

Researchers Find Ways To Combat COVID-19

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On January 16, 2023

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Ever since COVID-19 was discovered scientists had no idea how to stop this virus. After lots of research we were able to know that there were many different variants of  COVID-19. We understood that some variants were stronger than others according to research. There is an article that talks about how they can be able to stop all kinds of COVID-19 viruses and the different variants. In the article, Professor Seung Soo Oh had an idea on how to stop all kinds of variants in one go. He says that the virus can change its structure whenever. It will then bind to the angiotensin-converting enzyme receptor which is a receptor protein. His team developed a hybrid neutralizer that is able to bind to the virus which then cause the virus to not interact with the protein receptor. This neutralizer was able to be about 5 times more effective then what they first had when COVID-19 was discovered.

According to this article, Omicron which was found in November of 2021 in South Africa, is the most dangerous variant of COVID-19. It is a variant of COVID-19 and is one of the strongest variants. In December of 2019, sub-variants of Omicron began to appear. Some of the sub-variants include BA.5, BQ.1, and BQ.1.1. According to the article, the Omicron sub-variants were very effective and was more transmissible then the Delta variant. The neutralizer should be able to stop Omicron and the sub-variants.

According to another article, variants aren’t weakened by covid vaccines that were had a while ago. In order to help stop COVID-19, the article says that getting boosters will be more effective for any new variants that are discovered. This doesn’t mean they will 100% work. With this knowledge, the new neutralizer that was developed should be able to stop all these viruses from mutating and from entering the cell.

This relates to what we have learned in class this year because we have learned cell structure. When COVID enters the cell, it must bind to a receptor. Once it enters the cell the RNA or DNA would then reproduce. This is similar to what we have learned about how other things enter the cell such as glucose and amino acids. In receptor mediated endocytosis, the ligands must bind to the receptor and then enter the cell. This relates to what we have learned in class because we have learned how molecules are able to enter the cell and how receptors work.

 

SARS-CoV-2 without background

 

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

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On January 16, 2023

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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. 

 

A New Hope? Promising new research finds a way to treat COVID-19

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On January 5, 2023

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Despite the recent decline in COVID-19 cases, researchers and public health officials struggle to treat and prevent new cases of the disease.  A 2022 article in the Washington post outlined the recent efforts by researchers to treat and prevent COVID-19, particularly examining monoclonal antibody treatment, a treatment that utilizes human-made antibodies to aid in the Body’s natural response.

However, according to researchers, new mutations are quickly arising which undermine the effectiveness of these treatments, making it difficult for the medical world to keep up with the virus, so biologists are turning to more novel methods.  One Quebec-based company, Sherbrooke, thinks they’ve found the solution, “We saw a sharp decline in viral loads,” says the company’s chief medical officer Bruno Maranda.

Traditional monoclonal antibody treatment has had trouble inhibiting the binding between the spike protein of the virus SARS-CoV-2 and human cells because the binding location of the spike protein is mutating quicker than researchers can adjust antibody treatment.  According to Andrés Finzi, associate professor at the University of Montréal, “there is a huge immune pressure on the virus,” indicating that it will likely continue to mutate in this way.  

 

Novel Coronavirus SARS-CoV-2 Spike Protein (49583626473)

 

 

However, scientists have noticed that certain areas of spike protein have remained rigid as the virus mutates; one such area is the stem helix.  Because of its lack of mutation, scientists believe that this area is essential to SARS-CoV-2 and if disrupted can limit its ability to mutate and cause harm to our bodies.  

Although the new drug from Sherbrooke uses 2 antibodies that attack the spike protein in a more conventional way, the new third antibody attacking the more rigid areas of the protein has proven effective in all trials that have been undertaken.

Another recent paper has also attempted to amend antibody treatment to target more stable sections of the spike protein: the fusion peptide.  According to the chief of the Antibody Biology unit of the National Institute of Allergy and Infectious Diseases, this structure “acts like a grappling hook and inserts into the human cell membrane, pulling the membrane closer to the virus membrane.”  Researchers hope to use these rigid structures to help develop more reliable treatments and preventions for COVID-19.

This system of antibodies protecting our bodies from illness is similar to what we are currently learning in Biology class.  In class, we learned that in the body’s humoral response to pathogens, B-plasma cells secrete antibodies that bind to pathogens, thereby neutralizing them, allowing them to be quickly engulfed by macrophages and destroyed.  Monoclonal antibody treatment leverages this function of antibodies, creating artificial antibodies to facilitate this interaction more strongly.

