BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: antibodies (Page 1 of 2)

Miracle Drug for Drugs?

A fascinating new drug called CSX-1004 may be the cure to the fentanyl epidemic. Scientists who have recently discovered the drug have been conducting experiments on monkeys to fully grasp the effects of the drug before they begin their human trials. If the drug is found effective, there could be a revolution in the fight against drugs.

 Understanding Fentanyl Addiction

Fentanyl is a highly addictive synthetic drug that is nearly 50 times more potent than heroin and 100 times more potent than morphine. Fentanyl binds to the body’s opioid receptors, receptors responsible for pain reduction, emotions, and breathing regulation. Opioid receptors are G-coupled receptors. As we learned in AP Biology, the G protein receptor is first activated by a ligand, triggering the G protein to activate. The activated G protein causes GDP to turn into GTP. Then, the G protein binds with adenylyl cyclase, triggering ATP to become cAMP. The cAMP triggers the activation on Protein Kinase A, finally, triggering a response. In the case of fentanyl, fentanyl is the ligand. Typical responses of the drug include a feeling of euphoria, drowsiness, nausea, respiratory depression, confusion, and unconsciousness. The drug targets parts of the brain that control reward, causing users to take more of the drug. As abuse continues, the brain is no longer able to naturally produce dopamine, the neurotransmitter that binds to the opioid receptors. An addict quickly becomes reliant on drugs to give them the happiness and pain regulation that they once naturally had.

Antibody IgG1 surface

CSX-1004

CSX-1004 is an antibody that binds to fentanyl in the blood, stopping a great majority of it from reaching target receptors in the brain. As we also learned in AP Biology, antibodies are part of the humoral response and fight against infections. B-Plasma cells, which patrol the plasma, secretes antibodies. These antibodies bind to and neutralize the pathogen until a macrophage engulfs and destroys an antibody-coated pathogen. In conclusion, if CSX-1004 can bind to and neutralize fentanyl, it can potentially be killed or weakened before reaching receptors in the brain!

The Study

Scientists gathered groups of squirrel monkeys and began by giving them increasing doses of fentanyl over 28 days. They found extreme respiratory conflicts at the higher doses. They then repeated the experiment for another month. This time, they treated the monkeys with one dose of CSX-1004. They found that the dose decreased respiratory harm by 15% at all doses of fentanyl.

Timeline. Drug overdose death rates by sex, United States

The Future

If CSX-1004 is found effective and safe for humans, we could be looking at a decline in fentanyl addiction and deaths. Scientist Andrew Bennet stated that “If we can block the high produced by fentanyl, gradually people will stop using it as they realize it is not doing anything”. Fentanyl has been named the most dangerous illegal drug and was responsible for 28.8% drug related deaths in 2018. Drugs have a higher mortality rate than gunshots and automobile accidents. Does this statistic shock you? This is why drugs like CSX-1004 are so important to be in the works. CSX-1004 could be the key needed to prevent more lives lost at the hands of fentanyl.

The Other Mental Side of Covid-19

When thinking of Covid-19 most people think of a fever, cough, or lack of taste and smell. However, there is another symptom found in a recent study, a psychiatric symptom, that remains unknown to most people, yet is still quite dangerous. These aforementioned symptoms are paranoia, delusions, and suicidal thoughts, all of which were developed by teens in the midst of their Covid-19 infections. Luckily, scientists believe they were able to pinpoint the cause of these symptoms.

Scientists believe rogue antibodies, while trying to fight Covid, accidentally targeted their own brain. The antibodies were found in the patients’ cerebrospinal fluid (CSF), which is a clear liquid that flows in and around the hollow spaces of the brain and spinal cord. The rogue antibodies found do target brain tissue, however we can’t say for sure whether they are the direct cause of the newfound symptoms. This is due to the fact that the newly found antibodies target structures on the inside of cells, not the outside.

According to the study, Covid-19  may trigger the development of the brain targeting antibodies. The study also suggests that treatments that calm down the immune system could resolve the psychiatric symptoms. Both teens in the research underwent intravenous immunoglobulin treatment, which is utilized to reset the immune response in conditions related to autoimmunity and inflammation. Following this, the psychiatric symptoms of the teenagers either partially or completely disappeared. However, it remains a possibility that the patients might have shown improvement without any treatment, and due to the limited size of this study, this cannot be ruled out.

3 teens who were hospitalized due to Covid-19 at the researchers’ hospital were chosen for a new study. They tested positive with either a PCR or rapid antigen test. As taught in AP Biology, antigens are the foreign receptors on the surface of antibodies. Immune cells can transport a piece of the pathogen to T-cells for recognition once the pathogen is eliminated. T-cells play a role in triggering B-cells, which then produce antibodies targeted against that specific antigen. Of the 3 patients chosen, one had a history of unspecified anxiety and depression, and after being infected with Covid-19, they experienced delusion and paranoia. Another had pre existing anxiety and motor tics, and after getting Covid-19, they experienced mood shifts, aggression, and suicidal thoughts. The 3rd teen had no pre-existing condition, and after getting Covid-19 experienced insomnia, agitation, and disordered eating.

As part of the study, all 3 patients had a spinal tap which showed they all had higher than the normal amount of antibodies. However, only 2 of the patients carried Covid-19 antibodies, which created more uncertainty in the study. In conclusion, with this small a study, we can’t say for sure whether there is a causation between the antibodies and the psychiatric symptoms despite the evidence.

Based on the evidence presented, do you think there is a causation between the antibodies and they psychiatric symptoms of Covid-19 found in the teens?

Have you or anyone you know experienced these psychiatric symptoms or ones similar to those discussed in the study after getting Covid-19?(2020.05.08) Coleta De exames para Covi-19 (49870440091)

The Revolutionary mRNA COVID Vaccines

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

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

Covid Vaccine

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

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

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

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

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

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

New COVID-19 Vaccine

Did you know that different variants of COVID-19 can have SUB variants as well? Because the Omicron variant is now the world’s most prevalent strain, it has been able to mutate into different sub variants. The XBB sub variants stood out because they contain a high number of genetic mutations compared to other variants. These mutations or changes help the virus avoid the body’s immune response even if one has been vaccinated for COVID-19 already. Specifically the XBB. 1.5 sub variant (also known as Kraken) has a mutation that helps the virus bind to cells making it more contagious. Scientists believe that XBB. 1.5 binds “more tightly to cells in the human body that the predecessors” (Andrea Garcia). This was the dominant strain in June 2023. 

