#COVID19 – BioQuakes

Severe cases of COVID-19 result in respiratory problems and blood clots. Scientists are currently looking for a molecular solution to enhance therapeutic treatment. According to the authors, immunometabolic suppression seems to be the the main contributor to the shut down of the immune system, leading to a more severe response from SARS-CoV-2. In severe cases of COVID-19, it seems that a certain family of phospholipases has been associated with determining the outcome of symptoms in patients. Higher levels of the molecule secreted phospholipase A2 and its 12 other variants have been prevalent in cases of cancer, sepsis, bacterial infections and atherosclerosis. Similarly, high levels of sPLA2 were found in 127 blood plasma samples from severely affected COVID-19 patients.

These new findings provide a potential path towards effective treatment for Coronavirus. In new research led by the University of Arizona, the overabundance of the active enzyme, secreted phospholipase A2 group IIA, in the human immune system has been associated with increased severity of COVID-19 symptoms faced by infected individuals.

Maintaining host resistance and disease tolerance is an important part of successfully fighting Coronavirus related infections. Secreted phospholipase A2 group IIA (sPLA2-IIA) is naturally circulated by the human body in order to defend against bacterial invaders. The average healthy individual typically circulates around half a nanogram per milliliter of sPLA2-IIA. Researchers found that 63% of COVID-19 infected individuals being monitored at Stony Brook Medical Hospital who circulated amounts greater than or equal to 10 nanograms per milliliter of sPLA2-IIA died from the symptoms of COVID-19.

Why would certain infected individuals circulate 20 times the healthy amount of sPLA2-IIA?

When the human body encounters bacterial pathogens, the secretion of the enzyme sPLA2-IIA protects the body against the pathogens in an innate defense. Therefore, in an attempt to combat Coronavirus, the human body secretes a greater amount of sPLA2-IIA. This increased amount of sPLA2 can be considered a double-edged sword. On the one hand, the enzyme aids in attacking the virus. On the other hand, the enzyme acts as a “shredder,” tearing apart the membranes of vital human organs. The attack on the host’s cell membranes leads to organ failure and death. Interestingly, the active enzyme sPLA2-IIA resembles an isotopic enzyme found in snake venom, which similarly destroys microbial cell membranes. Much like the active enzyme found in rattlesnake venom, sPLA2-IIA has “the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of…muscles.”

By looking at the lipid metabolite levels in blood samples of Coronavirus patients, researchers were able to corroborate severe Coronavirus symptoms with an overproduction of sPLA2. It seemed that individuals whose circulatory systems contained elevated levels of lysophospholipids (lyso-PLs), unesterified unsaturated fatty acids (UFAs), acylcarnitines, and mitochondrial DNA as well as a decrease in plasma levels of phospholipids experienced higher mortality rates. Expectedly, there was cell energy dysfunction and unexpectedly high levels of sPLA2-IIA enzyme.

In the future, it is highly plausible that an sPLA2-IIA inhibitor may become a standard component of treatments distributed amongst patients with severe symptoms. Hopefully, such a treatment could help to diminish the ever rising mortality rate of Coronavirus and furthermore alleviate the suffering of thousands of patients.

Ultimately, our vast knowledge of molecular biology has an application beyond the mere observations of a published study. It is discoveries like this one that have the capacity to positively affect the course of a person’s life. My mother, for example, contracted COVID-19 a few weeks ago and had to endure days of intense fevers and coughing fits while she was confined to her bed. Although he never tested positive, my father too was bed-ridden with the same symptoms. In the meantime, I, a high school student, found myself taking care them as well as their household duties: cleaning the house, cooking three meals a day, doing laundry, etc. As a high school senior who has completed the college application process, I fortunately had the time to manage the extra workload. However, it is important to realize that many citizens around the world do not have the same privilege; some people are displaced from work while others catch the virus and never make a full recovery. With the robust power of anatomical science, we have the capacity to change people’s lives for the better.

How Diabetes Is Emerging In Patients With COVID-19

By allyle

COVID-19 has a plethora of underlying effects. However, researchers may have just identified the most dangerous long-term impact.

While researchers have been studying COVID-19 for the past two years, pharmacy technician Nola Sullivan of Kellogg, Idaho, has uncovered the virus’s extending underlying conditions. Sullivan faced an additional struggle as a result of being infected with COVID-19 last year, despite the virus’s long-term effects, which included a loss of taste and smell, nausea, and diarrhea. Many COVID-19 patients too are grappling with an additional struggle: the onset of diabetes. In a research involving nearly 3,800 patients infected with the virus, cardiologist James Lo and colleagues discovered that just under half of the patients acquired elevated blood sugar levels that were not previously present. How is it conceivable for COVID-19 patients to develop diabetes? Many researchers have been tackling this exact issue for a long time.

When a patient develops diabetes, he or she must learn to control the illness and live an active life due to an insulin shortage. Because diabetes is incurable, the prospect that it is a long-term side effect of COVID-19 is very troubling. Insulin is essential in the human body because it lowers triglycerides by boosting lipoprotein lipase activity, which degrades triglycerides into glycerol and fatty acids. A lack of pancreatic B-cells, which release proper quantities of insulin, has a direct impact on mitochondria and the glycolysis process which is utilized for energy synthesis by all cells in the human body, eventually prompting the pyruvate product to join the Krebs cycle for ongoing energy production. Both processes are required for continual energy generation. Glucose is broken down into pyruvate and energy during glycolysis. The process can take place in the absence of oxygen, making it anaerobic. Insulin promotes glycolysis by raising the rate of glucose transport across the cell membrane and the rate of glycolysis by boosting the activities of hexokinase and 6-phosphofructokinase.