While these new developments in COVID-19 treatment are exciting, Finzi warned that “we shouldn’t underestimate the capacity of a coronavirus to mutate.”  Other scientists, including Harvard professor of pediatrics Bing Chen, believe that antibody treatment research should not take the place of other disease-fighting tactics; according to Chen “we need much more effective vaccines, for sure.”  But one thing remains true, and that is that SARS-CoV-2 continues to mutate, and will continue to be a serious problem if we fail or adequately treat and prevent it, and while the number of cases is decreasing, it still remains strikingly high for us to write off the disease as harmless.

The APOE Gene: little known secret to COVID-19 survival

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On December 8, 2022

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I’m sure you all have heard it before – surviving COVID-19 is based on your age, sex, and pre-existing health problems – but what if I told you that another factor you should consider is your APOE gene.

A 22K fragment of APOE4 (APOE4) (IB68)

Apolipoprotein E, also known as APOE, is a gene that suppresses the spread of melanoma and is involved in anti-tumor immune responses. 60% of the population has APOE in its most common form, the APOE3 allele, but the other 40% of the population has APOE2 or APOE4. Unlike APOE3, APOE2 and APOE4 negatively impact the immune response against melanoma, and individuals with APOE4 are at greater risk of developing atherosclerosis and Alzheimer’s. These alleles can create such different responses by coding for proteins that differ by just one or two amino acids, which as we learned in AP Biology, can make a big difference in how a protein is structured and functions.

After studying APOE’s impact on the immune response against melanoma, Sohail Tavazoie’s lab at The Rockefeller University grew curious to research if APOE variants impact COVID-19 outcomes. By testing on 300 mice with a mouse-adapted version of SARS-CoV-2, they found that mice with the APOE3 allele were more likely to survive than those with the APOE2 or APOE4 allele. Mice with APOE2 or APOE4 had a less effective immune response, causing more virus to replicate in their lungs, more inflammation, and more tissue damage. The researchers further demonstrated APOE’s impact by analyzing 13,000 patients in the UK Biobank and discovered that patients with two copies of APOE2 or APOE4 were more likely to have died of COVID-19 than those with two copies of APOE3.

With more studies done in the future, clinicians should prioritize that individuals with these alleles receive not only COVID-19 vaccinations and boosters, but also antiviral therapies if they get infected. If testing for which APOE allele you have sounds important to you, you can easily get genetic testing with a saliva sample or a blood test in a commercial lab.

Pockets Galore! Pockets of COVID-19 Antigens are Stuck in the Body and are Causing Long COVID

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On December 8, 2022

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Do you know someone who has long COVID? It turns out that they may have pockets of SARS-CoV-2 hiding in their body! 

Researchers at University of Colorado’s Anschutz Medical Campus have found in a recent study that patients who suffer from long-term COVID symptoms (called PASC) have 100x more SARS-CoV-2 specific T cells than those who have recovered fully from the virus.  This discovery suggests that the virus itself lingers in the body, not that symptoms continue even after the virus has left.  

This evidence will allow doctors and researchers to shift the mentality surrounding treatment of PASC, as prevPaxlovidiously the only option was to treat exclusively the symptoms.  The shift has led them to antiviral medications (such as Paxlovid) and vaccines, both of which use adaptive immunity to their advantage.  The study found that the body’s natural adaptive immune response focused on systemic inflammation, pulmonary symptoms and reduced lung function because of the high levels of T-cells in the body.  The T-cells are very important in the primary stages of the infection because they help identify and destroy infected cells, however after controlling the infection, it creates longer symptoms, along with continued shortness of breath and lung damage.

About 20-30% of patients infected with COVID developed PASC.  Over the course of over 500 million COVID infections, healthcare systems are pressed to support 150 million patients with lasting symptoms, so a solution is a priority for physicians.  The upcoming solutions’ primary goal is to clear the virus from the body entirely so that T-cell levels decrease back to a normal level.  

In addition to identifying the higher levels of T-cells, the researchers found that the higher the level of SARS-CoV-2 specific T-cells there were in the body, the higher the inflammation levels there were in the body, showing that the T-cells play a role in creating lasting inflammation associated with PASC.  

The next step for the researchers is to continue to do research on the differences in lung cells between people with PASC and people who have not had COVID.  They claim that this research is vital because the “kitchen sink symptomatic treatments have not solved the problem” (Palmer).  