COVID-19 vaccines (2021) A

The updated COVID-19 vaccine is now being recommended by the CDC and has been approved by the FDA as of this September. It is a monovalent or single component version that specifically targets this sub variant of Omicron (XBB. 1.5). This vaccine is meant to broaden vaccine-induced immunity and provide protection from other XBB sub variants as well. This is similar to how the flu shot works in that the formula changes every year depending on which strain is spreading the most at the time. The vaccine will not prevent every version of COVID-19, however, unless there is a great change in the genetics of the virus, it should provide at least partial protection from other strains as well. The treatments for COVID-19 such as antivirals will still work against this new XBB. 1.5 sub variant. 

In AP Biology, we learned about the immune system and how memory T cells and B cells are made to fight the same virus in the future. A virus enters the body through a macrophage or dendritic cell. Viral antigens are then presented on the surface of the dendritic cells or macrophages and infected cells. The viral antigen then binds to the Helper T cell and causes cytokines to be released to stimulate B cells and cytotoxic T cells. This creates a memory helper T cell. B cells divide to create plasma cells and memory B cells. The plasma cells secrete antibodies for this virus. 

This process is why it is important to receive this vaccine even if one has already been infected by COVID before or if one has received the vaccine before because of the new variants such as XBB. 1.5 that are emerging. The previous COVID-19 vaccine does not necessarily protect against the XBB subvariants and having COVID-19 previously and getting those antibodies through the process described above does not mean you have the antibodies for the new strains.

I still got COVID after having the vaccine because it was a different strain of the virus than the one being targeted in the vaccine. This is very common but hopefully this vaccine means that there will be one less sub variant to worry about! 

Is Covid-19 Becoming Immune to Us?

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

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

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

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

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

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

SARS-CoV-2 without background

 

BQ- Outsmarting Bebtelovimab

Neutralizing antibodies for treating COVID-19

On November 30, 2022, the FDA released a statement stating Bebtelovimab, an antibody treatment previously approved to work against COVID-19, has now lost its authorization status, due to the presence of new Omicron subvariants, BQ.1 and BQ.1.1, which are believed to be capable of avoiding this antibody treatment.

 

But, how are BQ.1 and BQ.1.1 able to avoid the treatments? Well, this can be traced back to the spike proteins themselves. 

 

When the SARS-CoV-2 virus enters the body, it is able to bind to the ACE2 receptors and therefore be able to multiply and spread its genetic material to other cells in the body. Thanks to the development of the COVID-19 vaccine, however, our bodies are essentially programmed to respond the same way we would to an actual infection. As a result, we produce antibodies that learn to recognize the spike protein and therefore fight against it. This connects back to our lesson in AP Biology about immunity acquired from infection and vaccination.

 

However, the COVID-19 vaccine was made to protect against the original strain of the virus only (using the original spike protein), thus leaving people defenseless against mutations of the virus, such as Delta and Omicron. This is specifically happening with the newest subvariants, as BQ.1 has mutations of the spike proteins that our bodies don’t recognize as well.

 

Recently, a bivalent version of the vaccine was released to the general public to protect against other mutations of COVID-19 as well, including Omicron. The vaccine does provide protection against the original Omicron variants found at the end of 2021 and beginning of 2022, but because of BQ.1 and BQ.1.1 both having even more dissimilar spike protein mutations, they are able to bypass our antibodies produced by the vaccine, even faster than other subvariants of Omicron. 

 

As a result, it is no surprise that the antibody treatment was pulled by the FDA; considering the variants can even bypass the newest boosters, they would likely be resistant to antibody treatments that were made to treat previous variants of COVID-19.

 

But this decision made by the FDA leaves us with even more unanswered questions than before: without Bebtelovimab approved for usage, what will happen to those hospitalized as a result of the new subvariants? And what about those who become hospitalized with previous subvariants? What will be their best chance?

 

 

 

Coronavirus and Natural Immunity…Are You Protected?

Since the start of the pandemic, scientists have vigorously worked around the clock, conducting research experiments and clinical trials to fully understand how this relatively new virus affects us. How long do our antibodies last? Should I get vaccinated? Can natural immunity protect me forever? The UTHealth School of Public Health, located in Houston Texas, conducted a research experiment on 57,000 volunteers (over the age of 20) across the state to grasp a better understanding of natural immunity and the presence of  SARS-CoV-2 antibodies in our system.

Dornbirn-COVID-19 antibody testing-02ASD

In October 2020, these volunteers enrolled in the Texas CARES survey to provide resources to understand antibody quantities over time. Researchers used blood-drawn samples from Oct. 1, 2020, to Sept. 17, 2021, to analyze the data around levels of antibody presence. Some of the variables identified from the data analysis are age, body mass index (BMI), use of smoking and vaping products, and the severity of the previous infection. Suppose you are exposed to Covid-19 for a greater period of time. In that case, you are much more likely to have a more severe infection which would drastically increase the number of antibodies you will eventually produce. The opposite goes for someone who is very briefly exposed to the virus. However, even with these indicated variables, all volunteers showed a similar rate of decreasing antibodies over time. “Our research shows that the level of antibodies in those previously infected increases for the first 100 days post-infection and then gradually declines over the next 500 days and beyond” (Michael Swartz, Ph.D., associate professor and vice chair of biostatistics at UTHealth School of Public Health). The findings were published in The Journal of Infectious Diseases.

