COVID-19 – BioQuakes

Tag: COVID-19 (Page 1 of 5)

COVID-19’s use of a spike protein to attach itself to human cells has been known for a while. The original vaccines for COVID targeted this – the spike protein’s attachment. However, recent research by researchers at Yale School of Medicine (YSM), Northeastern University, and Rice University shows a novel understanding of how COVID infects human cells.

In class, we went over a video that showed the way COVID binds to a human cell and infects it as an example of cell communication. This video animates well the 2-step process that COVID undergoes. First, the spike protein attaches to a receptor on a human cell, then the spike protein is cut and the protein structure that brings the virus close to the human cell is revealed. The researchers investigated the second part of this process.

The advantage of looking at the second part of this process is that, unlike how the spike protein can mutate often, the structure that connects the membranes of the virus and the human cell is much more specific. This means that building a vaccine that targets the connecting protein structure will require a lower amount of vaccine updates.

Previously the intermediate steps of how the virus brings itself to the human cell were unknown, but the researchers used cryogenic electron tomography (cryo-ET) to image the protein structure of the intermediate steps of the second part of the process. Cryo-ET can capture images of biomolecules down to the subnanometer range. By using both these cryo-ET images and computer modeling, the researchers were able to see new details in the fusion of the virus and human cells.

The researchers modeled that antibodies that bind to the fusion proteins while folding can effectively prevent the fusion of the virus and human cells.

This connects to our AP Bio class on how antibodies work. Instead of binding to what antigens use to bind to human cells, the specific antibodies that the researchers created stopped certain proteins from binding during the fusion process. This prevented the structure of the fusion proteins from folding in on themselves like they would have without the new antibodies.

Would you take another COVID vaccine that would last through mutations?

Unpacking the Year-Round Spread of COVID-19

By miachondria

On January 22, 2025

In Student Post

Have you ever noticed how COVID-19 cases continue to rise in the summer months? While most illnesses thrive throughout winter, COVID-19 has shown the ability to spike in cases year-round. The BBC article titled “Why COVID-19 is spreading this summer” by freelance science writer David Cox discusses how epidemiologists have observed a “summertime surge” in COVID-19 cases in the U.S. over the past four years. Despite their extremely hot summertime climates Arizona, California, Hawaii, and Nevada have seen increased cases and hospitalizations during the summer of 2023. Similarly, in Europe, where positive test rates climbed significantly this past summer. Researchers believe this phenomenon is largely driven by the emergence of FLiRT variants (a part of the newer omicron strand). The FLiRT variant has developed mutations in their spike protein, which allow them to bypass immune defenses- giving me my interest in the topic. As we recently learned in Bio, the mutations can evade barriers found in the innate immune system such as the inflammatory response, natural killer cells, and phagocytic cells. What makes the virus so effective is that it attaches to human cells using the ACE2 receptor in the respiratory tract. As discussed in class, immunocompromised people have a difficult time for memory cells in response to the virus therefore it can often result in long-term COVID-19 or in rare cases death. While people have developed baseline immunity to older viruses such as RSV or the flu, COVID-19 is relatively new immunity, whether from infection, or vaccination wanes more quickly. In addition, Cox discusses vaccination trends throughout the article. Although covid continues to be a threat throughout summer, people have stopped getting the vaccine as consistently as something like the flu. Like discussed in AP bio, COVID-19 is crucial in building adaptive immunity which gives our cells immunological memory. Cox ends the article by discussing how COVID-19 will eventually settle into a more seasonal pattern, although this may take many years. However, these patterns that develop will be harder to read than those of the flu and RSV as the weather does not directly have an impact on the COVID-19 virus. The next question becomes- What does the future of COVID-19 look like as it transitions to a more seasonal virus? Will certain variants arise in certain seasons?

IBS aka COVID

By matomic

On January 22, 2025

In Student Post

In our Immune System Unit, we learned about the bodies Inflammatory Response.

Inflammation, as we learned, occurs when a foreign pathogen invades your body. Commonly, you may get infected by a cut or some other aberration in your skin. The Inflammatory Response is an example of innate immunity, meaning it is a general response to foreign antigens. Specifically, the Inflammatory Response will use Macrophages, Dendritic cells, and blood vessels to help combat foreign stimuli. Together these molecules performing their tasks, along with the invading pathogen, will result in your skin showing an anomaly of sorts.

Coronavirus may interrupt this process. Covid-19 may allow for certain harmful microbes to enter the infected cell that will in turn cause more inflammation. With time, this increased inflammation may damage the lining of the intestine. In turn, the intestine will become more permeable, causing an unpredictable amount of immune cells to be released when needed.

This phenomenon can lead to intense stomach problems even long after someone has begun to test negative. As an article from the New York Times outlines, Ms. Carter dealt with stomach issues long after she had stopped testing positive for covid. When she first contracted the virus in October of 2023, her diarrhea was so relentless that she had to be taken to the hospital. However, her problems only got worse as time progressed. In April of 2024, when after only eating bland foods such as plain toast or applesauce, she would experience intense diarrhea. Soon, she was diagnosed with irritable bowel syndrome (I.B.S). Given that various conditions such as norovirus or salmonella can lead to I.B.S, Dr. B. Joseph Elmunzer has theorized that covid may follow a similar trend. Although this conclusion does seem plausible, Dr. Elmunzer is just speculating as he has not or is not referencing any scientific study in regard to this issue. Therefore, I think Dr. Elmunzer’s ideas should be qualified a bit. However, you may think different; do you believe Dr. Elmunzer’s theory can be taken as fact?