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

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On December 8, 2022

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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!



The Covid Complacency Craze!

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On December 8, 2022

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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.

Clearing Up COVID-19 Brain Fog

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On December 8, 2022

In Student Post

Many people who have recovered from COVID-19 still suffer long-term effects from the terrible virus. From fatigue to loss of smell, to depression and anxiety, there are a wide variety of long-term conditions caused by COVID-19. One condition especially frustrating for patients is known as “COVID-19 brain fog.

Noun confusion 2900892.svgAccording to Harvard Health, COVID-19 Brain Fog is the term used by patients to describe their feeling that their thinking is “sluggish, fuzzy, and not sharp.” Doctors can run tests on patients who feel like they are suffering from this condition; however, oftentimes the tests come back normal. Scientists have several theories regarding the cause of brain fog. For one, COVID-19 can have lingering effects not related to the brain. As I mentioned earlier, patients can suffer from various conditions, which can distract them, impairing their ability to think clearly.

Health Matters interviewed neurologists Dr. Mitchel Elkind and Dr. Alexander Merkler to learn more about COVID-19 Brain Fog. The doctors noted that patients can sustain brain damage from a stroke during their  COBrain Exercising.pngVID-19 infection, and this would be an obvious cause for cognitive differences; however, Dr. Elkind mentioned that “some people seem to have this brain fog out of proportion to their illness.” In theory, patients who had mild coronavirus symptoms should not have long-lasting cognitive effects, but the medical community is finding that they do. One possible explanation is immune system activation.

Like any virus, when the immune system releases molecules to help itself fight off SARS-CoV-2 without background.pngSARS-CoV-2, some of the molecules can affect the nervous system. Sometimes the body can overreact and start attacking normal cells, which is when we start seeing effects such as COVID-19 Brain Fog. The immune system recognizes the viral proteins, but sometimes it mistakes similar-looking proteins in the brain and ends up attacking those. Fortunately, scientists are researching possible treatments for this devastating condition. 

At Augusta University, researchers are developing a drug to treat COVID-19 Brain Fog. It has not been tested yet, but the drug is a polyphenol molecule. One polyphenol molecule, EGCG, inhibits SARS-CoV-2 from binding to host-cell receptor ACE2, thus preventing the virus from entering the host cell. Dr. Stephen Hsu, Professor of Oral Biology and Oral Health and Diagnostic Sciences at Augusta believes that in combination with EGCG technology, EC16, will “yield benefits for Long-COVID relief and protection.”

AP Bio Sidenote 🙂

This connects to AP Bio through the possible treatment of brain fog. EGCG acting as an inhibitor connects to receptor-mediated endocytosis because it blocks the ligand, in this case SARS-CoV-2, from binding to ACE2 and so the cell does not accept the SARS-CoV-2.

I chose this topic because I am interested in the long-term effects COVID-19 has on individuals as well as society.

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

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On December 8, 2022

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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.



 

When You Want to Wake Up and Smell the Roses but You Can’t Smell

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On December 8, 2022

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Does it smell?! (8937541843)

It is March, 2020. Friends of friends of friends are beginning to contract COVID-19. What is one of the most common symptoms you hear about? The loss of smell. This  research article explains how COVID-19 has affected people’s sense of smell, why it’s important to restore this integral sense, and how researchers are working to do so. 

Icaro de A.T. Pires recalls when he realized that he had lost his sense of smell: his grape juice tasted flat. Two months after contracting COVID-19, he was unable to smell the beach on his vacation. Distraught by his inability to smell the salt of the sea, he realized how much he valued his sense of smell and its ability to bring up positive memories. Pires, an ear, nose, and throat doctor, recalled a deaf patient who had also lost her sense of smell, but instead of being unable to smell her vacation location, she was unable to smell at work, which was essential for her job at a perfumery. 

According to the British Medical Journal, about 5.6 percent of people, six months after having COVID-19, have not fully regained their ability to smell and taste. This is concerning if one considers that about 550 million people have had COVID-19. 

SARS-CoV-2 is not the first virus to eradicate people’s sense of smell, but the amount of people who have been affected by it has intensified the need for a solution to smell loss. 