Nonetheless, people with COVID-19 have experienced sugar surges. The elevated blood sugar levels were new after infection for the majority of the patients, suggesting that many of them had not been diagnosed with diabetes prior to contracting the virus. According to Lo and other experts, the mechanism by which COVID-19 causes diabetes is currently being investigated. Patients with ARDS caused by COVID-19 and a high blood sugar level were in the hospital three times longer than those with normal blood sugar levels. While the exact cause of diabetes is unknown, researchers have discovered evidence that the coronavirus attacks pancreatic B-cells, which produce insulin. This does not yet address the question because patients who received COVID-19 continued to generate significant amounts of C-peptide, indicating that pancreatic cells were still generating insulin. Despite this, their blood sugar levels remained elevated, suggesting that something else was at fault. The virus-infected fat cells must be stimulating other cells in a detrimental way, resulting in diabetes. As a result, Lo and colleagues observed that individuals with COVID-19 had low amounts of adiponectin, a hormone generated by fat cells that helps other cells respond to insulin’s urge to take up sugar. COVID-19 can clearly infect fat cells. The virus may also cause replication in human fat, which provides another indication as to how fat is implicated in the virus and, as a result, diabetes. While obesity has a significant impact on the onset of diabetes as a result of the virus, this is not always the case. The miscommunication of fat cells is to blame.

How may fat cell miscommunication be controlled, and who is directly affected? This is the next question that has to be addressed in order to develop a deep understanding of the long term effects of the virus.

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

By emzymes

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?

The Science Behind COVID Tests

By binturtong

My family and I have had a lot of questions about the COVID test, such as if I take the COVID vaccine and do a test, will it come positive? Well to answer a question like this we need information on how tests work.

Lets start with the basics:

There are two types of molecular tests, antigen tests and nucleic acid amplification tests. Rapid tests are known as Antigen Tests while PCR tests are known as nucleic acid amplification tests. I will talk about PCR tests first. The PCR tests test for DNA. However, the COVID-19 genetic code is actually RNA. So how do PCR tests pick up positive or negative results?

When your swab of DNA is sent back to the lab, they will isolate RNA and DNA with the process called gel electrophoresis. After isolating the RNA, it is mixed with enzymes (DNA polymerase and reverse transcriptase), DNA building blocks, cofactors, proves and primers. The RNA is transcribed into DNA by the reverse transcriptase. This transcription creates a complimentary DNA. The goal is to isolate the DNA now, and the DNA polymerase does so. The enzyme breaks up the RNA and isolates the complimentary DNA. That DNA is duplicated in order to amplify the molecule. Remember that this DNA is duplicated from the virus RNA.

To amplify the DNA for the equipment to read, the DNA is first heated, denatured, in order to separate the DNA strands. When cooled, primers and probes bind to the DNA strands. The DNA polymerase assembles new DNA strands from the DNA building blocks and when fully reconstructed, it has been successfully amplified. This is done repeatedly with the RNA and thus, creates many complimentary DNA’s ready to amplify.

If SARS-CoV-2 complementary DNA is present in the sample, primers copy the infected regions while probes, signaling proteins, stick to it and release a visual signal read by the equipment. Because there are millions of amplified DNA, there will be lots of signals being produced by the probes. If their is no virus, the probes do not stick and this no signal release and a negative result shows. Thanks to the power of signaling and cell communication, lab instruments can pick up on it and give us a positive or negative result.

The rapid test works in a very different way. Antigen rapid test takes about 15 minutes. The goal is to detect the spike protein of the coronavirus. The liquid drops onto the droplet. Antibodies are on the test pad, with three sets.

The testing pad, we’ll call pad, consists of the location for liquid drops, and a C and T line. At each segment of the pad there are different antibodies. Those antibodies will bind to the spike protein as well as the other antibodies. When the liquid is dropped in, capillary flow allows the liquid to move down the pad. The first antibodies will attach to the virus, which then move down the pad. Then the antibody will bind to primary and secondary antibody, not the virus. The combining of antibodies create the line which results in the positive or negative outcome.

To answer my question, no. The PCR and rapid tests should not test positive if one has taken the vaccine recently. This is because both tests are checking for active viruses and polymerase. Not immunity.

If you feel any symptoms take a rapid test, sometimes it comes negative when you really have COVID and that’s because at the early stages of COVID development in the body, there will not be enough active viruses going around. But that does not mean you are not contagious, please be safe and stay healthy!

Vampires and COVID-19? They may have something in common; and spoiler, it has nothing to do with bats

By shallele

Researchers from Trinity College Dublin and the University of Edinburgh think they may have found a new weakness of COVID-19; sunlight! More specifically, ambient ultraviolet B (UVB) radiation which provides the body with vitamin D. The researchers knew of previous studies of the susceptibility of those with vitamin D deficiency to not only receiving the virus, but also experiencing the entirety of it’s wrath. However, in most cases measures weren’t taken to rule out the possibility of confounding factors (other conditions that can cause both vulnerability to COVID-19 and vitamin D deficiency). In order to jump this hurdle, the researchers used “genetically predicted” vitamin D levels.

With this averaged sample, the researchers used an analytical process called Mendelian Randomization . The process allowed them to test correlations between Vitamin D levels and COVID-19. This process had been attempted in past studies, and the researchers results did not contradict previous conclusions; a link between vitamin D levels and COVID-19 was not evident. However, the researchers of Trinity and Edinburgh wanted to test the effects of UVB radiation. UVB radiation from sunshine is the most important supplier of vitamin D for many, yet it was not included in previous studies.