Coronavirus may not only affect you while you test positive for the virus. The effects of the virus may continue to present themselves much later in the form of stomach pain. As they had with Sarah Carter. It is even a possibility to develop I.B.S. The primary reason for these stomach problems stems from the effect of covid on our inflammatory response.

How We Prevent COVID-19 Beyond Vaccinations.

By bunsenbyrner

On January 9, 2025

In Student Post

In 2023, Chinese researchers conducted a study to determine the genetic diversity of COVID-19 before and after nationwide policies were instituted to prevent the virus’s further spread. A specific focus was placed on measuring the development of the more recent Omicron variant in terms of genetic diversity. This study was carried out from September 2022 to January 2023 and researchers gathered genomic data and concluded that, after the implementation of international global health policies focused on prevention and control (promoting the coronavirus vaccine for example), there were no particularly genetically unique Omicron variants across all samples (over 21,000 genomic sequences with 1,897 of those being from outside of China) that provide any new harm to human health and safety.

The immense genetic diversity of Coronavirus is primarily due to it being an RNA-based virus. A typical DNA based virus functions in a similar way that steroids cause gene expression in cells because they enter the cell (through endocytosis rather than simple diffusion for steroids) and then head to the cell nucleus to add and virus genes into the cell and cause them to be expressed. However, RNA0based viruses virus types only contain RNA in their genome, releasing RNA directly into the cell (bypassing the transcription phase in gene expression) and immediately interacting with the cell’s ribosomes to create more viruses. Not having DNA means that fewer regulatory processes take place to regulate genomic adaptation, causing more variations to occur among virus particles. This makes it very difficult for modern medicine to keep up with SARS-CoV-2 as antibodies manufactured through vaccines become less effective to newer, more differentiated strands of the virus with different targetable spike proteins. This process is also very beneficial to the replicative abilities of the virus, as RNA viruses are known to replicate at an increased rate than their DNA-centered counterparts. This is due to the fact that eliminating the need for DNA transcription makes the creation of new virus particles much more rapid, making such species typically more volatile. However, Chinese health policies have counteracted the danger presented by viruses such as COVID-19 by enforcing strict policies regarding the spread of the virus and vaccination policies in order to reduce the number of infected hosts and therefore limit the opportunities that these viruses have to mutate beyond our control. This has proven successful as no significantly dangerous strands have appeared since policies to spread vaccination and limit the COVID epidemic in China were implemented.

This study has proven the value that can be derived from taking preventative measures against viruses and that limiting the mutability of pathogenic viruses can lead to long-term health. Vaccinations are an incredibly valuable tool in our fight against diseases and their future usefulness is dependant on our ability to limit the spread and mutation of the pathogen the vaccine targets for. In order to keep ourselves and our neighbors safe, it is our responsibility to take preventative measures against contracting diseases to make sure that vaccines continue to keep us all immune.

This does add to the notion of the potential ineffectiveness of vaccinations given certain circumstances occurring within the virus genome and may show that medicine is overly reliant on the development of vaccinations rather than enforcing more strict prevention measures. The COVID-19 pandemic has shown the extreme unpreparedness that humanity has for the elimination of viruses. The results of this study beg the question if we focus less on the development of new vaccine models and more on limiting virus mutation or would this ultimately be detrimental to human health with minimal benefit? Due to the negative mental impacts that quarantine has had on humans globally, would people even prefer this strategy of prevention?

COVID-19: Could it Treat Cancer?

By mollybdenum

On December 17, 2024

In Student Post

In a study where mice were injected with a substance that mimics the effect that COVID-19 has on the immune system, their tumors decreased in size due to the alteration of particular immune cells. These immune cells are monocytes, which are white blood cells formed in the bone marrow that differentiate into dendritic cells and macrophages when a person is sick. Monocytes typically contribute to the growth of cancer because when they go near the area affected, the tumor changes them. The monocytes become cells that protect the tumor by surrounding it, blocking the immune system from attacking it. In a previous study researchers found that after extreme cases of COVID-19 patients had white blood cells with a receptor that bound to a sequence of COVID-19 RNA. In further experiments, the researchers found that these white blood cells had cancer-fighting properties and did not protect the cancerous cells as they typically do. Instead, the white blood cells activated natural killer cells which then targeted tumors, causing them to shrink.

COVID-19 Virus with Labeled Proteins

Unfortunately the COVID-19 vaccines do not cause the same effect. There are two main types of COVID-19 vaccine. One is a protein subunit vaccine. It is made with the spike protein of the virus, which the body recognizes as foreign, triggering an immune response. It causes plasma cells to release antibodies and activates immune cells to get rid of the protein. The other is mRNA vaccine. After the mRNA is injected, the body’s cells produce parts of the spike protein that are harmless and display them on their surface. This then triggers an immune response like the protein subunit vaccine does. Then, in the future your immune system is better able to protect you from COVID-19. These vaccines do not cause the same effect because they are only a part of the virus; however, something similar could prove to be valuable in fighting cancer. I think that it is fascinating that getting sick with COVID-19 could have such a positive side effect. Of course, there is much more research to do, but this is a really exciting possibility for the future of medicine. What do you think? If you have any thoughts, please share in the comments!