The olfactory sensory neurons work similar to the taste bud cells in terms of cell signaling. There are olfactory receptors in the olfactory epithelium (on the roof of the nasal cavity) that detect smells. There are dendrites within these receptors that are covered in cilia. When these cilia are stimulated by odorants that have entered the nose (in a G-protein-coupled receptor process), this depolarizes the olfactory receptor cells and sends electrical signals to the olfactory bulb, which are tied to the olfactory epithelium by axons, making the olfactory bulb the postsynaptic cell. These then send the signal to the brain that a scent has been received.  

Location of olfactory ensheathing cells (OECs) within the olfactory system

The olfactory sensory neurons are vulnerable to mucus, bacteria, and viruses that might inhibit their ability to work. Recent studies show that SARS-CoV-2 indirectly affects the olfactory system by killing sustentacular cells that support olfactory neurons. This attack harms the olfactory epithelium, causing the neurons to receive less odor molecules. Over time, the inflammation that effects the olfactory sensory neurons decreases, but for some people recovering from COVID-19, it can take up to months for them to regain their sense of smell. 

Researchers are exploring smell training, a process by which a participant smells four different smells 30 seconds each, twice a day for about three months. Generally, smell training seems to work, with about 30-60% of people having improved senses of smell after completing the training. 

The process requires discipline and endurance: taking even one day off can undo your weeks or months of progress. However, this is counteracted by the fact that there are no negative side effects, with the exceptions of frustration for those it does not work for. Doctors want to warn their patients about the possibility that, despite one’s dedication to smell training, it still might be unsuccessful in restoring your sense of smell. 

Researchers are not completely sure how smell training helps, but they have ideas of some possibilities. It is possible that the training stimulates growth of replacement olfactory cells, or it possibly strengthens pathways in the brain. There is also data that shows that smell training boosts the amount of olfactory sensory neurons; however, is unclear exactly how smell training works.  

There are other possible solutions to help restore one’s sense of smell, such as steroids, supplements, or more advanced solutions such as epithelial transplants. 

The article explains how that people do not recognize the importance of their sense of smell until it is gone. In fact, in a survey done on 400 people, 19% percent said that they would rather give up their sense of smell than their cell phone. Would you rather give up your sense of smell or your cell phone? What about giving up your sense of smell or your little left toe? 15% percent of people said that they would rather give up their sense of smell over their little left toe. 

Researchers are continuously researching solutions to restoring people’s sense of smell. People who have lost their sense of smell for an extended period of time from COVID-19 are struggling with their ability to live their lives to the fullest-they want to wake up and smell the roses, but they cannot. 

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

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On December 8, 2022

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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.

 

A New Way to Predict COVID-19?

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On December 8, 2022

In Student Post

SARS-CoV-2 without background

According to this article from the Karolinska Institutet, its researchers believe IL-26(Interleukin-26) is a possible biomarker for acute COVID-19 because of its correlation with patients with acute COVID-19 infection in conjunction with its correlation with an exaggerated inflammatory response.

IL-26 is an inflammatory mediator and a driver of chronic inflammation because of its ability to act as a carrier of extracellular DNA, and as an antimicrobial molecule through its capacity to form pores in bacterial membranes.

In addition, this article from the Yale School of Medicine states that high levels of neutrophils, inflammatory cells, are a biomarker for COVID-19 patients who become severely ill. The article also connects COVID-19 with obesity, believing obesity increases the risk of severe illness from COVID-19. Another biomarker is thrombomodulin, a soluble form of a protein on the surface of endothelial cells, which was highly correlated with survival among all COVID-19 patients

Here is an image of a neutrophil:

Blausen 0676 Neutrophil (crop)

 

In an older article regarding biomarkers for the early stages of COVID-19, Professor Burkhard Becher and his team at the Institute of Experimental Immunology at the University of Zurich discovered that the number of natural killer T cells in the blood is a biomarker to predict the severity of the disease. As you learned, killer T cells, also known as Cytotoxic T Cells, are part of the Cell-Mediated Response to kill infected or cancerous cells. In this case, these T-cells help fight against the cells infected with SARS-CoV-2 to get rid of the virus from the body. The reason the vaccine is so important is that it creates memory cells that help prevent reinfection and improves the body’s reaction to the virus

Here is an image of a T-cell:

Healthy Human T Cell

Biomarkers are significant because they give us an understanding of what the virus does to the body and how the body reacts to it. This information can be used to help find early suspicion of disease, confirm disease severity, classify the disease, rationalize therapies, assess response to therapies, and predict the outcome. I believe that by being able to better analyze COVID-19 using these biomarkers, we will eventually be able to control the spread of the virus and end this pandemic we are facing.