Studying almost half a million people from the UK, the researchers compared the genetically predicted levels effect versus UVB predicted levels effect on COVID-19 infection. “researchers found that correlation with measured vitamin D concentration in the circulation was three-fold stronger for UVB-predicted vitamin D level, compared to genetically-predicted” (Trinity College Dublin). The researchers found a correlation of high strength in the negative between UVB radiation and hospitalization and death due to COVID-19 as well.

While the researchers admit that the sample size of the study is not quite large enough to be entirely conclusive, especially considering the surprising deviation from the results of the genetically predicted study, they are optimistic that with time their theory will prove significant. The odds are with them as vitamin D has been found to be a benefactor of the immune system in general. A fact demonstrated by the presence of vitamin D receptor on both B and T cells, and the trend of higher susceptibility to infection of those with lesser amounts of vitamin D.

How are new COVID variants identified?

By ethanelab

On January 4, 2022

COVID variants are of high concern for scientists studying the disease. Some variants can be more infectious or cause more severe illness. Additionally, some variants can evade vaccines by having different surface proteins than the variant the vaccine was created for. This causes the antibodies produced from the vaccine to be less effective against other variants. In AP Biology class we discussed how the Delta Variant, first identified in December 2020, has a different spike protein structure than the original virus from which the vaccine was created from. This allows the variant to be more infectious, and make the vaccine less effective against it. But, what are COVID variants? And how are they discovered?

COVID variants are “versions” of the virus with a different genetic code than the original one discovered. However, not every mutation leads to a new variant. This is because the genetic code of the virus codes for proteins. Some mutations will not change the structure of the protein and thus not change the virus. So, COVID variants can be defined as versions of the virus with a significantly different genetic code than the original virus.

To detect new COVID variants, scientists sequence the genetic code of virus which appears in positive COVID tests. Scientists look at the similarity of the genetic sequences they find. Then, if many of the sequences they get look very similar to each other, but different to any other known virus, a variant has been discovered.

To sequence the RNA of the virus, scientists use what is called Next Generation Sequencing (NGS). To understand how NGS works, it is best to start with what is called Sanger Sequencing. Sanger Sequencing utilizes a modified PCR reaction called chain-termination PCR to generate DNA or RNA fragments of varying length. The ending nucleotide of each sequence is called a ddNTP, which contains a florescent die corresponding to the type of nucleotide. The addition of a ddNTP also terminates the copying of the particular sequence. The goal of this PCR reaction is to generate a fragment of every length from the start to the end of the sequence. The sequences can then be sorted by length using a specialized form of gel electrophoresis. The sequence is then read by using a laser to check the color of the fluorescent die at the end of each sequence. Based on the color and size, the nucleotide at that position of the genomic sequence can be found.

The difference with NGS is that many sequences can be done in parallel, allowing for very high throughput. In other words, with NGS many COVID tests can be sequenced in once.

Needle in a Haystack

By osmosisjohn

Immunization is defined as the action of making a person immune to infection by the process of inoculation. While the COVID-19 vaccine may be new, vaccines have actually been around for a lot longer than you may think. We’re used to getting vaccines through needles when we go to the doctors office, but what if I told you that that’s not the only way to receive one. Hundreds of years ago, Buddhist monks actually used to drink snake venom in order to build immunity to it. Though more formally, Edward Jenner is considered the founder of vaccinology after successfully inoculating a 13 year old boy in 1796 with a smallpox vaccine. The 13 year old actually demonstrated immunity and the first small pox vaccine was officially developed in 1798. While that may be just a brief recount of the history of vaccines, the significance of their revolutionary effects will follow humanity to the end of time. Through vaccines we’ve immunized viruses such as Chicken Pox, Polio, Influenza, Hepatitis A, Hepatitis B, HPV, Measles and many more. These viruses plagued the world in the past, but many of them are now obsolete.

While these vaccines may be different in nature, they all have one similarity… They are administered through needles. The “proper” term inoculation, however it is not specified how the virus needs to be administered. Monks used to drink snake venom and that was considered inoculation. So that begs the question… Does a needle really need to inject a vaccine? The answer is no.

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How does the COVID-19 vaccine work?

The COVID-19 vaccine is considered an mRNA vaccine. Normal vaccines would put an inactivated germ into our bodies in order to build immunity. An mRNA vaccine uses mRNA that is created in a laboratory in order to instruct our cells on how to make a protein. The COVID-19 is administered through the upper arm muscle and it enters muscle cells. Inside these cells, the mRNA is assembled in the Endoplasmic Reticulum to form spike proteins. The mRNA that is injected is coded to constantly recreate the spike protein and it is displayed on the surface of the cell and our immune system will respond with antibody production.

What are other Methods of Vaccination?

According to Victoria University, there is more than one way to administer a vaccine. While they’re usually administered with a needle, you could also administer one using Jet Injectors. These Jet Injectors date back to the mid 1860s. They penetrated the skin and administered the vaccine without a needle. The method included a spring-loaded injector where a spring is released to deliver the vaccine. Another method of administering the vaccine is a liquid jet injector that uses very small volumes of liquid that is forced through very tiny microscopic holes in your skin, also not requiring a needle. This method was used during clinical trials against HIV and it is also utilized in some influenza vaccinations. A third method of vaccination is a band-aid-like patch that contains 400 tiny needles. It is said that if the vaccine were administered through antigen-presenting cells in the skin than into muscle cells the chances of the DNA (A DNA based vaccine) entering the nucleus would increase. The researchers created a delivery system by attaching DNA sequences encoding SARS-CoV-2 spike protein on the surface of nano-particles. The tiny needles were then coated with the nano-particles. After this, the patch would then be applied onto the skin, painlessly penetrating it.