This relates to the AP biology topic of the immune system. Monocytes are white blood cells that play key roles in the beginning of the body’s immune response. Macrophages engulf and dispose of pathogens and infected cells while the dendritic cells call T cells to action by displaying the pathogen’s epitope on their surface. The COVID-19 vaccine relates to B and T memory cells and how they remain in the body ready to fight the specific pathogen if the person gets the same sickness. This is what makes the vaccine effective in preventing a person from getting sick.

Covid-19: Could it’s immune cells fight cancer?

By almoeba

On December 16, 2024

In Student Post

Were you one of many who faced an extreme case of COVID-19? You may have lost your sense of smell, but now you may have tumor shrinking immune cells!

A recent study suggests that the immune cells produced during a severe case of COVID-19 may be more helpful than you think. In her article Julia Goldenberg explains how COVID-19 immune cells may shrink cancer tumors.

The study was done by a group of researchers. They realized that certain monocytes lose CCR2, ultimately becoming nonclassical monocytes with anticancer properties.

Monocytes are a type of white blood cell built to destroy pathogens. With an infection or injury, white blood cells work together and collude to heal the injured or infected area.

In our AP Biology class, we learned how the immune fighting cells are created. These monocytes will ingulf the virus and produce interleukin to activate T-Helper cells. The T-Helper Cells then trigger a humoral response so B cells can split and create B plasma cells which secrete antibodies, and B-memory cells too prevent reinfection. These cells are the immune fighting cells that fight against the tumors.

Goldenberg goes on to explain how the inflammatory conditions during COVID-19 allow this change to occur. When blood tests of patients were taken, they found that the monocytes that were produced from COVID-19 contained a specific receptor. This even occurred with mice! The researchers studied a variety of mice with different types of stage four cancers. When the monocytes were induced, the tumors shrank for all four types of cancer. This is because the monocytes activated natural killer cells.

The researchers are hoping that this can work in humans. However, this wouldn’t work with the current COVID-19 vaccines that are on the market since they their RNA sequence is differs from severe COVID-19. But with more work, hopefully an advanced vaccine can be developed.

Throughout the years we have focused on how negative COVID-19 has been. As it is dangerous and has caused extreme long lasting symptoms for many people, one can only wonder, are there any more benefits to this nasty virus?

New Explanation for how Certain People’s Immune Systems Prevent them from Contracting Covid-19

By madnahallicase

On December 16, 2024

In Student Post

Researchers have completed recent studies of people’s immune responses to Covid-19 pathogens. They found that certain innate immune responses work better at preventing infection of the virus than others. In addition, the researchers were able to recognize patterns relating to the receptors on T-cells which may be able to help in the creation of new strategies to fight infections.

SARS-CoV-2

The experiment was conducted by researchers from Wellcome Sanger Institute, University College London, Imperial College London, and the Netherlands Cancer Institute. It included a group of participants who had never before been exposed to Covid-19, which was an important detail to the experiment as the researchers wanted to observe specifically the immune responses to pathogens it had not encountered before. Each participant was first purposefully exposed to the virus and then closely observed for a duration of time following that exposure. The researchers monitored the blood and linings of the nasal passages of each person daily, taking note of any immune cell activity. The researchers were then able to use single cell sequencing to create their dataset for this experiment. Single cell sequencing is a method of analyzing the nucleic acids within a cell to understand the function and behavior of different cells. Upon further analysis, the researchers were able to identify immune responses that had not been recorded among people previously infected with Covid-19.

The two most notable of the new immune responses found during this experiment were the activation of specialized mucosal immune cells and a significant decrease in inflammatory white blood cells throughout the body. These immune responses were only present in the people who did not experience infection or symptoms after being exposed to the virus. Typically Covid-19 patients have an immune response that is widespread throughout the body, yet these people showed innate immune responses specifically in the nose. On the other hand, the people who ended up becoming infected presented the opposite immune response, allowing the virus to establish itself in the nose. The researchers also suggest that activity of a certain gene preceding exposure to the virus further helped certain individuals to remain healthy. This gene called, HLA-DQA2, codes for a protein that is a part of the leukocyte antigen system which is an important part of the immune system. Using these findings, researchers hope to be able to develop new, better ways to fight off Covid-19 and other viruses.

This connects to the AP Biology unit of the immune system. The topics being studied in this experiment included innate immune responses. The mucosal cells in the nose and inflammation are both examples of innate immunity. In contrast with adaptive immunity, which is specific to each individual pathogen, these innate immune responses do not recognize differences between pathogens. I think that this research is important and will hopefully help in the creation of new medical technologies. What do you think of this research?

Is COVID-19 Linked to Diabetes?

By rebesomes

On January 15, 2024

In Student Post

Today’s children are being born into a world much different than what we once knew. The new reality of our world involves grappling with the effects of COVID-19. However, it seems that some children are experiencing greater effects than we could have imagined. As it was recently discovered, after a child is infected with COVID, he or she may have a heightened risk of developing Type 1 Diabetes. This adds another complicated layer to the pandemic that we thought we had mostly seen the end of. This article will detail the facts of the research while also providing insight from my AP Biology studies.

