COVID-19 – Page 3

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!

Paxlovid and Molnupiravir: Our First Steps Toward Covid-19 Treatment?

By jauharna

Currently, the new Covid-19 variant Omicron is taking the world by storm. Originating in South Africa as of late November, it was considered a variant of concern(VOC) by the WHO on November 26th and the first US case was identified on December 1st. While masks and current vaccination provide significant protection against Covid-19 strains, there is always a chance of breakthrough infections.

In response, both Merck and Pfizer have developed novel antiviral pills in attempts to treat Covid-19 symptoms. It is known that cures for viral diseases do not exist, since viruses tend to mutate extremely fast. However, there exist novel drugs that promise to alleviate Covid-19 symptoms in the early stages of infection, like Pfizer’s Paxlovid and Merck’s molnupiravir.

It is known that Covid-19 infects human cells by its outer spike proteins attaching to ACE2 receptors on the outside of the cell membrane. When in the cell, Covid-19 viral pathogens insert their viral RNA into our cytoplasmic ribosomes, which then codes for the creation of new viruses that then get excreted by the human cell. Merck’s molnupiravir consists of a five day treatment in which mutations to the viral RNA are introduced, since molnupiravir resembles viral nucleosides, causing irregular viral replication and, ultimately, an inability for the Covid-19 viral population to collectively survive in their human host. Pfizer’s Paxlovid pill, on the other hand, is administered in the early stages of Covid-19 infection to stop the progression of the disease and to prevent severe Covid-19 symptoms by inhibiting protease enzymes from functioning, which leads to the inability of virus proteins to become segmented and to spread, leading to dysfunctional Covid-19 viral pathogens and the ultimate death of Covid-19 viruses in the human host.

Fortunately, these two treatments are showing promising results in current clinical data trials. According to a Merck Sharp and Dohme (MSD) clinical study, 14.1% of placebo-treated patients were admitted to the hospital or had died of Covid-19, while only 7.3% of molnupiravir-treated patients were either hospitalized. In addition, at the end of the trial, 0 deaths were recorded in the monopiravir trial, while 8 deaths were reported among the placebo group. These results lead MSD scientists to deduce that the novel molnupiravir to reduce hospitalization or death by 50%.

Pfizer’s Paxlovid, on the other hand, is especially promising in its clinical results. According to a recent Pfizer clinical data trial, 7% of the placebo group was hospitalized, and 7 died, while a staggering .8% of Paxlovid-treated Covid-19 patients were hospitalized, with 0 deaths by the end of the trial. These results lead Pfizer to state that “Paxlovid is 89% effective at patients in risk of serious illness,” as reported by Pfizer CEO Albert Bourla.

In conclusion, although Covid-19 cannot have a fixed “cure,” outside of a vaccine of course, yet convenient, short-course antiviral pill treatments like Pfizer’s Paxlovid and Merck’s molnupiravir provide promising clinical trial results that show efficacy in reducing hospitalization and death rates due to Covid-19. While clinical data trials provide important markers of understanding Covid-19 treatment, it is still impossible to predict the practical applications of these pill treatments in the real world. Who will have access to these pill treatments? How will they get distributed? Will these treatments create global and regional socioeconomic disparities? In the eyes of these questions, our current vaccination protocols remain firm. While novel Covid-19 antiviral treatments are a huge step against Covid-19, the necessity for society to continue vaccination, as well as attempt to reach herd immunity levels, still holds utmost importance.

Omicron: The Latest Invader

By harrisynthesis

As it has been for the past few years, COVID-19 is the talk of the town. However, just when things seemed to be dying down, a new variant made its way into our lives. It goes by the name “Omicron”.

Unlike the past two variants, Delta and Mu, Omicron presents a whole new dilemma in the fight against COVID-19. After Delta took the world by storm with significantly greater infection rates than Mu, seemingly nothing could get worse. However, over 30 mutations to the spike proteins of the virus now trumps Omicron above all other variants. Identified in South Africa on November 24, 2021, Omicron has already made its way to many other countries around the world, including the US.

The threat of Omicron derives from its ability to resist the effects of the antibodies of the vaccine due to the changes in the protein structures. As we learned in our AP Biology class recently, the vaccine works by stimulating the production of plasma B cells, which secrete antibodies to identify and neutralize the antigen of the COVID-19 virus by recognizing the spike proteins, as well as B memory cells that exist to prevent further infection of the virus. The many changes to the spike protein make the antibodies unable to properly detect and neutralize it, allowing for the virus to continue to spread throughout our bodies. Virologist Penny Moore warns of the reduced effects the vaccine will have against Omicron, as well as the exponentially faster infection rates that pose threat to the world.

A recent study from a South African virologist, Alex Sigal, isolates blood samples from 12 Omicron infected patients who have been vaccinated with the Pfizer vaccine. The study shows that the antibodies from the vaccine are nearly forty times less effective against Omicron than the other two variants. This uncovers that the vaccine may not be efficient enough to combat the new virus. Sigal’s experiment also found that people previously infected with the virus held stronger immunity to Omicron than those with the vaccination. This is due to the fact that natural B memory cells made are able to evolve for multiple months to help fight against COVID-19 while B memory cells from the vaccine only evolve for a few weeks. Though, the experiment was not done with enough patients to make a certain conclusion.

Although, there is a glimpse of hope to retain some immunity against Omicron using the booster shot. Pfizer-BioNtech research has indicated that the third dose of the vaccine can produce antibody levels against Omicron that closely resemble the antibody levels of only two shots against the prior variants. Scientists have begun to branch off from the traditional concept of stimulating production of plasma B-cells to create antibodies in hope to find a new way to trigger the immune system to adapt to new COVID-19 variants. Biologist Jesse Bloom suggests a deeper dive into the function of T-cells, particularly cytotoxic T-killer cells, and their ability to destroy cells already infected with the virus.