Concluding this experiment, it is safe to say that you are most naturally protected from Covid-19 at 100 days after infection. After that period of time, your protection will gradually wane, slowly making you more vulnerable to severe symptoms again (similar to the covid-19 vaccine).  However, the data suggests that you will have some quantity of antibodies for well over a year after infection. As we learned in class this year, antibodies are a naturally formed secondary response from your immune system. The B-plasma cells secrete antibodies and can send them off to surround and immobilize the pathogen, allowing a macrophage to come and digest/destroy the cell. The B-memory cells are there to help prevent reinfection later down the road. This immune response is a way for our body to naturally protect us while storing information from previous infections for long periods of time. This is what keeps us safe!Antibody Opsonization

 

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

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.

Optimus Prime, Megatron, Proteins? The New Transformer Vaccine Candidate!

Amid the global outbreak of COVID-19, with no end in sight after nearly two years, the future wellbeing of humans is in danger. Coughs, fevers, and shortness of breath have lent way to millions of deaths across the globe. As thousands of researchers relentlessly work to find solutions to this virus, multiple vaccine candidates have emerged. Specifically, in the United States, millions of Americans have received doses of the Pfizer-BioNTech, Moderna, and Johnson & Johnson’s Janssen vaccines. However, scientists at Scripps Research recently recognized a new, self-assembling COVID-19 vaccine as a potentially more efficient and effective way to fight this worldwide battle.

 

Primarily, it is critical to understand how vaccines function as they help protect the immune system. The COVID-19 vaccines currently in effect are mRNA-based; in other words, the messenger RNA signals one’s body to produce a harmless viral protein that resembles the structure of a spike protein. The body, with the help of T-Helper cells, recognizes this structure as a foreign invader as B cells bind to and identify the antigen. The T-Helper cells will then signal these B cells to form B-Plasma cells and B-Memory cells. When getting the vaccine, the B-Memory cells are especially important as they prevent reinfection. This is a process known as adaptive immunity. Here, in the event of future infection with the spike-protein COVID-19, the memory cells would help carry out the same response more quickly and efficiently. Essentially, this process acts as the body’s training in case of any future infections.

 

While the Scripps Research COVID-19 vaccine would evoke a similar immune response to that described above, it differs from other candidates in how it assembles in the human body; this new vaccine would be comprised of proteins that are able to self-assemble. On their own, these nanoparticle proteins would transform into a sphere protein structure surrounded by smaller proteins, mimicking the coronavirus’s shape. Here, the self-assembled spike proteins are more sturdy and stable than in an mRNA-produced structure. Thus, it more accurately prepares the body for future infection with COVID-19. In fact, multiple tests found that mice who were given the experimental vaccine were able to fight off not only SARS-CoV-2 but also SARS-CoV1 along with the alpha, beta and gamma variants.

 

Nonetheless, influencing the public to get a newer vaccine instead of the well-trusted vaccines already in production requires proof of the candidate’s benefits. Primarily, as mentioned, early results find that this new candidate would perform well with many different strains of COVID-19. Additionally, researchers assert that this vaccine would be relatively simple to produce on a mass scale. Lastly, scientists found that this vaccine may well be more protective and long-lasting than current vaccine candidates. Although the process of vaccine approval is lengthy and often difficult, I am hopeful for the future of the Scripps Research vaccine if it is put into production. Moreover, I believe that such experimentation with self-assembling nanoparticle proteins transcends the current pandemic. The benefits of this field present a wide array of opportunities, and I look forward to seeing what its future may hold.

 

What do you think? Are these transformer-like self-assembling particles a gateway to the future of medicine or an unnecessary distraction from effective treatments already in circulation?

We’ve Been Programmed to Fight Coronaviruses since 6 Years Old

It was previously thought that after initial infection your body creates antibodies tohelp your immune system in the future. But did you know that a common cold you had at a young age can affect how your react to covid today? Depending on the specific spike protein, your body may have a positive or negative response to future variants. An article by Rachel Brazil describes this as “original antigenic sin”(OAS) and has been linked to the differing immune responses to COVID-19.

THE HISTORY BEHIND OAS.

In 1960, Thomas Francis Jr, a US epidemiologist, noted that the immune system seemed to be ‘permanently programmed’ to produce specific antibodies against the first strain of flu it encountered. These antibodies would then reactivate when a flu virus shared similar epitopes to that of the first strain. Relating to SARS-CoV-2, the varying coronaviruses cause different immune responses from person to person. Similar to this, we learned about memory cells in AP Bio. Once the adaptive immune response takes place memory B, helper T, and cytotoxic cell are created to support future immunity to that specific virus.

child sick

Microbiologist at the University of Pennsylvania in Philadelphia, Scott Hensley, spoke with the author of the original article about his team’s work with OAS. “Much like flu, most of us are infected with these common coronaviruses by the age of five or six,” says Hensley. It’s surprising to learn that a coronaviruses have been around for many years before the pandemic. What’s even more surprising is that a simple cold we had as a kid can affectus even today. Hensley and his group analysed blood serum samples taken before the pandemic. Their findings were that the samples had antibodies that defended against a ‘common cold’ coronavirus called OC43. These antibodies could also bind to the SARS-Cov-2 spike protein. Hesley’s group then took samples from before and after SARS-Cov-2 infection for testing. Results showed that infection boosted the production of the antibodies that bind to OC43. They also found that these OC43-binding antibodies bound to the S2 subunit of the SARS-CoV-2 spike protein(due to its similar structure to that in OC43). On the other hand, the antibodies did not bind to the S1 region of the SARS-CoV-2 spike and were unable to stop the virus entering cells.

IS THIS A GOOD OR BAD THING?

Hensly’s group once again were studying OAS, but focused on its effects during the 2009 H1N1 pandemic. Their study showed that past infection to other historical flu strains provided protection against the H1N1 virus. While this may seem good, OAS also has drawbacks. The body may produce antibodies that could be used for other virus strains, but they may not be the best fit for the specific virus. As a result of this the ill equipped antibodies bind to the antigens preventing the body from creating more protective response. 