Over the past three years, we have become all too familiar with SARS-CoV-2, known as the virus that causes COVID-19. We have seen its effects in many different ways in our own lives and the lives of those around us. Now, as research improves, new discoveries have been made about COVID’s link to Diabetes in children. This article from NewScientist by Chen Ly highlights these studies. The article mentions that inside the pancreas are these structures called islets of Langerhans. These islets are groups of pancreatic cells that are responsible for producing insulin and glucagon, the two hormones that are crucial for the regulation of our blood sugar. The body can develop an autoimmune response to these islet beta cells and then fight against them with autoantibodies. If enough autoantibodies are created, they can trigger the onset of type 1 diabetes after killing too many islets in the pancreas. In a research study conducted by Annette-Gabriele Ziegler at The Technical University of Munich in Germany, it was concluded that children who had COVID antibodies were twice as likely to develop islet antibodies than those who have not been infected. This information provides insight on the relationship between COVID antibodies and diabetes. If children’s bodies can create these autoantibodies that kill the islets, the insulin production in young children can be weakened by COVID infection.

As stated in this article from the University of Minnesota, diagnoses of Type 1 Diabetes increased as a result of documented COVID infections. The incidence rate of T1D was 29.9 from January 2020 to December 2021. This was a jump up from the 19.5 incidence rate recorded in 2018 and 2019. This jump suggests that COVID infection is correlated to an observed increase in T1D. In an article by the CDC, it was reported that people under the age of 18 were more likely to receive a diabetes diagnosis after 30 days from COVID infection. This highlights the importance of COVID prevention strategies in order to additionally prevent other chronic diseases. In addition, this PubMed states that during the pandemic, we observed an increase in cases of hyperglycemia, diabetic ketoacidosis, and new diabetes. Th alludes to the possibility that COVID may trigger or unmask T1D.

Recently in our AP Biology class, we have been learning about the immune system and cell communication. This can be related to the research mentioned above in that we have covered the topic of blood sugar regulation and studied the pathway of insulin and glucagon throughout our bodies. Insulin regulates our blood sugar by helping to store the excess glucose in the liver when there is too much of it in the bloodstream. Glucagon does the inverse of this by taking the stored glucose from the liver and bringing it to the bloodstream when blood sugar levels are low. Both of these hormones seek to maintain homeostasis. In addition, we have focused on how our bodies react to viruses, and the different kinds of cellular responses that are necessary to fight infections. This is related to my research for this article because it dives deeper into the concepts of immune responses and blood sugar regulation. Getting to read about these topics in relation to the COVID-19 pandemic has further enhanced my understanding of them.

I chose to write about this topic because of the impact that both COVID-19 and Diabetes has had on my family, which helps me to connect with these topics and heightens my curiosity. I welcome any comments regarding these topics and how they may have affected you or someone you know. What are your thoughts on these findings?

From Individual to Environmental: COVID-19 Antigen Testing Expands

By jamesome

On January 7, 2024

In Student Post

Until recently, testing for COVID-19 has focused on the individual rather than on the environment. However, newly introduced technology promises to expand the scope of COVID-19 detection. Researchers at Washington University in St. Louis have developed an apparatus to detect the presence of the covert virus in environmental settings. Previous attempts at this technology have been limited by the volume of air tested. Without adequate air quantity, the sensitivity of the technology is negatively impacted. The current system, however, is capable of concentrating up to 1000 m³ of air per minute, compared to the two to eight cubic meters assessed in previous attempts. The result is a system that increases viral detection sensitivity while maintaining specificity.

The newly introduced apparatus functions by using centrifugal force to approximate viral particles to a liquid matrix adherent to the wall of the test chamber. Within the matrix are found nanobodies, bioengineered antibody fragments derived from llama antibodies. As we discussed in class, the human immune system is composed of humoral and self-mediated factors. Antibodies fall into the humoral category. While human antibodies consist of a light chain and a heavy chain, llama antibodies are composed of two heavy chains. By isolating heavy chain llama antibody fragments sensitized to the COVID-19 spike protein and then splicing multiple sensitized heavy chains together, researchers were able to amplify the viral signal, in a manner similar to PCR.

While the device has yet to be approved, cleared, or authorized by the FDA, it holds promise for meaningful real-world application. For example, prior to a large public event, indoor spaces could be screened for the presence of COVID-19. If the virus were detected, remediation could be performed and the environment retested prior to the public event. In doing so, countless potential COVID-19 infections could be avoided.

This novel technology diverges from current efforts at viral detection in that it does not rely on the existence of an infected individual but rather focuses on environmental detection thereby constituting primary prevention. In the future, the technology could be applied to prevention of other infectious diseases, both viral and bacterial. Further work is needed to explore the potential application of this method.

I urge readers to respond to the above and offer opinions.

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

By cornophyll

On January 7, 2024

In Student Post

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

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

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

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

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

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

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

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

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

What is the difference between the Pfizer, Moderna and Novavax vaccines?

By ariatom

On December 15, 2023

In Student Post

After the COVID-19 outbreak, various vaccines were developed to fortify our immune response against the virus. However, questions have arisen regarding the distinctions among the three prominent vaccines: Pfizer, Moderna, and Novavax. Despite the emergence and spread of new COVID-19 variants, these vaccines continue to be recognized as effective measures in preventing severe disease.

The Pfizer vaccine is a messenger RN A (mRNA) vaccine, meaning that a small piece of mRNA will instruct the host cell to produce copies of the spike protein

from a harmless version of the COVID-19 virus. The immune system will then identify the viral protein and will begin to produce antibodies that will attach to and mark the pathogens for destruction. Isn’t the immune system so amazing! The immune system then deploys B memory cells to prevent reinfection by remembering the antigen so your immune system can quickly fight it in the future. Common side effects of the Pfizer vaccine include pain, redness, and swelling at the injection site, as well as tiredness, headache, muscle pain, chills, fever, or nausea throughout the body.