Omicron poses severe potential threats to the state of the world with its fast infection rate and immunity to the vaccine. The studies of the few infected patients with Omicron do not seem to promising, but not enough has been collected about Omicron to determine its true potential. The only thing we can do now is hope for the best!

How COVID-19 Antibodies Are Causing Long-Term Effects

By joelesterol

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.

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 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!

An Antidepressant Is The Next “Weapon” Against COVID-19

By allyle

On December 17, 2021

Is the COVID-19 vaccine the only way to lower death rates and hospitalization rates? While more individuals are becoming vaccinated against COVID-19, researchers have looked at how a low-cost antidepressant prescription could potentially tackle the virus. Fluvoxamine (Luvox), an antidepressant medication, has the capacity to reduce hospitalization and morality rates after patients receive COVID-19 within a few days. Although fluvoxamine is licensed by the FDA for the treatment of obsessive-compulsive disorder (OCD) and other disorders such as depression, it is not approved for the treatment of COVID-19. In a study, conducted in Brazil, 1,500 newly diagnosed COVID-19 patients were assessed. 741 of the participants received a 100 mg pill of fluvoxamine twice a day for 10 days and the remaining 756 participants received a placebo twice a day. 16 percent of those who took the placebo twice a day got ill enough to necessitate a lengthy hospital stay compared to 11 percent of those who took fluvoxamine. Researchers discovered that participants who took at least 80% of the fluvoxamine administered to them had a two-thirds lower chance of hospitalization! Furthermore, there was only one fatality among individuals that took fluvoxamine, compared to 12 fatalities in the placebo group. According to The Lancet Global Health, this research has shown that the drug has reduced morality rates by roughly 91 percent. The antidepressant drug can be easily prescribed by doctors for COVID-19 using their clinical judgement.

When the COVID-19 virus enters the body through the eyes, nose, or mouth and travels to the lungs, the immune system strives to protect itself from the invading pathogens by producing antibodies that, on occasion, eliminate invading infections. If the invading pathogen is unfamiliar to the body, B-memory cells will be unable to detect it, and B-plasma cells (antibody secreting cells) will be unable to manufacture antibodies, allowing the virus to enter the cell and flourish in the body.

Fluvoxamine is a 2-aminoethyl oxime ether of aralkylketones. The antidepressant medication, if taken promptly after receiving COVID-19, may be an additional method of minimizing viral transmission and accompanying medical concerns. Fluvoxamine is easy to get and inexpensive to manufacture, particularly as a generic drug. COVID-19 treatments, in general, serve as both a cure for severe sickness and a treatment for the beginning of illness. Fluvoxamine, as an SSRI (selective serotonin reuptake inhibitor), attaches to a cell’s receptor that governs cellular stress response and the generation of cytokines, proteins that alert the body of a problem and lead to extreme inflammation. Nevertheless, fluvoxamine has been shown to minimize inflammation. When people get COVID-19, it’s theorized that the damaged cells produce a slew of cytokines that generate inflammation in the lungs, making it difficult to breathe. Patients would be able to breathe better and require fewer hospitalizations if fluvoxamine was taken to help decrease inflammation.

Who knew that an antidepressant that inhibits the serotonin reuptake pump at the presynaptic neuronal membrane might reduce inflammation and allow you to breathe? Because fluvoxamine works by boosting serotonin levels between nerve cells in the brain, it is impressive that the medicine might be used for purposes other than treating depression or OCD. The lingering question is whether someone with COVID-19 who has been taking these antidepressants for a previous disorder has an edge.

Vitamin D Points to Potential Life-saving Therapeutics for Severe Cases of SARS-CoV-2

By rileybosome

On December 17, 2021

A promising new joint study by Purdue University and the National Institutes of Health (NIH) suggests that active metabolites of vitamin D are linked to reducing lung inflammation after SARS-COV2 infection. And no, before you break out your vitamin D pills, the vitamins inside your capsules are quite different from the active metabolites studied. Because of this, these researchers are warning those infected with COVID-19 against taking excessive supplements of vitamin D in hopes of reducing lung inflammation.

The researchers identified an autocrine loop involving vitamin D which allows T-helper (Type 1) cells to activate and respond to the active metabolites of Vitamin D which represses the signaling protein, Interferon Gamma. Distinguishing features of Interferon Gamma is the central role it plays in promoting inflammation.

Structure of interferon gamma. The two chains are colored in red (chain A) and green (chain B).

Although interferon gamma sounds wildly unrecognizable at first, we have actually learned about these proteins more broadly in our AP Biology class. Interferon Gamma is actually a type of cytokine! Regarding this cytokine’s structure, the proteins that compose interferon gamma are dimerized (sounds familiar? This is because we have also previously learned about dimerization through the tyrosine kinase receptor pathway in class!).

Along with the suppression of Interferon Gamma, Interleukin 10, a cytokine with potent anti-inflammatory properties, is amplified. This is significant because this cytokine prevents damage to the host and maintains normal tissue homeostasis by reducing inflammation.

Structure of interleukin 10 as published in the Protein Data Bank.

In the near future, these pathways could be exploited therapeutically to accelerate the shutdown program of hyper-inflammatory lung cells in patients with severe SARS-CoV-2 infections. But for now, before vitamin D is adopted to treat COVID-19, clinical trials are still needed. However, research findings like these are critical to creating effective treatment not just for those infected with SARS-CoV-2, but also other respiratory diseases as well.

What do you think about this new discovery? Do you think this could lead to scientific progress regarding the treatment of inflammation?

New Covid-19 Pill! Will it work?

By sydeousmembrane

On December 17, 2021

In a study conducted by Tina Saey, she looked at Merck’s Covid- 19 pill Molnupiravir and how it is affecting hospitalization rates of Covid-19. Molnupiravir, “an antiviral drug that can be taken at home” is the first medicine that can be taken orally that is approved to help fight off Covid-19. The drug is typically administered to patients who have mild to moderate Covid within five days of their symptoms appearing. Molnupiravir has been tested several times and is now waiting on the FDA for formal approval. This new pill could be a game-changer, but will it really be as great as it seems?