In her article Brazil mentions Aldolfo García-Sastre, director of the Global Health and Emerging Pathogens Institute at the Icahn School of Medicine at Mount Sinai in New York City. García-Sastre observed the levels of the OC43 binding antibodies in patients hospitalized with COVID-19 in Spain. He found an increase in levels of OC43 binding antibodies along with antibodies for HKU1(another betacoronavirus). García-Sastre claimed that, “We looked for a correlation between people mounting higher [levels of] antibodies against these conserved epitopes versus having less protective immunity against SARS-COV-2, and there was a slight correlation”.

THE VERDICT: THERE ISN’T ONE…YET

Because of the varying reactions that follow OAS, the debate on whether or not it is to be seen as beneficial is polarizing. Though th, scientists are still working to find ways to use it in potential vaccines. Comment below to let us know your opinion on the matter!

 

COVID-19 May Induces Cell That Produce Antibodies for Life

Once in our body, SARS-CoV-2, the virus that causes COVID-19, forces the body’s innate immune system to activate. However, the innate immune system response typically is deemed unsuccessful due to the complexities of the virus’s structural components, which then paves way for the body’s adaptive immune response to initiate. As we learned in Biology, adaptive immune response begins with a macrophage engulfing SARS-CoV-2 through phagocytosis. Then, the MHC proteins present on the macrophages, white blood cells that surround and kills microorganisms, remove dead cells, and stimulates the action of other immune system cells,” display the antigen on the surface, creating a ‘wanted’ poster for the immune system (Cancer.Gov). We also learned that eventually, a T-Helped cell comes along and binds to the displayed antigen, which activates the T-Helper cell which fosters the secretion of interleukin, a cytokine. Finally, both B and T cells are stimulated, which then begin the process of fighting off the virus, along with preventing reinfection. One of the cells that assists in the preventing reinfection are B-Plasma Cells, which are, “antibody-producing immune cells [that] rapidly multiply and circulate in the blood, driving antibody levels sky-high”(WashU School of Medicine).

Tingible body macrophageOne crucial step in determining a person’s ability to fight reinfection is testing to see if antibody secretion has either occurred or is currently occurring. While typical blood samples will suffice, “the key to figuring out whether COVID-19 leads to long-lasting antibody protection, Ellebedy [ PhD, and associate professor of pathology & immunology] realized, lies in the bone marrow”(WashU School of Medicine). The B Lymphocytes, which initiate a humoral response, mature in the bone marrow, and so, to determine the prevalence of antibody secreting cells, bone marrow samples must be received from past COVID-19 patients. To determine if antibody production increases after the body completes its fight against, Ellebedy collected blood samples and “As expected, antibody levels in the blood of the COVID-19 participants dropped quickly in the first few months after infection and then mostly leveled off, with some antibodies detectable even 11 months after infection” (WashU School of Medicine). However, people who exhibited mild cases of COVID-19, meaning that their body removed the virus after two to three weeks, antibodies continue to secrete antibodies, and will continue for an indefinite time period.

Covid-19 San Salvatore 09One problem introduced was rooted in the mainstream media, which spread a misinterpretation of data, being that “antibodies wane quickly after infection with the virus that causes COVID-19” (WashU School of Medicine). Ellebedy believes that this is a major misinterpretation of data, and actually means that antibody production is continuing inside of the bone marrow. Typically, antibody production plateaus after a certain period of time preceding infection, yet these numbers don’t go to zero.

Ellebedy concludes that this result is highly promising, especially for people who experienced a more severe infection from SARS-CoV-2, because an increased amount of circulating virus cells typically leads to a stronger immune response due to the body being required to secrete more antibody cells. Although she believes that more studies need to undergo in people who experienced moderate to severe infections, and show if they also have the same everlasting antibody production.

 

 

 

 

 

 

Is A Vaccine Update On Its Way?

On December 11, 2020, the Pfizer-BioNTech COVID-19 vaccine was approved for its first public use. Since that day, there have been multiple variants of the virus, varying in their mutations from the original strain. One of these strains, in particular, is the Omicron variant. This variant is a new strain of COVID-19 and was first identified on November 24, 2021, in Botswana. With the emergence of this new unknown variant, in addition to all of the past variants, has the time come for an updated vaccine that is tailored specifically to the variants? This question is explored in the Bloomberg article Third Pfizer-BioNTech Dose Is Ket To Fight Omicron’s Spread

Solo-mrna-vaccine-8

After researching the Omicron variant in relation to two doses of the COVID-19 vaccine, there was seen to be a 25% reduction in antibodies capable of fighting the virus. However, after a third dose of the vaccine, increased antibody levels close to that of those made for the original COVID-19 strain. With this information in mind, Pfizer stated that an Omicron-specific vaccine may be required. This new vaccine is projected to be ready for the public by March of 2022. The company also stated that their vaccine would change from a two-dose to a three-dose vaccine with the third shot being for Omicron. The third shot would be administered about three months after the first two doses have been given.

Fab fcfragment colors

While the public is waiting for the third dose from Pfizer, Pfizer says that people should use their current vaccine for a third dose, as it would give further protection against the virus. Then, once the Omicron vaccine comes out in early 2022, people should get a dose of that vaccine as well. This new strategy of getting the vaccine is due to new research from multiple labs on the effectiveness of the vaccine on the Omicron variant. An original observation saw a 25 times drop in antibodies, but two other labs found that there is actually a 40 times reduction with this variant. Globally, South Africa found a 41 times drop in antibodies, and a 37 times drop from a German lab. With this research, Pfizer is beginning to look into an Omicron vaccine but must find that it heavily increases protection against the new variant, and if not it will keep the current vaccine in circulation. There is also speculation about a yearly booster for the vaccine, but there must be research conducted on that as well.

The COVID-19 Vaccine: How, What, and Why

We have all seen the news lately – COVID, COVID, and more COVID! Should people get the vaccine? What about the booster shot? Are vaccines more harmful than COVID-19? Will my child have birth-defects? This blog post will (hopefully) answer most of your questions and clear up a very confusing topic of discussion!

