BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: #COVID19 (Page 1 of 2)

Is Brain Fog Becoming Clear?

Has anyone ever tried to talk to you the second after you woke up?  It’s almost impossible to comprehend what they’re saying within those first ten seconds that you’re awake, right? Now imagine if those ten seconds lasted weeks, months, or even years, and you’ll be imagining the life of someone with post-COVID-19 brain fog.

“Brain fog,” is a feeling of confusion, inability to concentrate, fatigue, and overall “cloudy” mindedness that is a common residual symptom of the SARS-CoV-2 virus, affecting about forty percent of people who experience “long COVID” symptoms.  Although unable to be detected through any sort of medical examination or test, post-COVID brain fog can have an overwhelming presence, causing people to be unable to work and frequently lasting for over a year.  However, because brain fog only became an extremely common complaint of patients since the COVID-19 pandemic started, scientists know very little about the symptom.

SARS-CoV-2 without background

In an attempt to discover more, scientists at Karolinska Institute, led by Carl Sellgren, researched how the SARS-CoV-2 virus affects the brain by infecting organoid brain cells with SARS-CoV-2.  The experiment revealed that the virus caused neuron synapses to be destroyed at an unnaturally high rate.  As we learned in AP Biology, neurons are signaling cells that exist throughout the body but make up most of the brain.  Neurons are not actually connected- a small gap, called a synapse, between the end of one neuron (or the presynaptic membrane) and the start of the next (called the postsynaptic membrane) separates the two cells.  Neurons signal each other by sending small particles called neurotransmitters across the synapse and into the next cell.  Another common brain cell is microglia, which are immune system cells that dispose of dead cells and repair synapses.  Microglia also destroy synapses, or connections between neurons, when they are no longer needed.  

Complete neuron cell diagram en

Sellgren’s study revealed that SARS-CoV-2 causes microglia in the brain to amplify the rate at which they destroy synapses, preventing many neurons from being able to make connections with other neurons.  Assuming that a full human brain would respond the same way as brain organoids, this discovery explains why long-COVID patients with brain fog experience difficulty thinking.  Amplified microglia activity is also associated with aging, which further supports the results of Sellgren’s experiment because people oftentimes become more forgetful with age.

With this new discovery to open the gates to more knowledge, scientists can begin to understand post-COVID brain fog more deeply and potentially hope for treatment for this symptom that affects the lives of thousands of people.

How is COVID-19 similar to Yellow Fever

Since the start of the pandemic, COVID-19 has affected millions of people around the globe. It’s an RNA virus that causes fever, cough, and death. Like other respiratory viruses, COVID-19 spreads quickly by particles that come out of your mouth when you sneeze, breathe, and cough.

Novel Coronavirus SARS-CoV-2

 

One similar virus is Yellow Fever. It’s also an RNA virus that transmits by mosquito bites. Depending on the person’s body, one might react differently from another. Most people either have no symptoms or mild symptoms that can be recovered in a week. However, people with weak immune systems might develop severe symptoms such as high fever, chills, and body aches. In addition, the fatality rate for people to develop severe symptoms is between 30%-60%.

YellowFeverVirus

Now you might wonder, what makes those viruses similar? Aside from them being RNA viruses, they also have similarities in symptoms. Still, most importantly, those two viruses both do something that I mentioned in my last post: Endocytosis. When these viruses enter our body, they use their special protein receptors to trick our cells into thinking it’s some proteins that benefit our body. Once viruses enter the body, using receptor-mediated cytosis, it uses its own protein and DNA to replicate themselves, including those false proteins. One thing to note is that those viruses can’t replicate by themselves. They would need to rely on living cells to multiply. Once the viruses replicate themselves, they carry on with exocytosis to exit the infected cell and infect more cells in our body.

Last but not least, Yellow Fever and COVID-19 can’t be completely cured since the viruses mutate so quickly that we don’t have enough time to find what can erase those viruses completely. However, as long as we receive vaccines and take care of our health, those viruses shouldn’t worry us too much.