Ms. Saey states that “finding an early treatment hasn’t been easy”, so when Molnupiravir came around experts praised its development. Initially, the pill showed great signs of preventing hospitalizations and death from Covid-19. The results were so promising, a 48% decrease in hospitalizations, that the trial ended early so that the pill might become available to the public faster. However, when all the data was collected and analyzed the reduction in hospitalization rate dropped to 30%. The unexplained decrease happened when participants in the placebo group were no longer experiencing severe symptoms. Due to the decrease in reported effectiveness, the FDA’s antimicrobial drugs advisory committee came to a split 13-10 decision on whether the drug should be available for emergency use.

The main concern for authorizing Molnupiravir is that the pill could create even more dangerous versions of the Covid- 19 coronavirus. The drug works by making mutations in the RNA. This is when a change occurs that affects nucleic acids, the building blocks of RNA. A handful of these mutations could land in the spike protein. Spike proteins interact with the cell receptors located on the host cell; in terms of Covid-19 it helps the coronavirus break into cells. The spike protein could also burst into other proteins making the virus more transmittable. James Hildreth, an immunologist stated that, “the potential for this drug to drive some very challenging variants into the public is of major, major concern.” Although this is a possibility it seems unlikely because, after five days of usage, infectious viruses in participants taking Molnupiravir were no longer detectable.

Spike Protein

Overall, there is much promise but also notable concerns to the new drug Molnupiravir. I believe that this new medicine, even with its downsides, could save hundreds of thousands of lives. As Ms. Saey states, “a 30 percent reduction in hospitalizations and deaths is worth giving the drug temporary authorization.”

How Does the New COVID-19 Pill Work? Has it Proven to be Effective?

By sydoplasm

On December 14, 2021

The COVID-19 pandemic has affected so many lives across the world. Many people wonder when society can return back to “normal life”. While vaccines are a great and effective way to begin the process of protecting people against SARS-CoV-2, a professional must administer the shot which may be time consuming and immunizations require more resources than other medications such as pills. Recently there has been more positive research on a new pill that helps the body fight SARS-CoV-2. This pill is a game changer to the future of the COVID-19 pandemic as it can be taken at home rather than vaccinations which must be administered by a healthcare professional.

A new study shows that an at-home pill cuts the chance of hospitalization of newly diagnosed SARS-CoV-2 patients in half. This pill is comprised of an antiviral drug called molnupiravir; molnupiravir is the first oral medication proven to be successful in reducing the viral COVID-19 RNA. The pill was tested in a pool of subjects who were at high risk of developing severe illness once diagnosed with COVID-19. Of the subjects, 377 patients received the placebo and 385 patients received the molnupiravir pill. Within 29 days of beginning the trial, 14.1% of patients who received the placebo were hospitalized, eight of which died. Within this same time frame, 7.3% of patients who received the pill were hospitalized, none of which died. It is important to note that not only did the pill decrease hospitalizations by about half, but this medication also worked for gamma, delta, and mu variants of SARS-CoV-2.

Once the SARS-CoV-2 virus has entered the body’s cells, it replicates its RNA. The complete virus particles exit the cell and begin infecting other cells which begins the virus’s rapid spread throughout the body. As we learned in AP Biology, helper T cells secrete cytokines which activate the adaptive immune response . However, when too many cells are infected there are a lot more helper T cells secreting cytokines into the bloodstream; this is referred to as a cytokine storm. A cytokine storm can result in dead tissue or damage to organs and is an unfortunate COVID-19 complication. However, this pill works to disrupt the SARS-CoV-2 RNA reproduction. Once the molnupiravir drug is absorbed into the virus infected cells, it is converted into defected nucleotides(building blocks of RNA). When the virus attempts to replicate, it is unable to because its genetic code is defective. Because it can not replicate, the amount of virus in the body will remain low. Due to the low SARS-CoV-2 viral count, the virus is less harmful which is made evident in the study summarized above.

It is evident that this pill is effective and can save many lives. Do you think this could be a turning point in the COVID-19 pandemic, leading the beginning of life as we knew it before March 2020?

Are Plant-Based Diets The Cure to COVID?

By jervoussystem

On December 14, 2021

We all know that unhealthy diets can cause medical issues, and thus sticking to healthy foods is better, but this conversation has not been so prevalent regarding COVID. Everyone is told to “mask up,” to “get vaccinated,” and to “wash your hands, yet I cannot recall the last time someone told me to “eat healthy” to stay safe from the pandemic.

In a recent study by Massachusetts General Hospital, over half a million people in the USA and the UK participated in a smart phone symptom study that analyzed each participant’s diet and gathered data for the results. Each participant added data about their diet, which was ranked by healthiness through a “Plant-BasedDiet Score that emphasizes healthy plant foods such as fruits and vegetables.” From March to December 2020, 31,831 participants were infected by COVID, and those with better diets had a “41% lower risk of developing severe COVID-19” symptoms. They also had a 9% lower chance of getting infected.

The researchers connected these sample statistics with the socioeconomic inequality caused and reinforced by COVID. They found a relationship between “poor diet and increased socioeconomic deprivation with COVID-19 risk that was higher than the sum of the risk associated with each factor alone.” Often poorer communities have less access to healthy food, specifically plant-based ingredients that led to less severe COVID results in this study. This means that they may have a higher chance at infection, and likely will have more dangerous outcomes to COVID. This means while plant-based diets can very much help prevent the dangerous nature of COVID-19, but is not a strategy many can employ.

Why does healthy eating help fighting COVID? Well, we know that the humoral and cell mediated immune responses are crucial in building immunity and fighting against COVID. Cytotoxic T-Cells destroy infected cells, and Plasma B-Cells create antibodies. Macrophages also destroy antigens to help out. With all these important parts of the immune system being so important, and being attacked by COVID, the body needs food to create more.