Similarly, the Moderna vaccine employs mRNA technology. It instructs host cells to replicate the spike protein, leading to the immune system generating antibodies that identify and target the foreign viral protein. B memory cells are then employed to prevent reinfection by remembering the antigen which allows your immune system to quickly fight it in the future. The side effects of using the Moderna vaccine are also pain, redness, swelling in the area where the shot was administered, and tiredness, headache, muscle pain, chills, fever, or nausea throughout the body. The key distinction between the Pfizer vaccine and the Moderna vaccine lies in storage requirement. Pfizer vaccine needs to be shipped in a special freezer that reaches very cold temperatures compared to Moderna that can survive in less extreme conditions.

In contrast, Novavax is the only non-mRNA vaccine available in the United States. It is a protein adjuvant vaccine. A protein adjuvant vaccine contains pieces of a harmless version of the COVID-19 spike proteins and pieces of an adjuvant. The immune system identifies the spike proteins as foreign bodies and the adjuvant aids in antibody production and activation of other immune cells to combat the spike proteins. The B memory cells are then used to prevent reinfection by remembering the antigen so your immune system can quickly fight it in the future.

Isn’t the way our bodies are able to fight off infection really amazing. Feel free to leave a comment and one fun fact you learned from this blog post!

Is Long COVID-Induced Brain Fog Also Related to Blood Clots?

By photosynthesaad

On December 11, 2023

In Student Post

-As learned in AP Biology, the virus that causes COVID-19 is the SARS-CoV-2 virus. It has spike proteins attached to it that bind to the ACE2 receptors on our healthy cells which allow the virus to fuse with them. The viral envelope attaches to the membranes of our cells and then releases its genetic information to the inside of them. Its RNA hijacks the cells and instructs its machinery to create more virus particles, causing it to further infect the body.

Shown above: SARS-CoV-2 virus with spike proteins attached.

After suffering from COVID-19, many people have experienced a condition called long COVID. Long COVID is a condition that causes either new or previously experienced symptoms from the COVID-19 virus to develop and linger for weeks, months, or even years after recovery. While scientists are constantly discovering more about the condition, they are still not completely sure what causes it. The variety of symptoms in addition to the lack of understanding regarding this topic result in the inability to properly treat the condition as a whole. Instead, doctors usually treat the symptoms individually and specifically to the patient. Some symptoms include chronic pain, shortness of breath, chest pain, intense fatigue, and brain fog. New research shows that long COVID-induced brain fog could possibly be linked to blood clots.

Data were collected from about 1840 unvaccinated adults in the UK who were hospitalized due to severe COVID symptoms. The patients provided blood samples when initially hospitalized, 6 months after hospitalization, and 1 year after hospitalization. They also completed cognitive tests and filled out questionnaires.

Blood clotting is a process that prevents uncontrolled blood loss when a blood vessel is injured. A type of blood cell called platelets combine with proteins in the plasma to form a clot over the injury. However, sometimes blood clots do not dissolve naturally or they can form when there is no injury, which can be very dangerous. Fibrinogen and D-dimer are two proteins involved in blood clotting, which were also later predicted to be linked to brain fog. Fibrinogen is created by the liver and is one of the main components in the formation of blood clots. D-dimer is a protein fragment that is released when the blood clot breaks down. People with more severe COVID cases and higher levels of fibrinogen proved to have worse memory and attention skills and overall rated their cognition more poorly on surveys. People with higher D-dimer levels also rated their cognition as poor and showed to have more trouble going back to work six to 12 months after recovery.

These proteins have already been linked to COVID-19 and fibrinogen has been linked to cognitive issues but scientists are still not completely sure how the proteins cause brain fog in long COVID. Dr. Maxime Taquet, a clinical psychiatrist at the University of Oxford, suspects that the blood clots could be blocking blood flow to the brain or directly interacting with nerve cells. Scientists wonder whether medicines used to treat blood clotting, such as blood thinners, could possibly reduce brain fog and other cognitive issues.

While I have not gotten an official diagnosis, I am very curious about long COVID because I experience many of the symptoms. I’ve had a lasting cough, brain fog, and reflux. Do you or have you ever experienced long COVID symptoms?

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

By charbonknioxide

On December 11, 2023

In Student Post

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

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

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

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

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

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

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

How HLA-B*15:01 Gives the Immune System a Head Start Against SARS-CoV-2

By alectron

On December 11, 2023

In Student Post

In the article I came across, it discusses how researchers have come across an ally within our immune system’s genetic coding. Human leukocyte antigen (HLA), otherwise known as the protein markers that signal the immune system, has been discovered to hold a secret that may revolutionize our approach to combating COVID-19. A specific mutation in the antigen, HLA-B*15:01, has emerged as a key player in asymptomatic infection of SARS-CoV-2. How did scientists stumble upon this discovery, and how does this mutation in the antigen actually allow infection without the presence of sickness?

Research conducted at the University of California, San Francisco (UCSF), led by Dr. Jill Hollenbach, didn’t hesitate to dive right into the genetic phenomenon, finding the very answers to those questions outlined above. Using a national marrow donor database and the COVID-19 Citizen Science Study (CSS) app, they tracked nearly 30,000 individuals through the first year of the pandemic, providing insights into genetic factors influencing COVID-19 infection and immune system-related reactions. In the end, the researchers revealed that a staggering 20% of asymptomatic individuals carried at least one copy of the mutated antigen HLA-B*15:01. Moreover, it was found that those with two copies were over eight times more likely to avoid falling ill.