 

COVID-19 and Its History Through The Variants

Since 2019 SARS-CoV-2, a positive-sense single-stranded RNA virus has impacted and changed human life. A Johns Hopkins article titled “What is Coronavirus,” states: “A coronavirus identified in 2019, SARS-CoV-2, has caused a pandemic of respiratory illness, called COVID-19.” Coronaviruses cause highly infectious disease, with variants known as SARS-CoV-2, SARS, and MERS. Although COVID-19 only recently sparked conversation – due to the pandemic –  Coronaviruses were identified in the mid-1960s, and even so, it has most likely been around for much longer than that. The first recorded case of COVID-19 spreading in the United States was on January 30th, 2020, and continues to apply to the current day: with 305,082 reported COVID-19 cases in the US this week alone (Day of writing December 1, 2022). Evidently, heavy research has gone into the post-COVID effects it has on adults aged 18 to 64 (although there has been less research done on the younger age groups). But, in current times with the Omicron and Delta variants researchers have begun testing to see if its post-COVID effects are the same or different than the original COVID-19 strand.

SARS-CoV-2 without background

In the original COVID-19 strand there were many different side effects that people encountered: difficulty thinking or concentrating – referred to as brain fog -, headaches, sleep problems, dizziness – when standing up – pins-and-needles feelings, change in smell or taste, and depression or anxiety. In Omicron, individuals had similar post covid complaints – regarding fatigue, cough, heart palpitations, shortness of breath, anxiety/depression. While individuals infected with Delta from 14 to 126 days found that even in acute (14-29 days), sub-acute (30-89 days), and chronic (90 -126 days) found that they were at a lower risk of having post-COVID complaints. The main difference between the original COVID-19 variant and the Delta variant is that the spike proteins have different structures, with the Delta variant infecting lungs more easily – making it the most contagious version of covid. As stated on the government’s site: “SARS-CoV-2 uses its viral membrane fusion protein, known as a spike protein, to bind to angiotensin-converting enzyme 2 (ACE2) as a ‘receptor’…causing severe pneumonia and acute respiratory distress syndrome.” In the immune system, our body’s ability to react and destroy antigens sufficiently depends on a few things. One of them is if the human body has experienced this antigen in the body before it would have made B Memory cells and would be able to fight it off more efficiently. The adaptive immune system response goes through B Cells, Helper T cells, and Cytotoxic T cells which are in charge of encountering, activating, attacking, and remembering this antigen for the potential next time the body faces this virus. Overall, not only do the viruses change but the way they affect the human body changes as well due to the humoral immune response.

 

 

 

NMT5: A New Enemy To SARS-CoV-2?

In the past few months, scientists in the United States have developed a potential new antiviral to SARS-CoV-2.   The drug, called NMT5, is effective against several variants of SARS-CoV-2, the virus that sent the planet into lockdown only a few years ago.

As stated in the journal Nature Chemical Biology, NMT5 coats SARS-CoV-2 particles as they travel through the body.  Thus, when the virus attempts to attach to the ACE2 receptor proteins of the cell, NMT5 attaches first.  The drug changes the shape of the cell’s receptor upon attachment, which makes it harder for SARS-CoV-2 to infect the cell, and on a larger scale, the organism’s body.

In order to ensure that the drug isn’t toxic, researchers tested NMT5 on healthy cells.  According to the National Institute Of Health, it was “found that NMT5 was non-toxic and only changed receptors that were being targeted by the virus. These effects lasted for only about 12 hours, meaning the receptors functioned normally before and after treatment”.  In fact, in an experiment that used hamsters as models for the human immune system, NMT5 reduced SARS-CoV-2’s ability to bond to ACE2 receptors by 95%!

A significant reason NMT5 is so effective is that it not only limits one particle of SARS-CoV-2, but the effectiveness of the virus as a whole, when present. When a SARS-CoV-2 particle with NMT5 attaches to an ACE2 receptor, it adds a nitro group to the receptor, which limits the ability of the particle to attach to the receptor for 12 hours by changing the receptor’s shape.  Thus, no COVID-19 particle can attach to the ACE2 receptor – even ones that haven’t been surrounded by NMT5.  Stuart Lipton, a professor at The Scripps Research Institute, states that “what’s so neat about [NMT5] is that we’re actually turning [SARS-CoV-2} against itself”, as particles surrounded by NMT5 serve to limit the ability of other SARS-CoV-2 particles.  The drug has excited scientists studying SARS-CoV-2 around the world, as they have “realized [NMT5] could turn the virus into a delivery vehicle for its own demise” (PTI, The Tribune India).