Vitamins and Minerals are crucial for this, and plants are the prime method of acquiring such nutrients. “Vitamin C, vitamin D, zinc, selenium, iron, and protein” all crutial in building and strengthening the immune system, as per Harvard T.H. Chan. Proteins in particular can be used by the body to create more white blood cells, which are made much of protein. Consuming too much fat and sugars will not go into the immune systems, which depresses it.

Healthy diets, including plant-based diets, are not a cure for COVID, but the data has shown it may help people. Unfortunately, it will not help everyone due to socioeconomic inequality, and is another reason why governments should focus on getting better access to healthy food in poorer communities that don’t currently have much. For those who are able to eat healthy, please do so. Not only does it help the fight against COVID, but in any sickness. These statistics are not specific to COVID, but it is important for this conversation to be had about eating healthy because the focus is often only about vaccines, masks and politics with COVID. It is not a cure, though. Getting vaccinated and wearing a mask is the best way to stop the spread, and I highly suggest everyone get vaccinated.

This study also supports the new plant-based diet trend. Many skeptics do not want anything to do with this diet, but from athletes like Serena Williams using it, to this study supporting it, plant-based diets are getting results.

Could This Chewing Gum Help Prevent COVID-19?

By angelatin

On December 14, 2021

With COVID-19 being the topic of discussion in the world right now scientists all around the world are trying to find any solution they can to help prevent this virus. A recent study has found that a specific chewing gum could actually reduce the spread of COVID-19. The research was led by UPenn’s School of Dental Medicine’s scientists. The study involved using samples of saliva from COVID-19 patients.

The transfer of COVID-19 to the body involves spike proteins and ACE2 proteins. The COVID-19 virus is surrounded by receptor proteins which are what actually bind to other receptors of our cells in our bodies. This binding is how the virus is able to enter our body and affect the different cells. The specific protein that the COVID-19 spike proteins bind to in our body is called the ACE2 receptor protein. Scientists began researching whether they could inhibit this binding to the ACE2 protein.

The research done at Upenn led by Henry Daniell actually had began their research before they knew it. Prior to COVID-19 the team was researching the ACE2 proteins to prevent hypertension. They were able to grow this protein in the lab using a plant based production system. This involved putting DNA that was specific to creating the ACE2 proteins into the plants. This plant material could be a new means of delivering this protein. The Dental School had been working on a chewing gum that also used such plant proteins to prevent plaque in their patients. Daniell began to wonder if his team’s ACE2 plant based proteins could combine with the chewing gum plant protein based compound. This sparked the collaboration of both teams to combine their research into one solution for COVID-19. When the ACE2 plant receptor proteins were implanted into the chewing gum they tested the saliva from COVID-19 patients to see the change in the cells. After the chewing gum was exposed to the saliva the viral RNA that was present in the cells was almost eradicated completely. This was able to work because the COVID-19 spike proteins bind to the chewing gum’s ACE2 receptor proteins instead of the body’s cell’s ACE2 proteins. It served as a barrier or replacement for the proteins to bind to distracting it from the human cells. This prevented almost all the viral cells from affecting the important human cells. Though this research is both new and in its early stages of development it could be a great asset in preventing the spread of COVID-19 in the future.

How Mice and Mental Health Led to This COVID-19 Treatment Breakthrough

By eukericotic

On December 8, 2021

An up-close visualization of the COVID-19 virus and its infamous spike proteins.

Ever since the initial outbreak of COVID-19, scientists have worked tirelessly to innovate and find the antidote to the virus which has infected millions and tragically killed hundreds of thousands. Such unprecedented times have led researchers to reconsider everything they already know and take intellectual risks.

One innovator whose experimental hypothesis may save many is Angela Reiersen, a child psychiatrist from Washington University School of Medicine in St. Louis. When she fell ill with COVID-19 in March 2020, Reiersen thought back to a study she had read about the effects of the lack of the sigma-1 receptor in mice and how the lack of this receptor protein led to massive inflammation and overproduction of cytokines. Cytokines are a part of the inflammatory response that occurs when pathogens sneak past the barrier defenses of the innate immune system and permeate cells. Upon entry of a pathogen, mast cells secrete histamines and macrophages secrete these cytokines. These cytokines attract neutrophils which then digest and kill the pathogens and other cell debris. Although cytokines are crucial to a functioning immune system, overproduction of cytokines can be extremely dangerous as it can lead to septic shock, in which the immune system becomes extremely overactive. This has become the cause of death for many COVID-19 patients.

As a psychiatrist, Reiersen worked regularly with SSRIS, or selective serotonin uptake inhibitors, in the treatment of conditions like depression and obsessive compulsive disorder. SSRIs help the human brain by increasing the level of serotonin available between nerve cells, but they also activate the S1R in the Endoplasmic Reticulum. Reiersen wondered, if the lack of the S1R causes fatal levels of inflammation, can we prevent extreme inflammation from COVID-19 through the use of SSRIs?

Scientists have turned to repurposing existing drugs, like the antidepressant fluvoxamine, to prevent COVID-19 related complications.

There have been multiple studies performed to test this line of reasoning, both including and independent of Reiersen. The most notable study was performed as part of TOGETHER, an international organization seeking to test possible unorthodox treatments for COVID-19. The trial was a collaboration between researchers from McMaster University of Canada and Cardresearch, a research clinic located in Brazil. The team in Brazil located 1,497 unvaccinated adults who were deemed “high risk” for COVID complications in their first week of showing symptoms of COVID. Conducted at 11 different research sites in Brazil from January to August, the study provided participants with a 10 days supply of either 100 milligrams of fluvoxamine, an SSRI, or a placebo pill. The researchers monitored the participants for 28 days after, as well.