COVID-19 May Induces Cell That Produce Antibodies for Life

By catebolism

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).

One 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.

One 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.

Protein Responsible for Increasing the Severity of COVID-19

By ethanols

The CDC reported that the first human COVID-19 case, originating in Wuhan, China, to enter the United States was on January 20th, 2020 via DNA samples. Present-day, COVID-19 has affected nearly three hundred million people worldwide according to the New York Times. Now, one would assume that this virus would have the same effects from person to person, yet it actually produces drastically different effects depending on the victim’s body composition. Some people “develop mild or no symptoms upon infection,” whereas others, “develop severe, life-threatening disease” (University Of Kent). But what exactly causes this alteration of symptoms from patient to patient? Well, researchers at the University of Kent have scrutinized through their resources to determine a possible source for this predominant world health issue.

As we’ve learned throughout units two and three, protein structure is pivotal for determining the protein’s function, and proteins as a whole are what viruses, for example, SARS-CoV-2, consist of on the molecular level. SARS-CoV-2 transmits itself through our body by binding its spike proteins to our healthy cell’s receptors, which then emits a signal to the cell, ultimately altering the genetic code of the cell, changing its function. One protein synthesized from our cells is called ‘CD47,’ a cellular surface protein, which, in broad terms, “tells circulating immune cells called macrophages not to eat these cells” (Stanford.edu). Once SARS-CoV-2 cells begin to synthesize this surface protein, the cells become ‘protected’ from our immune system, enabling the cells to continuously reproduce and flood the body without any interference from the macrophage and other immune system anti-virus functions. Virus-synthesized CD47 on the surface of SARS-CoV-2 cells allows for the production of higher volume of virus, ultimately resulting in a more severe disease infection.

According to the researchers at the University of Kent, CD47 is far more prevalent among older people, which may provide a reasonable explanation as to why they typically exhibit severer symptoms compared to those of younger people. One condition that high levels of CD47 typically produce is high blood pressure, which forces the body to deviate by over 1o mm Hg systolic and 10 mm Hg diastolic, according to the American Heart Association. High blood pressure, specifically caused by CD47, puts people ” [at] a large risk factor for COVID-19 complications such as heart attack, stroke, and kidney disease”(University of Kent). The researcher’s data demonstrates that both age and virus-synthesized CD47 greatly contributes to more severe COVID-19 by blocking a fully functioning immune response which increases tissue and organ damage.

This finding should provoke optimism within the scientific community, understanding what causes differing symptoms-severe or less severe- is incredibly useful for combatting both the virus’s spread and severity from person to person. Hopefully, scientists will be able to further utilize CD47 research to save lives of people who are at higher risk of experiencing more severe COVID-19 symptoms.

SARS-CoV-2 and Our Evolving Immune Systems

By anaplasia

A scientific study analyzed in a recent article by Monique Brouillette brings hope with the emergence of possibly more infectious COVID-19 variants. The study looks at the blood of people who are vaccinated, and people who recently have had COVID-19, to learn more about the cells in our immune system. Studying and seeing these cells create their own way to counteract mutations could mean the evolution of our immune systems in response to the variants. So the study poses the question: Along with our cells ability to respond to the initial SARS-CoV-2 virus invasion, do our bodies adapt so that those same cells can recognize the new variants?

An Immunologist at the Rockefeller University, Michel Nussenzweig, conducted a study along with his colleagues by testing the blood of individuals both one month and seven months after they had COVID-19. The scientists noticed that individuals had lower levels of antibodies, and equal or higher levels of memory B cells, seven months after having COVID-19 than one month after. This was expected as the virus had been fully cleared by the seven month mark, and memory B cells were created in response to the initial invasion of SARS-CoV-2.

Memory B cells are created by the humoral response. This is when macrophages or dendritic cells recognize a forign antigen (in this case SARS-CoV-2), and stay in the body near its lymph nodes with the ability to recognize the virus.

If someone were to get infected for a second time, these memory B cells would activate to quickly produce antibodies and block the virus. This is called the secondary immune response (pictured on the right).

The scientists then did another test in the study. They tested reserve B cells and antibodies someone produced in response to SARS-CoV-2 against a version of SARS-CoV-2 they created to be more like a new variant. The replica new variant virus was made to be more like the new variants by having a mutation in the spike protein, which is the part of the virus that binds to our cells. When they tested this, they saw that some reserve B cells produced antibodies that went and attached to the mutated spike proteins, showing that the reserve B cells and antibodies from SARS-CoV-2 were able to adapt and recognize a different or mutated version of SARS-CoV-2.

New COVID19 mutant (SARS-CoV-2 VOC-20201-01)

Example of SARS-CoV-2 Mutation

The SARS-CoV-2 variants have many similar elements to the original SARS-CoV-2, but also contain mutations in their spike proteins and receptor binding domains (for the most part), which allow them to usually go undetected by our bodies. This is why those who are vaccinated or have SARS-CoV-2 antibodies are not fully immune to the variants.

Most recently, Nussenzweig and his team conducted the same experiment again, but with new and improved viruses that more closely resemble the COVID-19 variants. One of the replica variants is of B.1.351, which contains mutations K417N, E484K, and N501Y, was tested against cloned six month old (previously exposed to SARS-CoV-2) B cells. Although it has not yet been reviewed and confirmed, this test did show that some of the antibodies produced by these B cells had the ability to recognize and attach to these mutated variants engineered to be very similar to the viruses of the Covid variants.