The secret of these genetic guardians is actually quite simple, and, through collaboration with researchers from La Trobe University in Australia, the UCSF team focused on the memory T-cell – a key element of the immune system’s ability to remember previous infections. Through their exploration, the researchers found that individuals with HLA-B*15:01, even without previous exposure to SARS-CoV-2, demonstrated T-cell responses to a specific viral peptide (the NQK-Q8 peptide). The researchers then concluded that exposure to a kind of seasonal coronavirus, which carries a strikingly similar peptide to SARS-CoV-2 called NQK-A8, enabled T cells in these individuals to quickly recognize Coronavirus and mount a faster, and, overall, more effective immune response. This led to minimal – if any – presence of symptoms within the study.  

Let’s link this research to what we’re currently delving into in our AP Biology class. In this unit in particular, we’ve been discussing and exploring the functions of cell signaling, as well as the ins and outs of the immune system. Thus, there are obvious associations between bodily response, antigens, and the immune system with SARS-CoV-2 to what we are currently uncovering in class. We learned how Helper-T cells kickstart the immune system by releasing cytokines that trigger mitosis in B – plasma B cells (which produce antigens) and memory B cells – and T cells – cytotoxic and memory. Knowing that this mutation in the antigen appears similar to SARS-CoV-2 NQK-A8 peptide, we can understand how this may have triggered an immune response in the past, and that a secondary infections would have been easier to take care of considering the memory B and T cells were already present in the body.

Can you see how it connects to what we’ve been learning in our AP Bio class? Isn’t our immune system fascinating? Let me know how you feel about this discovery!

COVID-19: Multiple Doors and Multiple Species

By atomicmass

On December 11, 2023

In Student Post

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

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

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

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

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

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

Long Term Health Risks From COVID-19 Infection

By evaporation

On December 7, 2023

In Student Post

A recent study examining the health records of 140,000 U.S. veterans suggests that risks of health issues such as diabetes, fatigue, or blood clots may persist for at least two years after a COVID-19 infection.

As learned in AP Biology, the fundamental method in which SARS-CoV-2 virus enters the cells involves the interaction between its spike protein (S-protein) and the angiotensin-converting enzyme 2 (ACE2) receptor present on the surface of human cells. Upon initial contact, the S-protein of the virus binds to the ACE2 receptor. This binding triggers a series of events that hijacks the host cell’s machinery to release viral RNA and replicate itself, finally generating new viral components. COVID-19 can also trigger an excessive immune response known as a cytokine storm, which might lead to T cell obliteration.

The study compared veterans who had been infected with the virus to nearly 6 million others who did not contract COVID-19, analyzing new diagnoses, lab results, and prescription records. The research identified health problems that emerged from a month after individuals contracted the virus.

The research team discovered that patients hospitalized during their initial COVID-19 cases had a higher likelihood of facing subsequent health problems. But those with milder initial infections showed a higher risk for approximately one-third of the medical issues analyzed compared to those who didn’t test positive for the virus. This group, comprising mostly milder COVID-19 cases, could potentially strain the healthcare system more, according to Ziyad Al-Aly, a clinical epidemiologist at the Veterans Affairs Saint Louis Health Care System.

The most prevalent issues observed align with commonly known long COVID symptoms found in other studies. These include fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems. Furthermore, patients initially hospitalized were approximately 1.88 times more likely to experience acute gastritis (stomach inflammation) two years after infection compared to those without a COVID-19 record, while non-hospitalized patients had a risk factor of 1.44 times.

Finally, Al-Aly and colleagues determined that among every 1,000 individuals infected with the virus, there was a collective loss of 150 years of healthy life due to persistent symptoms in these patients. This stark revelation underscores the severe impact of long COVID, highlighting its destructiveness, as noted by McCorkell. Other studies, such as the U.S. Census’ Household Pulse Survey, have similarly noted how COVID disrupts the day-to-day lives of many patients.

Ultimately, with recent increases in COVID-19 transmissions, I strongly advocate for maintaining our vigilance and adhering to health guidelines, such as practicing good hand hygiene, and staying updated on vaccination recommendations. As a fellow germaphobe myself, I will certainly take heed of these practices. These measures remain crucial in curbing the spread of the virus and safeguarding both individual and community health. As the article mentions, even a mild COVID-19 infection could potentially lead to health issues in the months or years following the initial illness.

Let’s all do our part to keep our communities safe and healthy!

The Long Term Effects of COVID-19 Hidden Behind the Fog

By shaliva

On December 7, 2023

In Student Post

COVID-19 was one of the biggest pandemics in United States history. It changed everything including schooling and many other aspects of life, but do you ever seem to forget what life was like before COVID-19? You may be thinking am I just getting old? Why am I losing my memory? Well, findings in Nature Medicine have shown that you may be suffering from what they are calling “Brain Fog”. This Brain Fog can result in recurring memory and concentration lapses that can make it difficult to function every day. You may be thinking, how does this even relate to COVID? Well, It is believed that this brain fog is developed from blood clots triggered by COVID.