Do you think the COVID-19 virus will have another surge or will it lessen and continue to infect us similar to influenza?

Threat of “Tripledemic” This Year

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On December 2, 2022

In Student Post

For the past three years, COVID-19 has been on everyone’s minds. Between the mask-wearing, quarantining, and social distancing performed over this time frame, it is understandable that the spread of other viruses was also curtailed by these measures. However, people are increasingly returning to pre-pandemic activities, and often unmasked – the potential for other viruses to spread rapidly and easily is back.

San Francisco COVID social distancing poster

This winter, influenza is a threat as always – the Centers For Disease Control and Prevention estimate that 2,100-6,200 Americans have already died this year – and fewer Americans have received flu shots this year compared to past pre-pandemic years. but the Respiratory Syncytial Virus (RSV) has the potential to be incredibly deadly this year too.

RSV primarily threatens children and infants, who lack protection with their weaker immune systems. Furthermore, there is currently no vaccine available for RSV. Experts suggest this season to be particularly dangerous because a generation of children have not had frequent exposure to various infections in their lifetime due to the social distancing required by the pandemic, combined with the gradual return of normal activity. When infected, the body’s innate immunity responds. If it fails to stop the virus from spreading, the adaptive immune response begins. Once the infection, in this case RSV, COVID-19, or Influenza are successfully fought off, T-memory cells and B-memory cells continue circulating to prevent serious reinfection. If reinfected, the secondary immune response that occurs will provide better long-term protection.

Children are typically exposed to RSV at least once before the age of two; that number has dropped drastically since the COVID-19 pandemic (not to say that these precautions were not vital and instrumental in controlling the spread of COVID-19). Therefore, they lack this immunity. Unfortunately, there is not much for medical professionals to currently do about this without a vaccine – simply wait for exposure to the virus to rise again. However, the effective vaccines developed for both COVID-19 and Influenza are capable of slowing the spread of both of these viruses – and have been doing so. Through consistent vaccination, we may be able to escape the “tripledemic” experts have been warning of this year.

One Generation’s Trash is Another Generation’s Treasure: How a selected mutation during the Black Death causes dangerous illness today

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On October 24, 2022

In Student Post

The Covid-19 pandemic has certainly changed millions of lives forever, but many scientists wonder how the pandemic could affect the human genome.  In a 2022 article in US news, researchers studied the Black Death, the 14th-century pandemic that wiped out nearly 25 million Europeans, and in particular, how it affected our bodies.

According to researchers, the Black Death led our bodies to select for certain genetic traits which at the time decreased their risk of infection.  These specific genes increased the activity of the immune system to better help fight the plague, however, today these mutations are having dangerous consequences.  Researchers have noticed a connection between such genes and the risk of numerous conditions, such as Crohn’s Disease, Lupus, and Rheumatoid Arthritis.  These illnesses are known as Autoimmune Diseases, a class of illnesses that occurs when the body tricks itself into attacking its own cells.

These specific genes increased the activity of the immune system to better help fight the plague, however, today these mutations are having dangerous consequences

According to LibreTexts, this phenomenon occurs when certain pathogens have a very similar molecular structure to the antigens that our bodies produce.  Therefore, our bodies are tricked into attacking their own cells thinking that they are pathogens.  This destroys important structures in our bodies, the absence of which causes illness, such as Crohn’s disease and Rheumatoid Arthritis.

According to Dutch biologist Henrik Poinar of McMaster University, “A hyperactive immune system may have been great in the past.” This hyperactivity may have led to an increase in activity against the plague, which in turn could have increased survival rates.  This groundbreaking research suggests that even the shortest event of monumental importance can forever change our bodies.  As stated by senior researcher Luis Bareirro, “Our genome today is a reflection of our whole evolutionary history.”

The obvious question here is: will our current Covid-19 pandemic affect our bodies and are our bodies evolving? Researchers say no.  According to Barreiro, Covid’s low fatality rate makes it unlikely to cause any significant genetic change.   However, Covid’s mutations are difficult to predict, and we have no way of knowing how future mutations will affect our bodies.  Furthermore, in a recent study from Stanford Medical school, researchers identified 1,000 genes linked to severe Covid infection.  It is theoretically possible for these genes to be selected for as we evolve, and it is unclear how that could affect our ancestors.