Discovery of monoclonal antibodies that inhibit new coronavirus(Wuhan virus)

First off, what are some potential effects of COVID-19? They include, but are certainly not limited to, shortness of breath, joint pain, chest pain, loss of taste, fever, organ damage, blood clots, blood vessel problems, memory loss, hearing loss tinnitus, anosmia, attention disorder, and the list goes on. So, our next question naturally is: what are the common effects of the COVID-19 Vaccine? On the arm that an individual receives the vaccine the symptoms include pain, redness, and swelling. Throughout the body, tiredness, a headache, muscle pain, chills, fever, and nausea can be experienced. To me, these effects seem much less severe than COVID-19’s!

COVID-19 immunizations begin

Now that we have covered effects, you are probably wondering what exactly the COVID-19 Vaccine does – will it make it impossible for me to get COVID-19? Will I have superpowers? Well, you may not get superpowers, but your cells will certainly have a new weapon, which we will discuss in the next paragraph! The COVID-19 Vaccine reduces “the risk of COVID-19, including severe illness by 90 percent or more among people who are fully vaccinated,” reduces the overall spread of disease, and can “also provide protection against COVID-19 infections without symptoms” (asymptomatic cases) (Covid-19 Vaccines Work).

So, how does the vaccine work? Many people think that all vaccines send a small part of the disease into us so our cells learn how to fight it at a smaller scale. However, this is not the case with the COVID-19 vaccine! As we learned in biology class, COVID-19 Vaccines are mRNA vaccines which use mRNA (genetic material that tells our cells to produce proteins) wrapped in a layer of fat to attach to cells. This bubble of fat wrapped mRNA enters a dendritic cell through phagocytosis. Once inside of the cell, the fat falls off the mRNA and the strand is read by ribosomes (a protein maker) in the cytoplasm. A dendritic cell is a special part of the immune system because it is able to display epitopes on MHC proteins on its surface.

Corona-Virus

After being made by the ribosomes, pieces of the viral surface protein are displayed on the surface of the dendritic cell (specifically the MHC protein), and the cell travels to lymph nodes to show this surface protein. At the lymph nodes, it shows the epitope to other cells of the immune system including T-Helper Cells. The T-Helper Cells see what they’re dealing with and create an individualized response which they relay to T-Killer cells that attack and kill virus-infected cells. This individualized response is also stored in T-Memory cells so that if you do end up getting COVID-19, your body will already know how to fight it! The T-Helper Cells additionally gather B-Plasma cells to make antibodies that will keep COVID-19 from ever entering your cells. T-Helper Cells are amazing! As you can see, the vaccine never enters your nucleus, so it cannot effect your DNA! No birth-defects are possible!

You are now equipped with so much information and able to disregard many common misconceptions about the COVID-19 vaccine! Additionally, you can make an educated decision about whether or not you should get the vaccine. I think yes! If you have any questions, please feel free to comment them and I will answer. Thanks for reading!

 

How COVID-19 Antibodies Are Causing Long-Term Effects

The COVID-19 vaccine has been essential in flattening the curve of the pandemic, but there have been reports of various side effects derived from the vaccine. These side effects include allergic reactions, heart inflammation, and blood clotting. These symptoms have been commonly thought to be because of the patient’s immune system. But, this question as to why these immune responses to both the vaccines and responses to the virus itself have been possibly answered in a new article in The New England Journal of Medicine.

COVID-19 vaccines (2021) A

Various types of the COVID-19 Vaccine

 

William Murphy and Dan Longo, both Professors of Dermatology and Medicine respectively, believe that the Network Hypothesis by Niels Jerne contains insight as to why these side effects occur. In this hypothesis, Jerne details the process as to which the immune system regulates antibodies. This process is a cascade, in which the immune system launches antibody responses initially to an antigen. These antibodies can trigger an antibody response toward themselves, causing them to disappear over time. Anti-idiotype antibodies, also known as secondary antibodies, bind and deplete the initial antibody responses. They have the ability to act like the original antigen itself, which would initiate side effects to the person. 

SARS-CoV-2

SARS-CoV-2 spike protein, the protein responsible for binding to ACE2 Receptors

SARS-CoV-2, the virus that causes COVID-19, enters the body by binding its protein spikes to the ACE2 receptor, thus gaining entry into the cell. The immune system then reacts by producing antibodies for the virus, which neutralizes the effects of the virus. However, these antibodies can cause immune responses with the anti-idiotype antibodies. These secondary antibody responses clear the initial antibodies, which results in the depletion of the initial antibodies and a weakened efficiency for antibody production. 

 

Murphy states that “A fascinating aspect of the newly formed anti-idiotype antibodies is that some of their structures can be a mirror image of the original antigen and act like it is binding to the same receptors that the viral antigen binds. This binding can potentially lead to unwanted actions and pathology, particularly in the long term.” He and Longo also believe that these anti-idiotype antibodies can also target the same ACE2 receptors. 

 

In an article published by The Conversation, the ACE2 receptors play an important role in the immune response against SARS-CoV-2. The authors, Krishna Sriram, Paul Insel, and Rohit Loomba, write that the “SARS-CoV-2 virus binds to ACE2 – like a key being inserted into a lock – prior to entry and infection of cells. Hence, ACE2 acts as a cellular doorway – a receptor – for the virus that causes COVID-19.” Personally, this fact baffles me, since it’s truly both amazing and terrifying that non-living viruses are able to manipulate and finesse their way into infecting the host cells. 

 

Returning to the main article, the ACE2 receptors could be responsible for the long-lasting effects being reported to both the vaccine and the virus itself. These responses can also answer why these long-term effects can occur, even long after the infection has passed. 

 

These terms are apparent in our AP Biology classroom, specifically regarding the Immunity System. The immune response used to combat SARS-CoV-2 is Adaptive Immunity, which develops after exposure to pathogens including bacteria, viruses, toxins, or other foreign substances. Due to the complexity of SARS-CoV-2, Adaptive Immunity is used because it’s a specific but slower response to the virus. Both B Lymphocytes and T Lymphocytes are used in the response against COVID-19 but during different stages of the infection. When the virus first enters the body, the Immune System performs Humoral Response, in which B Cells bind to the antigen and secrete antibodies that are made by B-Plasma cells, and these antibodies are stored in the B-Memory Cells to prevent future infection. In the case that COVID-19 enters and infects a cell, the Cell-Mediated Response is used to kill off infected cells using T-Killer Cells and T-Memory Cells are created to prevent future infection.