Before we get into the brain fog, I want to explain how the body first reacts to COVID-19 entering your cells. AP Bio we learned, that your body activates its innate and adaptive immune systems. First, the innate system releases mast cells which release histamine along with macrophages that secrete cytokines. Cytokines are small proteins that are crucial in controlling the growth and activity of other immune system cells and blood cells. When released, they signal the immune system to do its job. We then see natural killer cells take out any damaged or infected cells while cytokines attract smaller phagocytes called neutrophils and digest pathogens. Along with the Innate response we see the Adaptive response. The adaptive response relies on B lymphocytes and T lymphocytes. The B lymphocytes create the humoral response while the T activates the cell-mediated response. Both are just as important but different. When T-helper cells recognize the antigen it triggers both responses. In the cell-mediated response, the T-memory cells prevent reinfection while the T-killer cells go and kill any infected cells. In the Humoral response the B-plasma cells, secrete antibodies that bind to and neutralize the pathogen which is then engulfed by a macrophage, while B-memory cells also prevent reinfection. Even with all this protection people may still be left with long last symptoms including brain fog.

To find out if this brain fog really came from COVID, a psychiatrist from Oxford named Maxime Taquet took samples of over 1,800 people in the U.K. who had been hospitalized due to COVID-19 and made 6 six-month checks on their symptoms. When examining the blood, they found that people who still had “brain fog” tended to have elevated levels of at least one of two proteins. The first protein is called a D-dimer protein which is produced when a blood clot breaks down. Patients with high amounts of D-dimer tend to have memory problems yet the cognitive side seems to still be intact. Doctors believe these effects were caused by blood clots in the lungs, which lead to low oxygen levels in the brain. The second and seemingly more dangerous protein to find mass amounts of is fibrinogen. This protein is produced in the liver and causes clotting to stop bleeding. When patients have elevated amounts of fibrinogen during COVID-19, they seem to have memory loss along with scoring poorly on the cognitive test. These patients show signs of dementia. Taquet believes that fibrinogen may have caused blood clots in the brain or somewhere else that directly affects the brain.

After hearing about the findings Resia Pretorius was very excited. From her own research, she has found connections between COVID and brain fog. She believes that the spike protein of COVID binds to the fibrinogen and causes it to change shape. But she believes this discovery can help determine ways to cure long COVID symptoms. So have you been affected by COVID’s brain fog or are you just getting old?

Aftermath Mysteries of COVID-19

By mitochondriadriana

On December 5, 2023

In Student Post

Greetings, health explorers! Today, we’re diving into the twists and turns of a new study that unveils what happens in the aftermath of COVID-19. To put this into context, let’s picture this: you have now gotten rid of COVID from your body after suffering for a few days, but the health challenges still linger. A fresh study with 140,000 US veterans reveals how risks, from diabetes to fatigue, can play the long game for at least 2 YEARS! Crazy right?

The research revealed that patients initially hospitalized during their COVID-19 cases were more likely to experience these health problems. However, even those with milder initial infections were still at a higher risk for about one-third of the analyzed medical issues compared to those who didn’t test positive. The most common problems align with long COVID symptoms such as fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems. The study found that for every 1,000 people infected with the coronavirus, a cumulative 150 years of healthy life is lost due to persistent symptoms, highlighting the significant impact of long COVID.

The article notes limitations. Some of these limitations include relying on electronic health records and potential skewing due to the predominantly male and older veteran population analyzed. It also did not include individuals who may have been infected but did not receive a positive test result in the early stages of the pandemic when testing was limited.

Wow, the impact of COVID-19 on long-term health is truly eye-opening! What are your thoughts on how we, as a society, can better address and manage the challenges posed by Long COVID? Share your insights below!

To set the stage, the World Health Organization (WHO) defines Long COVID, also known as Post-COVID Conditions, as the persistence or development of new symptoms three months post-initial SARS-CoV-2 infection, lasting at least two months with no other explanation. The Centers for Disease Control and Prevention (CDC) expand on this, noting that Long COVID encompasses a large variety of health issues affecting various body systems, even emerging after mild cases or in those who never tested positive for COVID.

Delving into the ideas, Dr. Akiko Iwasaki of the Yale School of Medicine and director of the Yale Center of Infection & Immunity, underscores that Long COVID is NOT A singular disease. Her research puts forward 4 hypotheses, suggesting that persistent virus remnants, autoimmunity triggered by B and T cells, reactivation of dormant viruses, and chronic changes post-inflammatory response may all contribute.

In AP Biology, we learned about the immune system and B and T cells. The immune system plays a crucial role in identifying and eliminating pathogens, but in some cases, remnants of the virus may persist. This situation involves the adaptive immune response, where B and T cells are responsible for recognizing and responding to specific pathogens. Autoimmunity is triggered by B and T cells. The immune system is designed to recognize and target foreign invaders. Sometimes, it can mistakenly attack the body’s own health cells, leading to autoimmune disorders. B and T cells are crucial to the adaptive immune response.

How have your studies or interests in biology influenced your understanding of topics like the immune system and the function of B and T cells? Share your insights!

Some statistics addressed in the Yale Medicine article, address the question of Long COVID’s trajectory, the Household Pulse Survey in the U.S. shows a potential decline, with reported symptoms dropping from 19% in June 2022 to 11% in January 2023. The true prevalence remains elusive, with estimates suggesting 65 million affected globally, potentially underreported due to the rise in at-home testing since 2022.

Now, let’s connect this to the study involving 140,000 US veterans. The article showcases the persistent health risks associated with COVID-19, unveiling that even individuals with milder initial infections face a higher risk of enduring medical issues. Some problems at the top of this list include: fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems.

For every 1,000 people infected, the cumulative loss of healthy life due to persistent symptoms amounts to a staggering 150 years. While the study acknowledges limitations, like reliance on electronic health records and potential population skew, it underscores the importance of protecting ourselves from COVID-19, given its potential long-term health consequences, even from seemingly mild infections.