What these scientists discovered with SARS-CoV-2 is a process called somatic hypermutation. This is when the immune system adapts to recognize and attack forign mutations or viruses it has not seen before when they have previously fought off a virus with some similar elements. The occurrence of this process with SARS-CoV-2 gives us hope that after getting the vaccine or having had COVID-19, our bodies will have a better defense against the new variants, which will, hopefully, in turn, lessen the fear and stress surrounding the emergence of new SARS-CoV-2 variants.

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

By biosyntaysis

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!

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!

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.

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!

Omicron Variant: How Will it Affect the Vaccinated?

By photosamthesis

Different brands of COVID-19 vaccines

When looking back over the past 2 years, many think about the need for and effectiveness of the COVID-19 vaccines, but regardless of what many may think it has been proven that the COVID-19 vaccine is effective against the original variant of COVID-19 that was most prominent during the production of vaccines. However, what many people are wondering is if these vaccines & boosters are still effective against the Omicron variant?

Before going over the effectiveness of the current vaccines and booster shots on the Omicron variant, we first have to look at the Omicron variant itself. First off, we know that Omicron was “first identified [in] South Africa,” which is a place where full vaccination rates are at 25%: a low percent that is not high enough for herd immunity. Despite this, the Omicron is still viewed as a threat to more vaccinated communities. This is because in order for variants of COVID-19 to be labeled a variant, it needs at least one mutation to its spike protein, and Omicron has dozens of mutations to its spike protein, and the more mutations it has, the more potential it has to infect the vaccinated.

Omicron Spike Protein

It is important to note that the COVID-19 vaccines help to produce antibodies that latch onto and render spike proteins inactive. Since this Omicron variant has dozens of mutations to its spike protein. As seen through activities and lessons learned in our Bio class, different variants of COVID-19 just have pieces of the protein structure changed, which leads to a changed shape of their spike proteins. This leads to existing vaccines being less effective as the original vaccine was meant for a specific spike protein shape, not the shapes of the new variants. The changes to the Omicron spike protein makes it very different to the original COVID-19 spike protein, so the vaccine will be less effective.

Advertisement campaign for getting a “booster”

Even if a break through the vaccinations defenses doesn’t happen with the Omicron variant, “some version of this coronavirus is bound to flummox our vaccines.” Despite all of this information, we still know very little about the Omicron variant and its effects. It’s just too early to know what will happen. Because of this lack of information, it is important for people to make sure they are vaccinated and get their boosters as it does still make a difference. Overall, people, vaccinated or not, should err on the side of caution with this new potential threat of Omicron out there and should try to stay safe.

Why to Get the Vaccine and Booster Shot!

By rayceptor

The COVID-19 pandemic started almost 2 years ago on December 12, 2019. Since then, it took roughly 1 year to release a vaccine in the US. So far there are almost ~780,000 deaths in the US with 195M US citizens fully vaccinated or 59.1% of the US population. Now booster shots are available to ages 18 and older in some parts of the country, you might wonder if you should take them. Is there an incentive to?

Firstly, the ultimate goal of the COVID-19 Vaccine is to stimulate the B-memory cells so when someone comes in contact with the same pathogen, there is faster antibody production for infections. The antibodies bind to the COVID-19 virus in an attempt to inactivate them, and the virus will then be engulfed by the macrophages. In a recent study, a team of physicians and public health experts measured the effectiveness of the COVID-19 vaccine over time. They sampled health workers at San Diego Health use in their study. When the subjects got vaccines in March, their early effectiveness for preventing the contraction of COVID-19 was around 90 percent; however, by July, this percentage had fallen to approximately 65 percent. This is an expected response for most viruses. The immunity wanes over time since the memory B cells’ protection against the virus begins to decrease with time because there are just fewer memory B cells specific to the pathogen present in your body. Thus, booster shots are given to remind the body’s immune system about the COVID-19 virus and produce more memory B cells. In a time where delta was the most prevalent virus, the study also found that unvaccinated people were 7 times more likely more to test positive for COVID-19 compared to unvaccinated people, and adults who contract COVID-19 are 32 times likely to require medical attention compared to vaccinated adults who contracted COVID-19. Again, we have to keep in mind, this is not a simple random sample of the whole US population, therefore we cannot fully use these results to reflect what will happen in our community.

Now that we went over the reasons to get the booster, we have discussed what the booster shot is. The booster shot in essence is the same formulation as the current COVID-19 vaccine that you received if you are vaccinated. The only little variation is in the Moderna’s shot: it is half the dose of the initial vaccine. The shot injects mRNA in a Lipid nanoparticle that can bypass our cell membrane because of its small size and nonpolar properties.

Lipid Nanoparticle containing mRNA

The mRNA is used by the cell’s ER to synthesize spike proteins. Since it’s the same formula as the previous COVID-19 vaccines, this means that the booster doesn’t guarantee immunity against the delta and omicron variants. However, it does retrigger your memory B Cells. You should get the booster shot around 6 months after full vaccination since there is a big decreased effectiveness with the passage of time.

Covid’s Spike Protein

With new variants around the corner, Chira Alleles, a co-author in the study stated “Similar findings [in this study] are being reported in other settings in the U.S. and internationally, and it is likely that booster doses will be necessary.” Since there is no huge downside to getting the shot, and if you do not have any underlying health conditions that might put you in more danger than getting COVID-19, I strongly think you should get the booster shot as soon as it is available to you!

What are your thoughts on getting the vaccine/booster shots? Do you think there will be a point where we can achieve herd immunity, or will that be impossible with the rapid mutations?

Can a Plant Based Diet Protect You from Covid?