How do you think this research will be implemented for the prevention of these long-term effects? Let me know in the comments below and stay safe!

How Killer T Cells Could Increase Immunity Against New COVID Variants.

In recent news, there are concerns about the newly discovered COVID variant named Omicron. Preliminary evidence suggests an increased risk of reinfection with this variant, as compared to other variants of concern. Scientists are hopeful that T cells could provide some immunity to COVID-19, even if antibodies become less effective at fighting the disease.

Along with antibodies, the human body’s immune system produces a plethora of T cells which target viruses. Helper T cell’s stimulate killer T cells, macrophages, and B cells to make immune responses. T cells do not prevent infection because they kick into action only after a virus has infiltrated the body. But, they are important for clearing an infection that has already started. If killer T cell’s are able to kill virus-infected cells before they are able to spread to from the upper respiratory tract, it will affect how you feel and will be the difference between a mild infection and a severe one.

Studies by Sette and his colleagues have shown that people who have been infected with SARS-CoV-2 typically generate T cells that target at least 15–20 different fragments of coronavirus proteins. But, the protein particles that are targeted vary from person to person. This means that a variety of T cells will be generated, making it difficult for the virus to mutate in attempt to escape cell recognition. Research suggests that most T-cell responses to COVID variations or previous infection do not target regions that were mutated in recently discovered variants. If T Cells remain active within your immune system against specific variants, they might protect against severe diseases.

Ultimately, in my opinion, this is extremely important since researchers have been analyzing clinical-trial data for several coronavirus vaccines in attempt to find clues as to whether their effectiveness fades in the face of new emerging COVID variants such as Omicron. As of now, coronavirus vaccine developers are already looking at ways to develop next-generation vaccines that stimulate T cells more effectively. Antibodies only detect proteins outside cells, and many coronavirus vaccines target spike proteins, located on the surface of the virus. Since spike proteins are liable to change, it may be prone to mutating and raising the risk that emerging variants will be able to evade antibody detection. T cells, on the other hand, can target viral proteins located inside infected cells, and some of those proteins are very stable. This raises the possibility of designing vaccines against proteins that mutate less frequently than spike proteins, and incorporating targets from multiple proteins into one vaccine.

Biotechnology firm Gritstone Oncology of Emeryville, California, is designing an experimental vaccine that incorporates the genetic code for fragments of several coronavirus proteins known to elicit T-cell responses, as well as for the full spike protein, to ensure that antibody responses are robust. Clinical trials are due to start in the first quarter of next year. If approved, this vaccine could revolutionize how we approach the creation and experimentation of COVID vaccines in the future.

14 Days or 14 Months?

The Infamous “14-day” COVID-19 Illness Has Still Not Ended for Some.

Approximately one in four COVID-19 patients appear to have lingering symptoms, even after they have fully recovered from the virus, says the University of California Davis Health. Known as “Long Haul Covid,” it has been relatively unknown why each person’s immune response differs drastically. 

Feeling sick just two days after the world closed on March 11, 2020, my mom began to show all the symptoms of COVID-19. Tests were scarce, and by the time she was able to get one, it came back negative. However, she dealt with the severe and immediate symptoms of COVID-19 for six months straight. She maintained an on and off fever for months and has still not regained her taste or smell. Unsure of why everyone around her (including myself) contracted the virus and recovered after a mere 14 days, she searched for answers everywhere.

Luckily Dan Longo, Professor of Medicine at Harvard Medical School, published an article this past week in which he thinks he has discovered the reason. Antibodies mimicking the virus. You see, our body has a particular system for how it typically handles viruses.

When pathogens pass the body’s barrier defenses, they trigger innate cellular defenses. In the area of entry, Mast cells release histamine and macrophages (large phagocytic cells), which secrete cytokines. These cytokines attract dendritic cells, which engulf the bacteria (COV2 virus) and fuse it with a lysosome to break it down, preserving the foreign antigen (epitope). The dendritic cell will then display the foreign antigen on an MHC protein on the cell’s surface. A T-helper cell will then come and identify the foreign antigen. Now activated, the T-helper cells will release interleukin (a cytokine) to signal the beginning of the cell-mediated and humoral response. In the Cell-Mediated immune response, the T-helper cells will stimulate other T-cells to divide and create two types of cells. T-memory cells will circulate your body to prevent reinfection, and Cytotoxic T-cells will kill any infected cells. In the Humoral Response, B cells will bind to the antigen on the virus and recognize it, while selected B cells will be stimulated by T-helper cells and divide. The divided B cells will become B plasma cells whose job is to secrete antibodies that bind to and neutralize the pathogen. Or B-memory cells whose job, much like the T-cells, is to circulate the body, preventing reinfection. 

Primary immune response 1

In regards to COVID-19, however, why hasn’t our immune response been consistent for everyone? Longo’s article answers that by closely drawing upon the concepts of Nobel Laureate Niels Jerne’s Network Hypothesis, in which she states that, as usual, the B-plasma cells produce protective antibodies in response to an antigen. However, these same antibodies later trigger a new antibody response, only this time toward themselves. These secondary antibodies are called anti-idiotype antibodies, and they are created when one antibody binds to the set of unique epitopes of another antibody. These secondary antibodies bind to and deplete the initial protective antibody response, mirroring the original antigen itself. Quoted from Longo’s research partner UC Davis Vice-Chair of Research and Distinguished Professor of Dermatology and Internal Medicine William Murphy, “A fascinating aspect of the newly formed anti-idiotype antibodies is that some of their structures can be a mirror image of the original antigen and act like it is binding to the same receptors that the viral antigen binds. This binding can potentially lead to unwanted actions and pathology, particularly in the long term.” Binding to the ACE2 receptor, an angiotensin-converting enzyme identified as the receptor for the SARS-CoV-2 viral entry, the anti-idiotype antibodies could affect normal ACE2 functions. With a lack of research surrounding the theory, Murphy states that he believes some of the long-lasting effects of COVID-19 reported result from the critical tasks of ACE2 being tampered with. In terms of the vaccine, most of the research studies on antibody responses focus on initial protection instead of long-term effects. Thankfully, Longo concludes by saying that most of Murphy’s and his questions are testable and can be at least partially tested in their laboratory.

anti-idiotype antibody

It has been 21 months since my mom first contracted COV2, and thankfully she is doing much better. However, causing much frustration, she has not fully recovered. Similar to an autoimmune disease, she has periods where she feels fantastic and periods when she struggles. And so, while the information about Long Haulers Covid has increased dramatically, it is evident that there is still much to learn. 