Cell reception and signaling are incredibly important to both viruses and the human immune system.  A virus works by infiltrating a cell through cell receptors that line the outside of the desired cell’s phospholipid bilayer.  Viruses attach to these receptors and infect the cell as a result.  SARS-CoV-2’s process is depicted below, as it attaches to the ACE2 receptors described earlier.  The immune system works by recognizing the virus at hand and signaling B-Lymphocytes and T-Lymphocytes to destroy the virus and infected cells.  B-Plasma cells surround the virus, as shown below, which neutralize it and allow it to be engulfed and destroyed by macrophages.  Cytotoxic T-cells kill cells already infected by the virus.  Both B and T Lymphocytes are activated as a result of T-Helper cells, as T-Helper recognize the virus when a piece of it is displayed at the end of a macrophage, and signal the Lymphcytes by releasing cytokines (another example of cell reception and signaling).  This process is all shown in the image below, with the specific virus depicted being SARS-CoV-2.

Fphar-11-00937-g001

However, NMT5 prevents the initial infection from happening when SARS-CoV-2 enters the human body by bonding with SARs-CoV-2 particles before they attach to cells, which allows for the immune system to quickly destroy the virus.  By blocking SARS-CoV-2’s access to receptors, the drug stops the particle before it can infect a cell and do any damage. Since cell receptors are specifically shaped, and any change in form results in a loss of normal function, the ensuing change in shape of a receptor limits any SARS-CoV-2 particle from attaching to said receptor, further limiting the virus’s damage by blocking cell reception from occurring. Thus, the immune system kills the virus without major symptoms.

All in all, the development of NMT5 is exciting for scientists all around the globe.  If it is as effective as studies show, it could play a major role in limiting the effects of SARS-CoV-2.  Hopefully, all goes well, and you should be hearing a lot more about the drug sometime soon.

If you have any updates or questions on NMT5, I invite you to share them in the comments below.  Thank you for reading my blog post, and stay curious!

Got a weird COVID-19 symptom? You’re not alone

COVID-19 is one of the most commonly known diseases of the decade, for most people today are familiar with its many symptoms, including chills, cough, difficulty breathing, etc. Rarely, SARS-CoV-2 will affect people in ways not expected by a respiratory virus; however, people are starting to see it cause odd symptoms. Peter Chin-Hong, an infectious diseases physician at the University of California, San Francisco said that people have developed patchy tongues, puffy digits, and hair loss as a result of SARS-CoV-2.  Chin-Hong still notes that these symptoms may be less dangerous because they are capable of going away on their own.

It is not always confirmed that COVID tongue, COVID toe, COVID eye, or other strange symptoms are due to COVID-19, but the large scale of coronavirus infections means that SARS-CoV-2 has many chances to show the public how it affects people differently. The U.S. announced they already have had 98 million cases confirmed, and Chin-Hong informed Science New that “statistically speaking, you’re going to find people with more and more weird things.” 

In October, the  Journal of Medical Case Reports released a study done by Saira Chaughtai, an Internal medicine doctor, after a patient obtained unbelievable symptoms after ten days of testing positive for COVID-19. Their tongues swell up and eventually erupted in white-ringed lesions. Chaughtai told Science News “I was like, ‘Oh my god, COVID can do anything.'”

Chin-Hong has also seen patients with unusual tongues; however, they had that looked “as if they’d chewed a mouthful of tortilla chips.”  

Changhai was perplexed about how she was going to treat her patients with COVID tongue. She began by researching scientific literature while giving her patients various types of mouthwash to help in the meantime. She even went to such great lengths in teaming up with a sports medicine doctor who shined a low-level laser light on patients’ tongues, a photobiomodulation therapy normally used to treat muscle injury. Chaughtai thought laser light therapy could heal swollen tongues because it increases blood flow. It showed good results as her patient’s tongue lesions healed even though she still feels some sensitivity. 

Another abnormal effect of COVID-19 is COVID finger or toe which causes swelling in peoples’ fingers or toes. The symptoms also included toes or fingers turning a pink, red, or purplish color. It is know to be very painful. Michael Nirenberg of Friendly Foot Care has seen at least 40 people with this symptom who have been exposed to the coronavirus. He found that fingers or toes will normally heal within a couple of months. Nirenberg told his patient to apply nitroglycerin ointment which he thinks increases blood flow to their fingers or toes. 