By fertilivization

On December 17, 2021

The Covid-19 pandemic has affected and devastated millions of people all over the world over the past two years. Even after religiously wearing masks and more than half of the world’s population getting vaccinated, we still need to live in caution of getting infected with this virus every day. Although Covid-19 is known to be one of the most contagious viruses to exist, it has been discovered in a recent article that maintaining a healthier lifestyle and diet will decrease your chances of getting infected as well as minimize any symptoms if you do happen to get infected. We all know that overall if you are able to maintain healthy habits, your immune system will be stronger and therefore, able to fight off infection more effortlessly, but applying this same idea to Covid-19 may help us escape this pandemic sooner than expected.

Since data on this theory was lacking, Dr. Jordi Merino and his colleagues conducted an experiment to gather more evidence. 592,571 participants were selected and began by completing a questionnaire assessing their dietary habits before the pandemic. Participants who had healthy eating habits had a 9% lower chance of contracting the virus and a 41% lower chance of developing severe Covid-19. Merino concluded that in addition to wearing masks and getting vaccinated, we should all try to maintain healthy, plant-based diets to fight against Covid.

In addition to the health benefits of having a plant-based diet, it improves your immune system because of the antioxidants, vitamins, minerals, and phytochemicals found in plants. These components work to keep your cells healthy and working at their fullest potential to fight off infection. They resolve inflammation in the body by neutralizing toxins, processed foods, bacteria, and viruses. With all the benefits, why wouldn’t you go plant-based?

It may sound pretty simple: if I go plant-based and I won’t get sick, right? Not exactly. It is found that the risk of Covid-19 is greater in areas of high socioeconomic deprivation. This is because the people who inhabit these areas are unable to maintain the same lifestyle as people who are more fortunate. Plant-based diets and healthier lifestyles are generally more costly, causing them to be less accessible to everyone. This is one of the main reasons that Covid is still a great risk to our society. For more information about a plant-based diet decreasing Covid risks, click here.

In AP Biology we learned how your immune system works to fight against any invading viruses in your body. When you are contracting a virus, the pathogen first needs to pass through your barrier defenses. These are the natural defenses with which you are born. For example, they include mucus, skin, stomach acidity, blood and lymph proteins, etc.. If you are an unhealthy person and these defenses aren’t working properly, you are much more susceptible to disease and then need to rely on your internal defenses.

This diagram shows how the humoral and cell-mediated responses work in the body to fight off disease. When a pathogen enters the body, your immune system will attack either the pathogen itself when loose in your bloodstream and bone marrow or attack and kill an entire infected cell. Keeping your immune system strong by eating right and frequent exercise will also ensure that these defenses will fight off disease quickly and form antibodies to prevent future reinfection. A healthy person is by no means immune to a virus, but they will experience fewer symptoms as well as recover faster because their immune system works faster. This means that fewer cells will become infected and the virus will have less time to replicate and multiply.

As someone who runs track and cross country, it is very important to me to keep my diet as healthy as possible. Though a plant-based diet doesn’t suit my lifestyle best, I do make healthy food choices as often as I can to properly fuel myself and to ensure I don’t get sick. This seems to be working well for me as I am still yet to get infected with Covid-19 or show any symptoms.

The COVID-19 Treatment Pill: Destroying or Amplifying The Virus?

By caroplasma

On December 14, 2021

After seeing millions of people die from COVID-19, a new discovery has been found that could be the first long term treatment option to give patients suffering from COVID-19 a chance to fight it off, but how sure can we be that the treatment pill will work?

New data about an antiviral pill made by Merck with its partner Ridgeback Pharmaceuticals show that the treatment pill is not as stellar as first believed. The drug has drawbacks that could outweigh its potential to fight the coronavirus and keep people out of the hospital.

The U.S. Food and Drug Administration is now deciding whether to grant emergency use authorization for the drug called molnupiravir, after the agency’s advisory panel narrowly voted to recommend it on November 30. The drug was authorized to be of use in the United Kingdom on November 4, and if the FDA follows suit, it could wind up being just a temporary treatment. Some advisers have already urged the agency to be ready to withdraw the authorization as soon as something better comes along.

Finding an early treatment for COVID-19 hasn’t been easy due to the constant trial and error that scientists keep facing, so when the development of molnupiravir came out a lot of experts hailed it as they thought it could be a potential game changer for the pandemic. It would be utilized as a pill that could be given to people early in the infection, keep health care systems from being overwhelmed, and spare people at high risk from the most severe complications.

In a clinical trial, the drug showed early signs of preventing hospitalization and death from COVID-19 in people who are at high risk. In fact, the results were so promising — a 48 percent reduction in the relative risk of hospitalization or death — that the trial was stopped so that the drug might potentially reach the public earlier.

But on November 26, Merck announced in a news release that when all the available data from the trial was in, the reduction in relative risk fell to 30 percent against hospitalization and death compared with a placebo. The shift stemmed from an unexplained decrease in severe disease among people in the placebo group in the last part of the trial.

Overall, among the 709 people in the molnupiravir group, there were 48 hospitalizations and one death compared with 68 hospitalizations and nine deaths among the 699 people who got a placebo, dropping the effectiveness from the initial 48 percent to 30 percent.

Taking that lower-than-expected efficacy into account, the FDA’s antimicrobial drugs advisory committee came to a split 13–10 decision about whether the antiviral drug should be granted emergency use authorization, with experts on each side of the vote often agreeing with points made by the opposing side. The debate and vote reflected a storm of uncertainty about the drug’s efficacy and who should use it — the list of people who would not be eligible is far longer than those most experts would give the drug to. The panel also looked into whether the drug could lead to even more dangerous versions of the coronavirus, whether it can cause growth delays in children or mutations in human DNA, and other unanswered questions.