In the end, 15.7% of participants who were given a placebo pill ended up having major complications from COVID-19, compared to 10.1% of participants who were given fluvoxamine. The gap may seem slight, but this is because not all patients took their full dosage due to gastrointestinal complaints. However, out of patients who completed their course of medication, 66% were safe from any complications and the mortality rate was cut by 91%!

Thanks to the research of Reiersen and many others, fluvoxamine is now considered a solid treatment plan for COVID-19 infections, especially in high risk individuals. As COVID-19 continues to infect millions around the world, who knows what new scientific breakthroughs will be made?

“US braces for Omicron!”…Whats all the hubbub really about?

By merrillenmeyerflask

On December 8, 2021

I was studying for AP Bio one day, when I first heard about the fears around the omicron variant. All over instagram, facebook, I even received emails about it: there seems to be major concern among many, including prominent medical researchers, according to WHO.

“What is the omicron variant?” You may ask. This variant was first reported from South Africa Wednesday, November 24th. In the recent weeks, cases of infection have been increasing rapidly in South Africa, likely as a result of this mutated variant. According to WHO, this variant has a large number of concerning mutations (discussed in detail below), some of which increase the risk of infection. Luckily, current SARS-CoV-2 PCR tests still can be used as a marker in detecting this new omicron variant. Because of this fact, officials have been able to detect this variant faster than previous surges in infection cases.

Despite being able to detect this variant faster than previously, researchers are still concerned over the mutations this variant poses and the implications that could have in this pandemic. Being the fastest spreading variant yet, some of these concerns include the specific mutations on the spike proteins. As we learned before, Spike Proteins protrude from the SARS-CoV-2 cell, allowing for it to bind to receptors on the host cell. Penny Moore, a virologist at the University of the Witwatersrand in Johannesburg, South Africa, says there are more than 30 mutations to the spike protein in omicron, which could possibly make it more contagious and/or allow this variant to evade our vaccines.

Many of the mutations detected on the omicron variant have been found in the delta and Alpha variants, and are linked to heightened infections, as well as the ability to evade infection-blocking antibodies and other immune responses. Mutations to regions of the spike protein in the omicron variant has changed the way the antibodies recognize the pathogens, hindering their ability to bind to the spike proteins. If the spike proteins have mutated and changed shape, then the antibodies will not be as effective in binding. Additionally, hints from computer modeling have revealed the omicron variant could dodge the immunity given by the T cells. However, Scientists have yet to understand the true significance of these mutations and what it means for the response to the pandemic. Penny Moore and her team hope to have their first results in two weeks.

What does this mean for vaccine efficacy?

Well, two quarantined travelers in Hong Kong have tested positive for the omicron variant despite being vaccinated using the Pfizer vaccine. Additionally, Moore says that breakthrough infections have been reported in South Africa among people who have received the vaccine. Again, researchers in South Africa will soon find whether this omicron variant causes illness that is more severe or milder than that produced by the other variants. We should hear their results soon. According to Researchers, the greater threat that this omicron variant poses beyond South Africa is unclear. In the meantime, a way to fight for a healthy future would be to continually take the measures necessary to reduce the risk of COVID-19, including proven public health measures such as wearing masks, hand hygiene, social distancing, and getting vaccinated.

Let me know your thoughts below on this new variant! Stay Safe!

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.

Could This Common Spray Help Prevent COVID-19?

By angelatin

On November 1, 2021

A recent study has found that the use of nasal spray can put people at a lower risk for COVID-19. The study was done at the Cleveland Clinic and the data was taken from already existing COVID-19 patients in the healthcare system. The study compared those who used nasal spray and those who didn’t and saw how they were affected by COVID-19. The study concluded that those who used the nasal spray were 22% less likely to be hospitalized, 23% less likely to need intensive care, and 24% less likely to die from the virus.

The study focuses on the effects of the COVID-19 on the nose. Research in this area has come to learn that a certain protein receptor is very important when it comes to actually acquiring COVID-19. This is the ACE2 protein receptor. A protein receptor is the way the virus actually enters the cells of the body. The receptors are all around the cell and are used to allow certain type of bacteria, molecules, and many other structures into the cell. The COVID-19 virus is aligned with spike proteins which are what connects to the ACE2 receptors. The only way something can successfully enter the cell is if it can successful attach to the receptor by having the corresponding configuration and shape. The ACE2 receptor can actually be found all over the body, but it was found to be crucial in the spread of coronavirus to the rest of the body when in the nose. When there are more of these receptors is when a person is more susceptible to COVID-19.

There are certain nasal spray steroids that are known to reduce the ACE2 receptor activity and Dr. Ronald Strauss, a member of the Cleveland Clinic, wondered if this could affect COVID-19. The study consisted of 72,000 patients who had been positive for the coronavirus between April 2020 and March 2021. Approximately 10,000 of those patients were on a nasal spray prior to the virus. Those using ended up having less admittance to the ICU, less hospitalization, and less cases of death. The nasal spray that was used to block the ACE2 receptors for other reasons was actually able to limit the amount of COVID-19 virus cells that could bind successfully to the cells and spread through the body. The nose is a very important part of our body that serves as an entry way to the rest of our body. Nasal sprays are a great way to prevent the spread of COVID-19 and are available over the counter at a low-cost.

Dr. Kizzmekia Corbett…the brains behind it all

By maxotope

On March 10, 2021

Dr. Corbett attending a NIH conference

As the month of February is regarded as “Black History Month”, it allows us to reflect on and acknowledge those who put their lives on the line to better our safety and who don’t always get recognition. In regards to COVID-19, the deadly virus that struck the world last January, many have spent countless hours researching new therapeutics and vaccines that counter the symptoms of this deadly virus. We tend to gloss over the founders of research and key discoveries pertaining to COVID-19, and instead use these findings as signs of hope for ourselves for the future. As we sit cocooned in our homes and limit our exposure to the virus, first responders and researchers are working day and night to preserve our safety of this great nation. Meet Dr. Kizzmekia Corbett, a 34 year old researcher and scientific lead for the Coronavirus Vaccines & Immunopathogenesis Team at the National Institutes of Health (NIH), National Institute of Allergy and Infectious Diseases, Vaccine Research Center (VRC). Dr. Corbett is a highly prestigious African American women who was one of the leading scientists at the forefront of the COVID-19 vaccine development. She along with her colleagues paved the way into the development of the well-renowned Moderna vaccine.