Covid’s low fatality rate makes it unlikely to cause any significant genetic change

This selection is similar to the selection we are performing on fast-growing flowers in Biology class.  Like the removal of flowers without hairs, certain human genetic traits (probably not hairs) perform more favorably in a pandemic environment and may prevail due to natural selection.

While it is impossible to know what the future will hold, it is interesting to analyze how major historical events, like the Black Death, have affected our bodies.  While there isn’t consensus around how the current pandemic will affect our ancestors, scientists agree that these events are clearly linked to our evolution as a species.  According to Barreiro, “It’s not going to stop. It’s going to keep going for sure.”

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.

The Promise of Messenger RNA Therapy

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On February 25, 2022

In Student Post

A recent article about messenger RNA therapy outlines the evolution of messenger RNA therapy and how it has gone from an idea to a globally used treatment in just the past seventeen years. Recently, messenger RNA therapies such as the Pfizer-BioNTech and Moderna COVID-19 vaccines have been used by hundreds of millions of people around the world. 

The author Drew Weissman, a vaccine research professor at the University of Pennsylvania, and his colleague Katalin Karikó created mRNA molecules back in 2005 that would not cause harm when injected into animal tissue. Then in 2017, Weissman and Norbert Pardi found that this mRNA creation could be brought into human cells through a fatlike nanoparticle without harm, and that bringing this modified mRNA in protect mRNA from being broken down by the body and resulted in the immune system generating antibodies and more effectively neutralize the invading virus. Vaccines-09-00065-g001This mRNA fatlike nanoparticle is known as mRNA-LNP (pictured to the left). mRNA is able to enter cells without harm because it is carried in by this liquid nanoparticle which is known for its role in transportation. The Pfizer-BioNTech and Moderna COVID-19 vaccines use this mRNA-LNP, and in clinical trials have shown to successfully prevent over 90% of treated people from contracting COVID-19.

The positive results from many trials and studies of the Pfizer-BioNTech and Moderna COVID-19 vaccines have provided a lot of information on the success of mRNA-LNP. It has been found that mRNA-LNP is much more effective and quicker than other approaches to COVID-19 treatments such as growing vaccines in laboratory cell cultures. 

41541 2020 159 Fig1 HTMLMessenger RNA therapy works by making cells create proteins that induce a reaction from the immune system in response to invading viruses (pictured to the right). This reaction in response to invading viruses is called the humoral response, where cytotoxic T cells are made to release proteins that destroy infected cells. The humoral response also trains the immune system to respond to and attack that virus in the future by creating memory B cells to recognize it, which is called a secondary immune response.  This method of instructing cells to create these proteins yields a greater quantity at a time that conventional protein and monoclonal antibody therapies. 

The success of messenger RNA therapy in COVID-19 vaccines has inspired the further research and use of this method for other viruses, as well as cancers, food, allergies, and autoimmune diseases, and many clinical trials are underway. Messenger RNA therapy could be a much more time and cost efficient alternative for a lot of conditions and treatments. More research still needs to be done, and there are many improvements that could be made (such as smaller doses of or a better supply chain for the vaccine), but overall messenger RNA therapy is very promising for treatments of the future.

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.

Is The Virus That Has Turned Our World Upside Down Able To Be Solved With a Pill?

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On January 30, 2022

In Student Post

The scientific method of developing a hypothesis, testing the hypothesis, collecting the data and presenting the data to other scientists has led the world to many of its greatest scientific accomplishments. As we face greater and greater scientific problems each year, it is necessary to continue this method to find the best treatments for the world’s diseases. Covid-19 and its variants will continue to be at the top of the world’s problems since we see that vaccines don’t stop the spread of the disease and we just don’t know what new variants will do. To solve this, scientists are working hard to create new drug solutions to treat this deadly virus once a patient has been infected. The most recent being the Merck and Pfizer’s pills: Molnupiravir and Paxlovid. Both of these drugs are to be ingested soon after noticing symptoms. Both have shown promising results, but if we want this pandemic to be over with so we can get back to normal, we need assurances that these pills work now and for the coming variants.

Pfizer tested their antiviral combination Paxlovid pill and found that their pill works with an astonishing 89% decrease in hospitalization given in a 3 day symptom onset. When given within 5 days it was slightly less, yet still an improvement from our current numbers. Their research found three of the 389 people with Covid-19 (.08%) were hospitalized, compared to a 27 out of 385 (7%) in the placebo group. The pill is a protease inhibitor, just like the ones used to help stop the spread of HIV. It stops the action of protease, which halts the ability of the virus to replicate. Paxlovid uses a decades-old HIV drug, called ritonavir, that accelerates the protease inhibitor. With this data, the FDA approved Paxlovid just before Christmas.