The antiviral pill works by making mutations in viral RNA so that viruses are rendered noninfectious and eventually stop replicating. Such mutations happen throughout the virus’s genetic instruction book, or genome.

Some of those mutations could land in the spike protein, which helps the coronavirus break into cells, or other proteins and make the virus more transmissible or more evasive to vaccines. As learned in AP Biology, the spike proteins enable the host cell to be taken over by the virus and multiply and infect the surrounding cells. The vaccine that is being administered to people all around the world contains the antibodies that you would get if you were to be infected with the COVID-19 virus, so that if you were to get the virus, your body would go into its secondary immune response. This is when the memory cells facilitate a faster, stronger and longer response to the same COVID-19 antigen. Getting the vaccine would protect your body from having a life threatening reaction to the virus. If there is a mutation that lands on the spike protein, then the vaccine will be of no use to people since that is a completely different makeup of the virus. That’s especially a fear if people don’t finish the full five-day course of the drug needed to render the virus inoperable, leading potentially to highly mutated new forms of the virus that could infect others.

Merck representatives said that possibility is unlikely, because after five days of taking even a half dose of the drug, infectious viruses were no longer detectable among study participants tested. In one study, the company found seven patients who had changes in the coronavirus’s spike protein after taking molnupiravir, but there was no evidence that the viruses spread to other people or affected the patient’s health.

Molnupiravir might also create mutations in human DNA, researchers say. The drug is a nucleoside analog — an artificial RNA building block that can mimic the bases cytosine and uracil. Some enzymes in human cells might convert those RNA subunits to a DNA building block, which may lead to mutations in human DNA, especially in rapidly reproducing cells, such as blood cells. How likely that is is an open question.

Still, there are no good remedies for people with mild to moderate COVID-19. As of November 30, more than 82,000 people in the United States are being diagnosed with COVID-19 each day and more than 800 die. Those numbers are expected to increase as case counts surge in some parts of the country. The new omicron variant might add fuel to that fire if it proves more contagious than the currently dominant delta variant.

So even with all of molnupiravir’s drawbacks, federal regulators might decide a 30 percent reduction in hospitalizations and deaths is worth giving the drug temporary authorization.

The drug might be helpful for “the right patient population, the right virus at the right time,” said Lindsey Baden, an infectious diseases doctor at Brigham and Women’s Hospital in Boston who chaired the FDA’s advisory committee. “To me that at least suggests there are populations where there may be benefit.”

But more studies need to be done to address concerns about the drug, he said. “It’s the absence of data that makes many of us uncomfortable.”

President Joe Biden said December 2 during remarks laying out a plan to combat the omicron variant that the government has secured a supply of the drugs and, if authorized, will distribute them similarly to vaccines.

How does the Omicron variant of COVID-19 compare to the deadly Delta variant?

By cytokinesav

On December 6, 2021

With news of the new variant of the COVID-19 virus reaching 16 states here in the US, many are asking: What is this Omicron variant?

The Omicron variant of COVID-19 was first reported to the World Health Organization by the Head of South African Medical Association, Dr. Angelique Coetzee. As of December 6, 2021, there are about 59,000 Americans hospitalized due to said variant. The Delta variant, more than twice as contagious than previous variants according to the CDC, still continues to be the leading cause of COVID-related hospitalization and deaths today in the US and many other countries. However, medical experts are saying that Omicron has a few different key mutations that make it very likely to outperform Delta. How does this Omicron variant compare to the deadly Delta variant which we’ve been battling this year? Here are the main things you need to know.

Symptoms of the Omicron variant:

Fever or chills
Cough
Shortness of breath or difficulty breathing
Fatigue
Muscle or body aches
Headache
New loss of taste or smell
Sore throat
Congestion or runny nose
Nausea or vomiting
Diarrhea

Infection and Spread:

So far, people who have been diagnosed with the Omicron variant of SARS-Cov-2 in the US have or had mild symptoms, yet it is said to be much more contagious. Why? The difference in the structure of the spike protein. Variants of COVID-19 have mutations present in the spike protein due to copying errors in our DNA.

Omicron Structure pictured

The Delta variant has 18 mutations in its spike proteins…Omicron has a whopping 43! That is many, many more than Delta. Jeremy Kamil, associate professor of microbiology and immunology at Louisiana State University Health Shreveport, said, “The number of changes blew people’s minds…It’s an exaggeration to say we’re back at square one, but this is not a good development.”

Around 30 countries have detected said variant so far; 19 states in the US have. The high number of mutations it contains does not necessarily mean it’s more dangerous. As previously stated, Omicron patients have thus far exhibited milder symptoms. Dr. Coatzee said that she first discovered Omicron’s appearance as her patients exhibited “unusual symptoms” in comparison to the Delta variant. However, don’t be too scared; experts say our immune systems have grown more equipped to fight the COVID-19 virus.

We still have yet to learn more about Omicron and its nature, infection, etc., as it is very new.

The original COVID-19 virus’s structure is pictured above

With Omicron having more than double the mutations as Delta, the likeliness of transmission/level of contagiousness is quite high–also meaning that the efficacy of our vaccine could be compromised. The Omicron spike protein has similar components that of the Delta, beta, and gamma variants, meaning that the rate of transmissibility is similar. With Omicron having the largest number of mutations, however, transmissibility can be increased more than 2x!

What should you do?