Kizzmekia Corbett graduated from Maryland University and received a B.S. in Biological Sciences. She was a Meyerhoff Scholar, which is an aggressive program that mentors minorities and women in science. She was then enrolled at the University of North Carolina at Chapel Hill, where she obtained her Ph.D. in Microbiology and Immunology in 2014. Dr. Corbett then used her expertise to propel novel vaccine development for pandemic preparedness. When president Trump paid a visit to the NIH last March, the leads of the vaccine research center explained their life-saving mission. The focal point behind that mission was no other than Dr. Kizzmekia Corbett. Two weeks after the president’s visit, Corbett’s team began their first stage of clinical trials. Corbett expressed that “they took a lot of the knowledge they have gained in the last six years and applied it to a vaccine platform in collaboration with Moderna…..The vaccine rolled out 10 months later”.

President Trump visiting the NIH back in March

Dr. Corbett explains the vaccines effectiveness at the molecular level, as “the vaccine teaches the body how to fend off a virus, because it teaches the body how to look for the virus by basically just showing the body the spike protein of the virus….the body then says ‘Oh, we’ve seen this protein before. Let’s go fight against it”. The Center for Disease Control and Prevention reports that 6.5 million Americans have received the first dosage of the COVID-19 vaccine thanks to Dr. Corbett, and that number is expected to rise daily. Dr. Anthony Fauci, the head of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, credited Dr. Corbett by stating “The vaccine you are going to be taking was developed by an African American woman and that is just a fact”.

President Biden visiting Dr. Corbett at the NIH

As we continue to reflect on inspirational African American men and woman around the world risking their lives to ensure our safety, let us take time to dig deeper into where these research discoveries come from. Let us not shroud the remarkable findings that scientists all around the world work endlessness to uncover. “In a time where vaccine skepticism is high among African Americans, Corbett hopes Black people will put faith in the vaccine and faith in the scientists working behind the scenes to bring it to the American people” states CBS news. If you are one of the fortunate people that have received this vaccine, maybe take some time to reflect on the countless hours of research that scientists such as Dr. Corbett experienced, because with out them the world would be a much different place.

Dr. Kizzmekia Corbett, Vaccine Visionary

By hydrolexandra

Despite the recently-approved Moderna Covid-19 vaccine’s place at the forefront of many STEM-related discussions, the fact that a Black woman played an integral role in its development is comparatively underpublicized. During a month intended to celebrate both historical and current Black trailblazers, it is of the utmost importance that the American public properly recognize Dr. Kizzmekia Corbett, who – through both her illustrious career and her contributions to the vaccine – remains a fine example of Black excellence in science.

Portrait of Corbett

Per BlackPast, Corbett was born on January 26, 1986, in Hurdle Mills, North Carolina. Even at an early age, Corbett was considered by her mother (Rhonda Brooks) as a “sweet little, opinionated detective” due to her intellectual curiosity. While attending Hillsborough High School, she interned for numerous research labs and enrolled in ProjectSEED, a program dedicated to providing supplemental STEM courses for exemplary math and science students. During her summers off from UMBC (which she attended on a Meyerhoff scholarship), Corbett worked under the National Institute of Health alongside Dr. Barney Graham in studying the way that the respiratory syncytial virus develops in children. According to Graham, her ambition and desire for success were apparent from the start; upon his asking of what she wanted to accomplish in her life, Corbett informed him that “[she wanted his] job.” Soon after she earned her PhD and became a postdoctoral fellow of the NIH, Corbett started working on the creation of a vaccine to combat SARS and MERS, two coronavirus diseases. She and her team were responsible for identifying the spike protein of both viruses; as a result, she was asked to lead a team of scientists enlisted by Moderna to finish developing an effective mRNA-based vaccine (NOTE: Per the CDC, “mRNA vaccines contain material [from the SARS-CoV-2 virus] that gives our cells instructions for how to make a harmless protein that is unique to the virus. [Once] our cells make copies of the protein, they destroy the genetic material from the vaccine.” After recognizing that the protein is an invader, the body will create T-memory cells and B-memory cells, which are responsible for preventing re-infection). Luckily for the general public, her and her team’s efforts proved to be successful, as the Moderna vaccine has an impressively high efficacy rate.

Corbett’s road to success wasn’t always easy; due to her race and gender, she was often deprived of a voice to share her research during times when it was desperately needed. Corbett was the only woman and Black person who was invited to now-former President Trump’s conference with leading figures of the NIH (including Dr. Anthony Fauci and Graham) regarding progress on the vaccine; according to NBC, no one at the meeting asked her a single question, despite her position as the head of the aforementioned scientific team leading the vaccine’s development. This treatment is not an anomaly: despite Graham’s stressing of the fact that Corbett is the leading expert on the project, many scientists around the globe defer to, direct questions to, and even double check her work with him instead. Even more egregious is the fact that Corbett is the subject of racist and sexist cyber abuse, as shown by this tweet telling her to “go back to McDonalds where [she belongs].”

Nevertheless, Corbett has made it clear (via an interview with Black Enterprise) that she never intends to change who she is and what motivates her in order to fit the expectations of the (increasingly diverse, but still largely white) STEM community. “I am Christian,” she says. “I’m Black. I am Southern, I’m an empath. I’m feisty, sassy, and fashionable. That’s kind of how I describe myself. I would say that my role as a scientist is really about my passion and purpose for the world and for giving back to the world.” By giving back to the world in such a formative way through her research, Corbett has proven that the growing desire for diversity in science is not just an option, but a necessity.

