#COVID19 – Page 2

Similar to any other virus, the symptoms of COVID-19 are amplified in patients who are of old age, have additional complications, or are unvaccinated. For instance, researchers found that unvaccinated individuals ages 50 and older are 12 times more likely to die from COVID-19 than individuals who are vaccinated with boosters (Hesman Saey). Additionally, cancer patients, especially those who are immunosuppressed, are at a higher risk of facing the serious impacts of COVID-19. Research suggests that baseline immunosuppression increases the risk of a cytokine storm. Cytokine storms result in extreme immune responses towards a pathogen which can result in harmful conditions for the body or in some cases death.

These factors play an important role in the severity of COVID-19, however, there are still some severe cases that are unaccounted for. Throughout the COVID-19 pandemic, one question that has perplexed many scientists is: why do certain healthy patients contract severe cases of COVID-19 while others merely experience the symptoms of the common cold? Recent research has found that genetics may be the answer. Studies have revealed that genes passed down from our ancient ancestors can both help and hurt individuals infected with COVID-19. A global study that took DNA samples from 28,000 patients infected with Covid-19 and about 600,000 healthy patients confirms this theory.

The two main genes taken into account are toll-like receptor 7 (TLR7) and TYK2. Variants in these genes are what can control the severity of a COVID-19 case. TLR7 is a gene whose protein is responsible for initiating an immune response by sending signals to other cells that a pathogen has invaded the body. If this process is not operating correctly, it is more difficult for the body to defend against a virus. So, if SARS-CoV-2 enters the body, a variation in TLR7 can cause a more severe case of COVID-19. TYK2 is responsible for producing interferons. A variation in TYK2 can cause an overproduction of interferons. When there is a virus present, such as SARS-CoV-2, the production of interferons can be helpful in the body’s defense.

The processes impacted by TRL7 and TYK2 directly relate to the body’s innate immune process. Innate immunity is the body’s first line of defense once a virus has passed through our innate immune system. The innate immune process involves mast cells which release histamines and macrophages which release cytokines. Interferons work in a similar way. All parts of innate immunity are focused on keeping the pathogen from advancing. Cell signaling is central to innate adaptive immunity, so any alterations in it would result in a less effective defense and therefore a more severe case of COVID-19.

I found this COVID-19 study to be intriguing because this past January a few members of my household were infected with COVID-19. However, only one experienced extreme symptoms. Since all were vaccinated, it may be possible that the alterations in TLR7 and TYK2 are the reason for the differences in reactions among my family.

Ever wonder if you were exposed to COVID-19? This new device may be able to help.

By lukewarm

Riding a public train. Traveling on an airplane. Or just shopping in a public mall. These are all ways someone may contract COVID-19 without realizing that a stranger around them is infected. Traveling via public transport can expose you to unwanted germs, especially when travel times exceed 15 minutes resulting in longer exposure to a possible carrier of the virus. According to the CDC, being exposed to someone with COVID-19 for more than 15 mins results in a “Higher Risk” scenario of contracting the virus. According to Johns Hopkins Coronavirus Resource Center, there have been over 600 million cases of COVID-19 across the globe. What if you could detect COVID-19 particles around you and then change your seat accordingly to reduce exposure?

Well, scientists out of Tohoku University have created a battery-less device which can detect COVID-19 particles in the air, causing a signal response on the device telling you of the virus’s presence. The device generates power via “alternative magnetization caused by vibration” which can detect “bending vibration energy” and transmit the detection wirelessly. The scientists first objective was to modify a “0.2mm thick Fe-Co/Ni plate with a rectifier/storage circuit”. This unit can detect substances that adhere to the clad plate through the change in vibration and resonance frequency. The ability to use this device without power as well as the ability to adjust triggers for its response are the key reasons it was chosen.

The next task for the scientists was to adjust the transmission device to detect type “229E (HCoV-229E)”, one of seven strains of human coronavirus. Coating the clad surface of the plate using targeted proteins, in this case a CD13 protein caused the resonance frequency or vibrations of the device to decrease when exposed to this certain COVID-19 strain. Through repeated tests, they were able to verify that these coated plates could transmit the detection of the type “229E (HCoV-229E)”virus without needing an external power source, “something not capable with current biosensors“.

Proteins stimulating responses in our cells when fighting a virus like COVID-19 occur during the Cell Signaling process that we are studying in AP Biology. Through the process of an Immune Response to a virus, after the virus is broken down inside a macrophage, a MHC2 protein will bring part of that virus to the outside of the macrophage to signal a helper cell. The Helper T Cell then has a protein of its own called a CD4 protein which will pair with the MHC2 protein to identify the shape of the virus. In this part of the Immune response to a virus, we see a protein transferring information to a helper t cell, similarly we see a protein on the surface of these coated clads identify a strain of COVID-19 and then send a signal.

As the scientists continue their research on batteryless biomedical devices, they hope to further “develop our device and see if it applies to other viruses, such as MERS, SARS and COVID-19“.