Well, continue to follow the standard COVID-19 measures. Wear a mask, social distance, wash your hands, travel less, and just be careful. These methods have proven time and time again to help. Travel restrictions on the rise can be tough with the holidays coming, but remember that they are only in place for the sake of our safety. It is important to follow these rules as the pandemic is not over.

Robert Malone: The Man Behind the Ideas for the COVID Vaccine

By photosamthesis

On November 1, 2021

Salk Institute (19) Salk Institute for Biological Studies

When you think of the COVID-19 vaccine, the first things that might come to mind are the companies that facilitate it (such as Pfizer & Moderna), if it is safe or not, or even that it is a new type of mRNA vaccine that is unfamiliar to many. However, people tend to overlook and not give any thought towards who made this all possible, and that person is Robert Malone.

Robert Malone, born in 1959, started his medical career at University of California Davis, and later got his MD from Northwestern University. After Malone’s traditional education at both an undergraduate and graduate level, he conducted research at the Salk Institute for Biological Studies.

During his time at the Salk Institute, Robert Malone performed a “landmark experiment.” In this experiment, Malone mixed strands of mRNA with droplets of fat (lipids). Human cells reacted with this mRNA lipid mix and began producing proteins from it. Robert Malone had some foresight and realized that this discovery has some potential in the medicinal world. He decided to jot down some notes, stating that if cells could create proteins from mRNA delivered to them that it might be possible to “treat RNA as a drug (written January 11, 1988).”

These revelations from Robert Malone had a huge contribution towards the mRNA COVID-19 vaccines.

After seeing all of this information on how Robert Malone made scientific contributions towards the COVID-19 vaccine, it is important to show how it works. Since we know (as seen in Malone’s experiments) that mRNA mixed with lipids that enter a human cell can lead to the production of proteins, scientists just had to tweak the mRNA until it could create pieces of “spike protein.” These pieces of spike proteins would have to match the shape of the spike proteins found on the surface of the COVID-19 virus. This required an impressive feat of biomedical engineering, but it was done.

Robert Malone’s work did not just contribute to the first strand of COVID-19 discovered, but his work applied towards different variants as well.

The idea of spike proteins and how spike proteins can be counteracted through an mRNA vaccine applies to all different variants of COVID-19. As seen through activities and lessons learned in our Bio class, different variants of COVID-19 just have pieces of the protein structure changed, which leads to a changed shape of their spike proteins. This leads to existing vaccines being less effective as the original vaccine was meant for a specific spike protein shape, not the shapes of the new variants. This means that mRNA vaccines are still very much effective towards different variants of COVID-19, but they would have to be modified mRNA vaccines.

Despite all of this, Robert Malone’s research’s applications might not stop at the COVID-19 vaccine. The COVID-19 vaccine was able to show us the power of mRNA vaccines, so it is not unreasonable to be expecting more mRNA vaccines in the future.

The Potential End To COVID-19: How An Antiviral Pill Could Decrease Death Rates

By allyle

On October 27, 2021

When will the world return back to normal? In recent years, people have questioned the longevity of the COVID-19 outbreak. While concentrating on vaccine delivery and vaccination capabilities, a pill has been developed in the hopes of preventing future COVID variations. Hopefully, the pill will eventually be administered to patients; this would make it the first oral treatment for the virus.

A current study on molnupiravir, an antiviral pill, has published data demonstrating that the medicine has the ability to lower hospitalization and fatality rates as a result of COVID-19. The study dealt with two groups of people. One group of 377 people were given a placebo, and the other group of 385 people were given molnupiravir to examine how the antiviral affected patients with COVID-19. The findings were substantial. Within 29 days of starting the trial, 14.1 percent of the group given the placebo were hospitalized. Fortunately, of the individuals who were given molnupiravir, only 7.3 percent of them were hospitalized.

Molnupiravir is a prodrug of N4-hydroxycytidine (NHC), a nucleoside analog (meaning that it contains a sugar and a nitrogenous base).

Molnupiravir is similar to the genetic coding of the coronavirus’s RNA, as is remdesivir (a FDA-approved medication). By interfering with the polymerase enzyme, the “fake” basic elements impair the coronavirus’s RNA synthesis, preventing the virus from replicating. Despite the fact that the two medications serve the same goal, they serve different actions. Remdesivir penetrates a growing RNA strand, slowing and ultimately blocking the polymerase enzyme. Unlike the COVID-19 vaccine, the structure of molnupiravir gives it the ability to target the polymerase enzyme instead of the virus’s spike protein. Molnupiravir enters the cell and is transformed into RNA-like building components. The active medication binds to the genome of RNA viruses, setting off a chain of mutations; this process is known as viral error catastrophe. In simpler terms, it disrupts how the virus replicates RNA.

Molnupiravir could theoretically be administered as soon as a patient receives a positive COVID-19 test, thereby preventing floods of COVID-19 patients from overburdening medical systems while the highly infectious delta variant continues to spread. Although the side effects of the drug remain unknown, it has been reported that the side effects of COVID-19 are much worse than those of molnupiravir. The antiviral drug has the potential to save lives, but the primary concern is about the long-term repercussions. When contemplating molnupiravir, the fear of birth abnormalities or cancer comes into play because it is a mutagenic medication. In response, the drug’s creator, Merck, stated that there is no indication of the possibility for mutagenicity. Although the manufacturer is confident in the treatment and believes that the long-term consequences are insignificant, it is logical that parents might have concerns about molnupiravir.

Ultimately, if patients receive the vaccination that targets the spike protein and are also able to take molnupiravir, hospitalization and mortality rates may dramatically reduce.

Inequality in the Sciences: Can we stop it?

By Alex Douglas

On March 25, 2021