Why are there inequities for people of color in the healthcare system, specifically in the COVID-19 pandemic, and what are the solutions?

By droeschdna

Show the effects on stress on the human body.

Throughout the past few months, the push for social justice has grown significantly. Throughout the COVID-19 pandemic we have heard about the inequities for people of color. I have taken in interest in this topic through my psychology class as well as my portfolio project. In my psychology class was where I started to really learn what inequities emerging majorities face in the healthcare system, and as someone who is white I think it is so important to learn what some people go through. Though I will never understand what it is like, I want to do my best to understand and create change for those people. I would like to enter the healthcare field, so I want to educate myself on these problems within the healthcare system and strive to create solutions.

In my portfolio project, where I focused on effectiveness and accessibility to COVID-19 testing, I researched an article that dove into a divide for people of color trying to be tested. These people were not able to go to drive-thru testing centers because they didn’t have a car, and therefore could not be tested. This is one of the problems that minorities have faced throughout the pandemic.

This article focuses on the problems of emerging majorities during the past few months. According to the article, in New York City, black people and latinos have a mortality rate from COVID-19 that is 1.6 to 2 times higher than white people. In Arizona, 16% of the deaths are Native Americans. Many people who work in the healthcare system, as well as officials and the general public, are working to solve this issue. The article addresses specific reasons why these inequities exist.

People of certain races, ethnicities, social position, and economic status could be more exposed to the virus because of their jobs, size of their family, child care, public transportation, etc. Some jobs don’t allow people to work from home and their children might be in child care. Some also rely on public transportation or live with many people at home. People who have faced poverty or discrimination often have chronic pychosocial stress that can eventually lead to inflammation. This develops a maladaptation that can cause an impaired response in the immune system to COVID-19. Unfortunately, these people may not have access to a primary care provider. To learn more about psychosocial stress I found an article that explains this in minorities. Oftentimes, minorities face stress because of economic status and not as much access and delivery to healthcare. Stress is associated with cardiovascular disease, hypertension, and inflammation.

Black leaders in the healthcare profession have proposed immediate solutions such as recording data for races and ethnicities, access to current treatments, mobile testing, and communication with leaders that are trusted. The Vanderbilt University Medical Center (VUMC) has worked to address these problems identifying and preventing inequities. They have created resources for COVID-19 to people who speak languages such as Arabic, Nepali, and Spanish. I didn’t realize that there were also inequities for people based on the language they spoke, so this was surprising to learn. I found an article that talks about inequities for Spanish speakers in healthcare. The article discussed how latino children who have limited English proficiency (LEP), are more likely to have compromised healthcare and parents have less communication with the provider which makes more dissatisfaction with the healthcare system. Although there are many inequities for people of color right now, there are so many solutions and people working to fix these problems. This relates to our goal in biology to learn about inequities in the healthcare system, especially during Black History Month.

Bias in Science: History, Representation, and Medicine

By alagapplasmamembrane

A cell culture of HeLa cells undergoing mitosis. HeLa cells are used in biomedical research to this day.

Science is not objective. Scientists may value fact, but they are still people too, influenced by identity and implicit and explicit biases in their research. Racism has pervaded every aspect of society since the country’s founding, and scientific institutions are no exception. From historical racist research practices to a modern reluctance to support Black Lives Matter or actively diversify the field, scientists have participated in and promoted racism for centuries. Scientists cannot claim objectivity now as an excuse to not be antiracist.

Throughout American history, unethical, racist research has contributed to scientific “progress”, but that is not regularly acknowledged. Although the past cannot be undone, fields should at least recognize the horrific means by which some research was done. For example, gynecology was borne of unethical experiments done on enslaved women and children. The “Tuskegee Experiment” withheld treatment of syphilis from hundreds of Black men just to see how the disease progressed. Henrietta Lacks, a Black woman with cervical cancer in 1951, had some cells taken from her tumor without being informed of this. The cells from her tumor, now known as HeLa cells, have been used since the 1950s for biomedical research. Since cancer is characterized by an improperly regulated cell cycle, with either too much cell growth or too little cell death, cancer cells can grow and divide excessively. This particular line of cells has been able to grow and divide endlessly, due to the presence of an active version of telomerase during cell division. This enzyme prevents the typical shortening of telomeres in cell division that leads to cell aging and death, making the cells “immortal” and the cell line usable to this day. Though they have been used in various research advances, her name was only connected to them in the 1970s. Her family, still with limited access to healthcare themselves, received no financial benefits and had no say in how the cells were used. Henrietta Lacks’ case is a more recent example of unethical research practices affecting Black people.

The questions scientists choose to study, whom they choose to include, and how they apply their results all bias research. Scientists of marginalized identities are much more likely to explore topics relevant to minority groups. So then, the lack of diversity among scientists also contributes to biased research priorities. In 2016, only 9% and 13.5% of science bachelors degrees were given to African Americans and Latinos respectively, and only 5% and 3.8% of doctoral degrees in science and engineering went to women and men from underrepresented minorities. Almost 70% of scientists and engineers employed full time are white. When issues like COVID-19 and climate change disproportionately affect marginalized groups, the lack of diverse representation can prevent representative research or solutions. Scientific institutions need to work on hiring and retention of Black, Latinx, and Indigenous scientists, in part by creating less hostile work environments and increasing DEI efforts.

The lack of diversity in clinical trials also decreases the inclusivity of science and medicine. Even though about 40% of Americans are nonwhite or Hispanic, the clinical trials for new drugs tend to have much whiter samples, with some having 80 to 90% white participants. Since these drugs will be used to treat all people, diverse samples are needed to determine the efficacy and side effects that can vary across ethnicity and sex. The 1993 National Institutes of Health Revitalization Act that required greater inclusion of women and minorities in NIH research samples did improve the proportion of female subjects, but not so much for minority groups. Even for diseases that disproportionately affect marginalized groups, those groups are grievously underrepresented in the clinical trials.