The Revolutionary Face Mask

By migottlieb

Since the start of the pandemic, society has struggled to develop an efficient way to detect the presence of the SARS-CoV-2 virus in the atmosphere around you. Well, this is no longer the case thanks to young inventor Yin Fang. The intelligent Yin Fang has developed a complicated face mask that can detect the virus in the atmosphere, and on the mask. Though this does seem extreme, it is ultimately revolutionary as it will allow the us to detect COVID-19 everywhere, which will help stop the spread of it.

How the virus spreads

SARS-CoV-2 is an airborne virus that hitches a ride between hosts when we breathe in and out. The virus can spread from an infected person’s mouth or nose in small liquid particles when they cough, sneeze, speak, breathe, ect…

How the mask works

The mask uses special sensors that react when the viral proteins connect to the face mask. It uses an extremely thin chamber that is filled with the virus proteins so that they bind together and cause the sensor to activate. When the connection is active, the sensor communicates with an app on your phone, to tell it the virus is present.

How the face mask works is quite similar to what we have learned in our AP Biology. The protein spikes on the virus bind to the mask, almost like how the COVID-19 virus enters the cell. COVID-19 enters a cell when it binds to a receptor and when it does, it enters the cell through phagocytosis and forms a vesicle around it. Though the virus does not get engulfed on the mask, it binds to the receptor, which activates the alarm on your phone, similar to how a virus binds to a cell.

Physical features on the face mask

According to Fang, the mask is extremely lightweight and portable. It has a similar design to your N95 Which allows for a mixture of protection and comfort while wearing the mask.

The Future of the Mask

The new face mask will ultimately allow us to be in indoor spaces while staying safe during a viral breakout. It will enable us to be cautious of our surroundings if the virus is detected. But most importantly, Fang says “The system on the mask could also be updated with aptamers that recognize different pathogens”

Is Covid-19 Becoming Immune to Us?

By shaminoacid

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

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

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

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

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

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

BQ- Outsmarting Bebtelovimab

By anbhatia

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

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

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

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

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

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

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

Can Keeping Indoor Humidity at a “Sweet Spot” Reduce the Spread of COVID-19?

By papanagopoulos

On December 6, 2022

The COVID-19 pandemic has taught us that indoor air quality matters. It has also taught us that indoor spaces need clean air in order to protect the health and well-being of the people inside. According to a study done by MIT, researchers found that indoor relative humidity may also influence the transmission of the virus.

In a recent study appearing in the Journal of the Royal Society Interface, the MIT team reports that maintaining an indoor relative humidity between 40 and 60 percent is associated with relatively lower rates of COVID-19 infections and deaths, while indoor conditions outside this range are associated with worse COVID-19 outcomes. To put this into perspective most people are comfortable between 30 and 50 percent relative humidity, and an airplane cabin is 20 percent relative humidity.

To conduct this research, the MIT team focused on the early period of the pandemic when vaccines were not yet available. This is important because with vaccinated populations it would be unclear the influence of any other factor, such as humidity.

In order for the MIT team to find this “sweet spot” between 40 and 60 percent relative humidity, the researchers found that whenever a region experienced a rise in COVID-19 cases and deaths, the estimated indoor relative humidity was below 40 percent or above 60 percent.

According to co-author Lydia Bourouiba, director of the MIT Fluid Dynamics of Disease Transmission Laboratory, “indoor ventilation is still critical.” However, “maintaining an indoor relative humidity in that sweet spot — of 40 to 60 percent — is associated with reduced Covid-19 cases and deaths.”

This study relates to AP Biology as COVID-19 affects the immune system. When the virus first enters the body, the body’s response starts by engaging two kinds of immune cells: B cells, which produce antibodies that fight off the virus, and T cells, which destroy infected cells. After this initial response, levels of antibodies in the bloodstream begin to fall. The humidity in the air also relates to biology because in low humidity environments below 40 percent our mucous membranes dry and this “mucociliary clearance” process is impaired. This leaves us more susceptible to airborne infections, like the flu or common cold. When the relative humidity is above 60 percent, as in the case of humid weather, the sweat your body produces cannot evaporate, leaving our bodies feeling hot and sticky. To cool off, our bodies must work even harder. This results in excessive sweating, increased rate and depth of blood circulation and increased respiration. This generates a negative feedback loop to help our body return to a normal state (homeostasis).

Pink Toe? Red Toe? Purple Toe? What does COVID do that we don’t know?

By riwang

On December 6, 2022

Michael Nirenberg, a podiatrist at Friendly Foot Care, encountered peculiar symptoms related to COVID. Over 40 patients had “lesions that look like chilblains” typically associated with exposure to cold weather. In a recent article published by Meghan Rosen on November 21st, she revealed some of the unsuspected symptoms of the SARS-CoV-2 virus. Among these symptoms include “patchy tongues, puffy digits, and hair loss” associated with other rare symptoms like COVID tongue, toe, and eye.

At a closer look into the particularly unusual symptom of the COVID toe, the American Academy of Dermatology reveals insight into the symptoms underlying it. Specifically, the association stated swelling, discoloration, pus, pain, and itch. These symptoms could last up to 14 days with some abnormal cases lasting up to 670 Days! Since COVID-19 is a relatively new disease Dermatologists are still researching the underlying causes of this symptom.