Antibody Concoctions: Possible COVID-19 Prevention and Treatment?

We all have heard the exciting news about Pfizer’s COVID-19 vaccine: a possible savior and source of hope for years to come. According to a LiveScience article by Nicoletta Lanese, “an antibody cocktail designed to prevent and treat COVID-19” entered late-stage trials over the summer. Scientists have been working to find an effective treatment that doesn’t have as many limitations as current findings. A treatment known as convalescent plasma therapy has been circulating clinical trials. It is not FDA-approved and therefore not available to the public. Antibodies are extracted from recovered COVID-19 patients and injected into sick patients in order to boost their immune systems. This method is too unreliable and unpredictable.  The plasma donors all have a variety of antibodies. Some have proven to be effective against the virus by not letting it enter cells in the first place. On the other hand, nothing is guaranteed and a patient could be injected with antibodies that have no effect against the virus. To reduce this risk, drug developers have noted the effective antibodies against SARS-CoV-2 and mass produced them in a lab.

This is a representation of what a spike protein would be under a microscope. The clinical trials are testing to see which antibodies can bind to the spike proteins and prevent them from entering/infecting healthy cells.

Another possible therapy called REGN-COV2 has also entered a late phase in its clinical trial. It supposedly has two antibodies that can prevent the virus from infecting healthy cells by binding to the spike protein. Hopefully the FDA approves the drug at the end of its current phase (phase 3), so short and long-term effects can be monitored. The Co-Founder, President, and Chief Scientific Officer of Regeneron, Dr. George Yancopoulos, released this statement: “We are running simultaneous adaptive trials in order to move as quickly as possible to provide a potential solution to prevent and treat COVID-19 infections, even in the midst of an ongoing global pandemic.” Many other pharmaceutical companies continue with their trials to search for antibody treatments against the SARS-CoV-2 virus. The universal goal is to find a longer-term solution and stop the rising mortality count.

I originally chose the topic of prevention, because I thought it was only going to include mask-wearing and social distancing. It’s incredibly interesting that this article is another scientific take on preventative measures. The article shows how hard scientists and companies are working on developing a treatment. My main intention for this topic was to show how important it is for everyone to partake in the effort to stunt the spread of the pandemic. With recommended safety procedures as well as current trials, I’m optimistic that there will be great progress in our near future. I was able to link this to our AP Biology class, because we recently covered the immune system! The article refers to antibodies, and I know that they are the humoral defenses that go for pathogens. These antibodies are originally secreted from B-Plasma cells in order to bind to and neutralize the pathogens. By using plasma from recovered patients, I assume they are relying on the B-Memory cells to prevent infection/re-infection in other patients.

Please let me know what your thoughts are in the comments! How much longer do you think we’ll have to wait? Do these new updates give you hope about returning to a state of normalcy? I’d love to know.

UPDATE

Since the summer of 2020 (when this article was released), a lot has changed. Regeneron’s antibody cocktail was granted an Emergency Use Authorization in November. While this seemed to be heading the trials towards an optimistic future, that was not the case. Presently, only the Moderna and Pfizer mRNA vaccines are FDA-approved for public use. What happened to REGN-COV2? According to this Washington Post article, 80% of the allocated dosage supply is remaining unused in overcrowded hospitals. There is a common sentiment that resources should not be going towards an “unproven treatment”. The only FDA-approved antibody in the Regeneron cocktail is bamlanivimab. Although we are all eager to return to normalcy, we must be conscious of what is the best for our health.

Testing!

When you hear the word “COVID -19 testing” what comes to mind? I have this vivid image of a cotton swab being pushed up my nose. But what exactly is testing? Why is it so important? And what are the types of testing available for our use?

We’ve all heard that testing is important but why? To summarize a supplementary article, COVID testing “leads to quick identification of cases, quick treatment for those people and immediate isolation to prevent spread” (Dr. Eduardo Sanchez). When discovered at an early stage, COVID will be less a threat to a person because doctors can plan accordingly while COVID is still less severe. Even when a person discovers they have COVID not as early as hoped, testing helps to identify anyone who came into contact with infected people so they too can be quickly treated. Contact tracing would not be possible without testing because a person would never know if they are spreading the virus. The only way to be better safe than sorry is to get tested. Someone may show symptoms that are COVID-like but there is still a chance that it could be a common cold, or allergies. It is important to confirm COVID suspicion.

Now that we know why testing is important, what kind of testing is out there? What I found in this FDA article is what I like to call a family of tests; there are numerous different tests to take.

To start things off, let’s talk about Diagnostic testing. Diagnostic testing shows if you have an active coronavirus infection. As of right now, there are two types of diagnostic tests: molecular and antigen tests. Molecular tests detect the virus’ genetic material in a sample from the patient’s nose or throat. This is where test results will take longer because they are sent to labs. From there, the lab essentially converts the virus’s RNA into DNA, and then make millions of copies of the DNA to be processed in a machine. The test is “positive” for infection with SARS-CoV-2, the virus that causes COVID-19. Examples of molecular diagnostic tests include nucleic acid amplification test (NAAT), RT-PCR test, and the LAMP test. Next, there is Antigen diagnostic testing. Antigen tests provide results from an active coronavirus infection faster than molecular tests. The downside to these tests are that they have a higher chance of missing an active infection. Sometimes an antigen test may come back negative, but a doctor might still order a molecular test to confirm.