One such disease is COVID-19. Even though the rates of infection, severity, and death are greater for Black, Latinx, and Indigenous Americans, these groups are underrepresented in clinical trials. Trials for drugs to treat COVID-19 did not accurately reflect the most affected populations at the research sites. Some studies also did not report the race and ethnicity of participants as required by the FDA. Remdesivir has shown to somewhat decrease recovery time, but since disease severity and outcomes are worse for minority groups, the benefits of improvement may not necessarily extend to them. This is why proportional representation of affected populations is so important in clinical trials for drugs.

One cause for lack of diversity in clinical trials is that minority groups can be unwilling or unable to take part, for reasons including fear of discrimination, lack of time or resources, inaccessibility of recruitment centers, language barriers, and fear of exploitation based in historical precedent. However, these barriers should be on the researchers to address, not on the marginalized groups. A possible solution could be to have the FDA enforce that drugs should be tested on samples that demographically reflect the populations that will be using them.

In the end, research institutions and scientists need to examine their biases in order to determine who they are serving, and then who they mean to serve. Efforts to increase diversity cannot be passive, but instead should involve active recruitment and work to eliminate the barriers in place. In an academic institution, that might mean a more inclusive work environment and better outreach and mentorship programs. For clinical trials, this could be reducing the financial burden of participation and building better relationships with minority communities that may have been hurt in the past. Science is meant to help people, so we need to be better moving forward, as well as acknowledge the damage scientists have done in the past.

COVID-19 and Environmental Racism: A Fatal Pair

By lizsosome

In his article “Environmental Racism Has Left Black Communities Especially Vulnerable to COVID-19” published by The Century Foundation, Caesar Berkovitz speaks of research surrounding environmental racism, air pollution, and their impacts on vulnerable populations concerning COVID-19. After outlining the pre-existing inequalities that harm Black individuals during the pandemic (increased risk of exposure due to work hours, disparities in wealth-income, and racism within the healthcare system), he goes into the meaning of residential and environmental racism. Environmental Injustice regards inequality in poor or communities of color that increases exposure to pollution and health risks. Environmental injustice is often paired with minimal environmental protection and environmental quality through government regulations. One aspect of environmental injustice regards the disparity in the location of pollution and bad air quality. Due to the pre-existing residential segregation, often Black individuals are placed in communities that have lower property value, and therefore a lower price on the industrial market. With more industrial factories, highways, shopping malls, and businesses in Black communities, air pollution worsens, decreasing the physical health of those who live there, hence a form of environmental injustice is created. Wealth disparities have allowed white community members to buy property away from these areas such as rivers used for dumping trash, and areas with landfills. Many individuals in these environmentally challenged neighborhoods also do not have a large legislative presence- often financial power comes with political power.

Air pollution has also been found to have links to lung cancer. For example, China is a country with a high lung cancer rate. Despite the low smoking prevalence, the large exposure individuals have to air pollution has created around 260,000 lung cancer cases in Chinese women annually. When cells are damaged, altered, or there are changes in their DNA (which can be caused by air pollution), they can become a defective part of the body system. These damaged cells then divide through mitosis without receiving the proper signals at the mitosis checkpoints. Once they do so, they continue to divide and they can create clumps of cells called a tumor. Once cancer cells metastasize, they spread through the blood vessels and they can move through the body to spread cancer to other parts.

So, you may ask, “how does this all apply to COVID-19?”. Well, when pollution from fossil fuel and industrial emissions are released into the atmosphere, PM 2.5 (or carcinogen) is released with it. The tiny particles of Carcinogen have been proven in a study by Harvard University to increase health risks when someone gets the COVID-19 virus. After looking at more than 3,000 countries all over the world, researchers in this study found that individuals who lived over a decade in a county or place with high levels of PM 2.5 (in comparison to the rest of the world) are 8% more likely to die from COVID-19. Therefore, adding another layer to environmental injustice, with increased pollution from environmental racism comes a higher fatality rate for individuals living in these areas from COVID-19.

“Wait, but I thought the environment was getting better because pollution and emissions were decreasing during the pandemic?”. This statement is true, but it doesn’t overpower the pre-existing exposure of pollution present within populations that experience environmental racism. A study done by CREA (Center for Research on Clean Energy and Clean Air), found that due to the lack of oil and coal production and demand, 11,000 air pollution-related deaths have been avoided in Europe, and there has been a 40% reduction in average level of nitrogen dioxide (NO2) pollution. However, as CREA also found, the net presence of PM2.5 and NO2 in the atmosphere is increasing- Tangshan, south Hebei, and Shanxi, China for example exceeded their pollution levels from last year.

Photo with “no filter” taken by someone in Taipei, Taiwan where the PM 2.5 level was 152.

Solving environmental racism includes untangling a web of pre-existing inequitable environmental, social justice, and healthcare legislation- there is no one clear solution. Caesar Berkovitz suggests that both pre-existing improvements and new changes can be made. He argues increasing funding of the Housing Choice Voucher Program at the federal level and increasing rental assistance programs would help reduce residential injustice. In addition to that, one of the main problems many towns face concerning building affordable housing is the “zoning town boards’ ‘ which approve or disapprove the development. Improving the structure of zoning town boards to ensure that at all times, both sides of the community are voiced in the discussion would be a step towards reducing residential inequalities. Redlining and inefficient zoning boards within towns should be the main focus, as it is the root of the unfortunate placement of the individuals harmed by environmental injustice. Increasing federal transportation funds to create the equitable street design and increasing funding for public transformation to reduce fossil fuel emissions from cars as Berkovitz mentions is also another option. Since environmental injustice covers a wide range of legislation and areas, there are various platforms and ways in which humans can help fight it. As we reach what seems like the end of the pandemic, what do you think would be the best solution to fighting environmental injustice? Comment down below!

The Truth Behind Health Disparities: COVID-19 Edition

By lindsosomes

On March 7, 2021