Especially as we enter the Winter season and with the virus still taking a toll everywhere, we must recognize that we still haven’t seen all effects of the COVID. With many mutations, variants, and mandates being removed, the question becomes “How can it be sustainable, sensible, bearable even, to get a virus that floors you, in the same way, multiple times a year?” Aimee Cunningham, a biomedical writer, further extends this discussion to a larger context. Warning us of the problem that many unforeseen symptoms can manifest, Aimee signals that if we don’t control the spread who knows how dangerous COVID can become.

In the context of Biology, we can pinpoint solutions by understanding how COVID enters our system and why existing methods/practices like social distancing and masks work. The virus bypasses the first and second defense of our immune system by attaching to the ACE-2 receptors of our cells, hijacking and replicating its RNA code in the cell: A process known as clathrin-mediated endocytosis. We learned receptor-mediated endocytosis which is like clathrin in that COVID has to bind to a receptor before fusing with the membrane. After all, symptoms are recognized days after contracting them. Though it may seem daunting to bring back mandates, there are drawbacks if we don’t.

In more recent news, China’s zero-tolerance policy is exemplary in showing a societal perspective of regulation. Even though COVID is recognized as a legitimate dangerous virus, we also recognize that it’s hard to live in constant regulation. I believe that as of now we don’t fully recognize the effects of all existing variations and that to stop the spread it simply comes down to doing our due diligence. In our school community, students still come to school when they are sick increasing the likeliness of more spread. Simple changes like staying at home can make a major difference.

Is CRISPR the COVID-19 Cure?

By microshoreganism

On March 20, 2022

New Developments In CRISPR Gene Editing Technology Show Promising Advances In Possible COVID-19 Antiviral Pill

CRISPR Gene Editing. If you have never heard of it, don’t worry, I hadn’t either. When google searching CRISPR Gene editing, I went straight to Wikipedia for the simple answer that it is a procedure done in molecular biology, in which the genomes of a living organism can be modified with extremely high precision. One of its many applications is the treating and prevention of disease, enabling researchers to edit DNA and use the natural defense system of bacteria to target and destroy the genetic material of viruses. In a new study from this summer, Dr. Sharon Lewin and her team of researchers at the Peter Doherty Institute for Infection and Immunity at the University of Melbourne believe they may have harnessed CRISPR’s gene editing abilities to block the replication of COVID-19.

Very similar to the replication of DNA, RNA replication begins with a single strand of “Template” RNA. In DNA, because it can only be replicated in one direction (5’-3′), and the strands run antiparallel, each strand is built in opposite directions creating one leading strand and one lagging strand. However, RNA only needs one strand made because it is single-stranded instead of a double. In SARS-CoV-2, an enzyme called RNA-Dependent RNA Polymerase adds nucleotides in the 5’-3′ direction, replicating the template RNA. Because humans have DNA, we don’t copy RNA; instead, we transcribe it to make proteins. Therefore this RNA replication process does not occur in humans and only in viruses.

Lewins’ team designed the gene editing to target single strands of RNA, like those found in COVID-19. CRISPR is most commonly associated with Cas9, an RNA-guided enzyme that cleaves foreign nucleic acids. However, Lewin and her team used a different enzyme, Cas13b, which could cleave RNA instead. Targeting specific sites on the RNA strands of SARS-CoV-2, Cas13b binds to the RNA and destroys the part of the virus needed to replicate, “Once the virus is recognized, the CRISPR enzyme is activated and chops up the virus,” said Lewin. She continues to explain that although the COVID-19 vaccines are highly effective, there is still a clear and urgent need for treatment once the disease is contracted. The ideal treatment would be an antiviral drug that could be taken shortly after the patients tested positive for COVID-19, “That’s what we hope to achieve one day with this gene scissors approach.”

Having written in previous blog posts about my mother’s struggles with COVID-19, my dad also had a very different yet real struggle. Like most people, my dad, having somehow not contracted COVID from my mom at the beginning of quarantine, was very fearful of getting sick himself. Fortunately, my dad has still never had COVID (knock on wood). This is great because he has remained healthy; however, it also had downsides. For my brother and me, being both kids and relatively healthy, when we contracted COVID in mid-August, it was nothing more than a rough cold. A cold that, after ten days, not only was gone but enabled me to feel some sense of temporary immunity to the virus and allowed me to feel comfortable going out with friends and returning to some level of normalcy. My dad never got this. Because he never contracted COVID, he lived a completely secluded life until this past February (when he gave up and began going out in public). If my family and I went to a mall, he would wait in the car. If we ate out, he would wear a mask the whole time and not eat until we got home. The fear for my dad was not specifically getting covid but not having some antiviral drug to take once he contracted the virus. A solution like Dr. Lewins would have been and still would be a life-changer for many families who still live in fear of getting sick from COVID-19.

Although this breakthrough in RNA CRISPR technology is remarkable, the study was performed in lab dishes and is still waiting for testing on animals or humans. Additionally, CRISPR technology medicines have not been approved to treat any diseases. Unfortunately, we are probably a couple of years away from a widely available treatment.

The Compound with the Potential to Decimate COVID-19 Morbidity

By elendometrium

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