Different from Diagnostic Tests, there are Antibody (different from Antigen) tests. These tests looks for antibodies that are made by your immune system in response to a threat, such as a specific virus. As we learned in biology class, antibodies can help fight infections. These tests are taken by finger stick or blood draw, and the results are quick. The antibody test only shows if you’ve been infected by coronavirus in the past. But do antibodies help diagnose COVID-19? As we learned in class about the Immune System, our body can fight pathogens, bacteria, and viruses that we have been previously exposed to. While this was a popular belief earlier on in the year, sadly, researchers do not know if the presence of antibodies means that you are immune to COVID-19 in the future. It is possible to contract COVID-19 for a second time, therefore adaptive immunity does not apply.

The most common testing that I knew of before researching was rapid testing. Rapid testing can be both a molecular or antigen diagnostic; a doctor uses a mucus sample from the nose or throat. The test can also be taken at home only by prescription of a doctor. The results are available in minutes. There is also saliva testing where a person can spit into a tube; this also keeps the doctor or worker safer from the potentially infected person.

Testing is the best way to keep yourself and those around you safe. While testing is still not 100% accurate, there is currently no better way to confirm if someone has COVID-19 unless he/she get tested. With this pandemic, we can never be too safe!

 

 

 

 

 

The Reoccurring Virus?

The spread of the SARS-CoV-2 virus, the virus that causes Covid-19, which is more notoriously known as the coronavirus, has been deemed by some to be one of the worst pandemics ever seen. With over 13.5 million cases and over 200 thousand deaths, the pandemic has taken the world by storm. In an article, Jop de Vrieze speaks on a topic that is of concern in regards to the subsiding of this virus, the topic of reinfection.

In our body, antibodies are our natural defenders. These antibodies are part of the body’s adaptive response to pathogens. Generally, B Lymphocytes(B cells) binds to an antigen and recognize it. T-Helper cells then cause the selected B cells to divide into B-Plasma cells and B-Memory cells. The B-Plasma cells then secrete antibodies which bind to the pathogen and then neutralize it, allowing Macrophages to engulf and destroy the antibody-covered pathogen. B-Memory cells help the cell be able to remember the pathogen, ultimately preventing reinfections. Antibodies are defined by Mayo Clinic as “proteins produced by your immune system in response to an infection. Your immune system — which involves a complex network of cells, organs and tissues — identifies foreign substances in your body and helps fight infections and diseases.” When you contract the virus, your body develops these antibodies that can help provide protection. But there’s a catch. The CDC says that ” we do not know how much protection the antibodies may provide or how long this protection may last,” which opens up the possibility for reinfection.

Specific to de Vrieze’s article, a man in Hong Kong tested positive for the coronavirus in March and tested positive again in August, becoming the first official reinfection case. Neurologists have, reasonably, expected much milder symptoms from reinfection cases, but that hasn’t been the case for some. As the CDC stated, the amount of protection and the protection’s longevity is still a big question. The leading case in de Vrieze’s article was that of Sanne de Jong. After having the virus and mild symptoms in Mid-April, she tested negative in May and then tested positive again in June. What is so special about her “reinfection” case is that when her virus samples were taken, they were very similar. This is of significance because it correlates to another, yet more unlikely, theory mentioned in the article. When the article was written, “no proof exists of mutations that would make the virus more pathogenic or that might help the virus evade immunity. But a recent preprint by a team at the Swedish Medical Center in Seattle suggests one may exist. The team describes a person who was infected in March and reinfected four months later. The second virus had a mutation common in Europe that causes a slight change in the virus’ spike protein, which helps it break into human cells. Although symptoms were milder the second time, neutralization experiments showed antibodies elicited by the first virus did not work well against the second, the authors note, ‘which could have important implications for the success of vaccine programs.'”
The possibility of reinfection is rare but is still very possible. And other mysteries of the coronavirus are still present. Here is my advice: Play it safe. With the uncertainty and danger surrounding the virus, the best thing we can do is prevent the spread and protect ourselves and others. The need for concern can pass if we are simply patient.

The Superhero Powers of COVID-19 Antibodies!

Antibodies are superheros that could save many people from the devastating effects of COVID-19. Defined broadly, antibodies are proteins in the blood that are formed in order to fight against antigens and foreign substances. An article put out by the CDC on November 3, 2020, states that there is not enough information to make a formal conclusion regarding the ability of COVID-19 antibodies to protect someone from being infected again by the virus. Nonetheless, a more recent article released by Nature on December 7, 2020, counteracted that statement by analyzing a study in which Dan Barouch and his colleagues tested which elements defend against COVID-19 using rhesus macaques (monkeys). According to the study, only a very low level of antibodies is required to defend a host against COVID-19. Furthermore, when antibodies are low, T cells are found to contribute to immunity.

In the study, the team took antibodies from masques recovering from SARS-CoV-2 and distributed the antibodies to healthy masques. The antibodies successfully protected the masques from the virus and even activated antibody-dependent natural killer cells, boosting immunity. These results suggest that the injection of antibodies could be very successful in defending individuals from COVID-19.

This information regarding antibodies connects to topics covered in AP Biology. Our immune system protects our body against pathogens such as SARS-CoV-2 through adaptive immunity. Two types of lymphocytes are necessary for an adaptive response: B Lymphocytes and T Lymphocytes. B cells are responsible for a humoral response (or antibody-meditated response) and secrete antibodies. Thus, when someone contracts COVID-19, the activated B cells in their body secrete antibodies that will bind to and neutralize SARS-CoV-2.

The fact that only a low level of antibodies is required to defend a host against COVID-19 is vital information for scientists. Extracting the antibody-producing B cells of an infected patient, medical experts could use the genetic information to create a massive amount of antibodies to be turned into a drug for distribution. This injection would help patients infected with SARS-CoV-2 fight off COVID-19. Thus, antibodies could save many lives and are, therefore, real life superheros!

Page 1 of 2

Powered by WordPress & Theme by Anders Norén

Skip to toolbar