Pfizer (2021)

Merck partnered with Ridgeback Therapeutics to produce their molnupiravir pill. It is a nucleoside analog, meaning it is an artificial building block of RNA, this introduces errors into the DNA of the Covid virus so it can’t replicate. The early trial stages gave a 48% reduction of the chances of hospitalization or death. The trial stopped once these results were revealed in hopes that it would be distributed to the public early. It was approved by the FDA one day after the Pfizer drug, but can’t be used in kids because of side effects. The effective success rate of the drug later dropped to 30%, so much lower than the Pfizer drug. After staying at a 30% success rate, there were more problems that arose. Due to it being a nucleoside analog, it was shown to be able to potentially harm human RNA in pregnant women. There were animal tests completed that showed both growth problems which would make it impossible to give the pill to pregnant women, children, or adolescents. Lindsay Baden, an infectious disease doctor who was apart of the FDA’s advisory committee said the drug might be helpful for “the right patient population, the right virus at the right time.” Ridgeback and Merck recently decided to let developing, poor countries make molnupiravir so that the drug can help countries that can’t usually afford expensive medicine we buy in the USA.

Merck & Co

Although a lot of the world is desperate for a swift end to the virus that has changed our lives over the past 2 years, these studies have shown how difficult this virus is to prevent and treat. Paxlovid looks like the most usable and safe drug to take when it is compared to molnupiravir.

Omicron’s Effect on the Vaccinated by Vaccination Status

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On January 17, 2022

In Student Post

As the world continues to be stricken by the seemingly everlasting wave of strains of Sars-Cov-2, the vaccine began to give people hope as it was extremely effective against the original disease as well as all the other strains up until now. With sudden jump in corona cases, researchers have discovered that there is a new virus that is soon to take over as the most prevalent virus in the world. It’s been named Omicron but the question that is on a lot of people’s mind is if this new strain will be hindered by the vaccine or will it continue on its rampage across the world.

Study Participant Receives NIAID-GSK Candidate Ebola Vaccine (3)

Studies show that the answer is dependent on vaccination status. Omicron has accounted for “90% of COVID cases in areas like the Midwest” states Doctor Rochelle Walensky. The article later goes on to state that the booster vaccination shot ” increased by 25-fold people’s levels of virus-fighting antibodies.” Ultimately the amount of vulnerability you have to this new strain is directly tied to how many vaccination shot you have. But why do we even need a booster shot if the first two doses should have been enough? Well to answer this question we first need to look at how the initial two doses work. The CDC states that “Vaccines work by stimulating your immune system to produce antibodies, exactly like it would if you were exposed to the disease.”  As we learned in our AP Biology class, by giving you a small amount of sars-cov-2, the dendritic cell is able to enlist the help of plasma B cells and memory B cells by sending out T helper cells. This is known as theHumorale Immunantwort humoral response and is what gives you the ability to fight off breakthrough infections as well as help hinder the symptoms of sars-cov-2. It is able to suppress symptoms as well as prevent reinfections because once your body has fought off a little bit of the virus with the antibodies created by B helper cells your body is able to make a copy of how to deal with it in your B memory cells. The memory B cells are what give you your immunity to the virus. However over time they do run out as you were only given a small amount of the virus so this is where the booster comes into affect. The booster shot is designed so that your body is able to continue to get stimulated by the virus so that you B plasma and helper cells are able to keep memorizing and keep fighting off small (in the case of the vaccine) or big (in the case of an actual infection) Covid cases. There may continue to be more booster that you must take in order to keep your immunity, and no its not because the chip is running out of battery or they want to keep injecting you, but its due to the fact that your body simply can’t remember such a small amount of the virus for very long and if you don’t get the booster you are 25x more likely to contract Omicron than those who have all three. Ultimately the vaccine is still effective against Omicron, however Omicrons ability to be more infectious than any other variant before it is why it was able to take over the world so quickly. That being said there is a very real possibility that there will be a Omicron centered booster shot that will be significantly more effective than the past three shots against this devastating variant. Feel free to let me know how you feel about Omicron, a special new booster, or about how that Vaccine works down below.

 

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