Long COVID demands continued attention, research, and comprehensive strategies for prevention and management. As we reflect on these findings, it is evident that understanding and addressing Long COVID is crucial.

What are your thoughts on this?

Shifting gears, another article from The Centers for Disease Control and Prevention (CDC) delves into new guidance for healthcare providers treating patients with post-COVID conditions. The term “long COVID” is introduced, emphasizing that these conditions can affect individuals regardless of their initial symptoms. The CDC highlights a broad spectrum of symptoms, including heart palpitations, cognitive impairment, insomnia, and post-exertional malaise (PEM). While primary care providers can manage many cases, the CDC warns against relying solely on diagnostic results. People with post-COVID conditions are advised to continue preventive measures, and COVID-19 vaccines are highly recommended. The guidance is subject to updates as more information becomes available.

The FAIR Health study mentioned in the CDC article, indicates that over 23% of COVID-19 patients experience post-COVID conditions, with pain, breathing difficulties, hyperlipidemia, malaise, and fatigue being common. Half of hospitalized patients developed post-COVID conditions, and there’s a higher risk of mortality following severe treatment, more so for hospitalized individuals. The American Academy of Physical Medicine and Rehabilitation admires the CDC’s guidance for improving healthcare responses for long COVID.

As I did my research surrounding a health challenge that stretches far beyond the initial impact of the pandemic, the significance hits close to home. It’s not just data; it’s the lived experiences of individuals moving through the long-lasting effects of COVID-19. This isn’t just a call to action; it’s a call for our collective attention, research efforts, and a compassionate response. This health issue isn’t confined to statistics; it touches the lives of millions worldwide, making it a cause that resonates deeply within us all.

New Injection Provides Hope for Regaining Smell Following COVID-19 Infection

By garfboxylgroup

On December 5, 2023

In Student Post

Did you or someone you know ever contract COVID-19 and lose your sense of taste or smell? This is called Parosmia. There are people on social media who have tried to theorize ways to regain the ability to smell normally. For example, burning an orange peel. However, if your nasal cavity is damaged, regardless of the strong orange aroma, it may be believed that you will not be able to regain your sense of smell.

So, how was your nose damaged in the first place? The olfactory system contains a zone that detects scents towards the top of the nasal cavity. When molecules diffuse up into the nose, they dock in receptor proteins which ultimately initiates a cascade to create a cellular response. Hence, we are able to smell aromatic molecules.

When someone is infected with the SARS-CoV2 virus, the olfactory epithelial cells are damaged. Doctors have analyzed singular cells following a biopsy in order to examine the effect of the virus on healthy cells. They were able to conclude that the body ignited a innate immunity response, in which swelling occurred where the nerve endings are located. While in some cases the swelling decreased following the innate response, other times, the swelling remained and damaged the tissue.

This can be explained by what we have learned in AP Biology. During an innate immune response, cells release histamines. These dilate blood vessels, while macrophages secrete cytokines. Cytokines attract phagocytes that allow the infected cells and pathogens to be destroyed. The proteins that attempt to interfere with the viruses cause more histamine to be released and overall more swelling. Therefore, the nasal cavity can remain damaged.

However, new research has found that an injection just might help patients with long COVID symptoms to regain their sense of smell. According to Dr. Adam Zoga, one way that patients have begun to smell again is by injecting stellate ganglion blocks into the neck on either side of the voice box. This reaches the stellate ganglia which contains nerve bundles that control your body’s fight-or-flight responses, known as the sympathetic nervous system. Patients also received a steroid injection to decrease swelling.

The patients that participated in the study did not all benefit from it. However, 22 of the 37 that followed up with administrators following the trial injection noticed improvements in one week. Dr. Leigh Sowerby analyzed this data and theorizes that this may work to treat Parosmia because the sense of smell is affected when the sympathetic nervous system is overactive. He believes that this injection “resets” the nervous system, allowing the nerve bundles to return to normal and patients to regain their sense of smell. However, because only 37 of the original 54 patients followed up after the injections, and there was no control group, researchers cannot further extended this claim.

Universal cure for all variants of Covid-19?

By jouleian

On January 16, 2023

In Student Post

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.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: COVID-19 (Page 1 of 5)

Mutations Schmutations: How Revolutionary COVID Research Could Bring a Long-Lasting Vaccine

Unpacking the Year-Round Spread of COVID-19

IBS aka COVID

How We Prevent COVID-19 Beyond Vaccinations.

COVID-19: Could it Treat Cancer?

Covid-19: Could it’s immune cells fight cancer?

New Explanation for how Certain People’s Immune Systems Prevent them from Contracting Covid-19

Is COVID-19 Linked to Diabetes?

From Individual to Environmental: COVID-19 Antigen Testing Expands

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

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

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

What is the difference between the Pfizer, Moderna and Novavax vaccines?

Is Long COVID-Induced Brain Fog Also Related to Blood Clots?

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

How HLA-B*15:01 Gives the Immune System a Head Start Against SARS-CoV-2

COVID-19: Multiple Doors and Multiple Species

Long Term Health Risks From COVID-19 Infection

The Long Term Effects of COVID-19 Hidden Behind the Fog

Aftermath Mysteries of COVID-19

New Injection Provides Hope for Regaining Smell Following COVID-19 Infection

Universal cure for all variants of Covid-19?

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