“We can’t predict who’s going to get what,” Chin-Hong states, for he feels people should be aware that COVID-19 is capable of causing a wide variety of symptoms. He noted that strange symptoms occur mainly with unvaccinated people. “If this is a reason why some people might get vaccinated,” Chin-Hong says, “I think that would be great,” for these symptoms may seem less severe and harmful as symptoms involving the heart or lungs, but they still can be alarming to see. 

In AP Biology this year, we discussed how there are specific receptor proteins integrated into the plasma membrane. The binding between the receptor protein and a ligand, or signaling molecule, is highly specific. Recent studies found that SARS-CoV-2 enters the cell through a specific receptor protein called ACE2. SARS-CoV-2 spike binds to its receptor human ACE2 (hACE2) and an enzyme called proteases activates it. We also talked about enzymes in AP Biology; they are proteins that function and set off reactions or processes. It is important to understand how the unfamiliar virus enters into cells to learn more about its influence on the human body; this can help scientists discover more information on how and why these strange symptoms occur.

HOLD up COVID-19, HOLD Technology Just Developed A COVID-19 Neutralizer

At the time of this blog post being written, it has been 998 days since Covid-19 was declared a pandemic. Scientists have been able to lessen the severity of deaths due to COVID-19, but they have not stopped people from falling ill. This post will discuss why and what new technology is being created to stop people from falling ill.

Recycled RoomCoronavirus is not different from many other viruses in that COVID-19 uses a protein on its surface to attach to and enter our cells. So, to battle this, scientists created an mRNA vaccine. mRNA is a genetic material that instructs our cells to make proteins. mRNA is covered in a layer of fat to diffuse through lipid bilayers. Ribosomes read the vaccine mRNA, leading to pieces of the viral surface protein being made and displayed on the surface of a dendritic cell. The dendritic cells release cytokines, which leads to lymph nodes making a copy of the surface protein, leading to  Cell-Mediated and Humoral responses. This leads to the killing of infected cells and the prevention of reinfection, but the coronavirus repeatedly mutates and changes its structure. So, the antibodies that the B cells created don’t fit onto and block the newly mutated coronavirus surface protein. Don’t fret; there is hope, Professor Seung Soo Oh is working on a coronavirus neutralizer.

Professor Seung Soo Oh uses Hotspot-Oriented Ligand Display technology (HOLD) to create this coronavirus neutralizer.  The neutralizer contains a protein fragment and nucleic acids, which strongly bind to the protein spikes of the coronavirus. The HOLD COVID-19 neutralizer is created using technology that operates on the principle of natural selection, which makes it significantly better at dealing with the mutating virus. Professor Seung Soo Oh refers to it as “the world’s first self-evolving neutralizer-developing platform.” His discovery led the neutralizer to be much more effective against the mutating virus. The neutralizer is effective against the Alpha, Beta, Gamma, Delta, and Omicron variants. In fact, it is five times more effective than the current vaccine for Omicron. So, almost 1000 days after COVID-19 was anointed to be a pandemic, Professor Oh has made a tremendous leap in halting the effects of COVID-19.

 

COVID-19 on the Genetic Level

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 inSARS-CoV-2 without background​​​ 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 i3D Structure of Legumin Proteinnto 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.

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

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. 

3M N95 Particulate Respirator

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…

Coughing icon

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. 

Fphar-11-00937-g001

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?

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

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

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

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

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

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

SARS-CoV-2 without background

 

BQ- Outsmarting Bebtelovimab

Neutralizing antibodies for treating COVID-19

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

 

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

 

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

 

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

 

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

 

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

 

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

 

 

 

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

Sars cov2The 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).

105 Negative Feedback Loops

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

COVID-19Foot Clan

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?

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.” 

CRISPR Cas9 technology

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  

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.”

Several vaccines (2021)

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

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

3D medical animation still of Type One Diabetes

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.

WHO EN Be SAFE from CORONAVIRUS COVID-19 9Mar2020COVID-19 biểu trưng

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.

Glycolysis metabolic pathway 3

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!

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

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?

Test de antígenos Covid 3

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

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.

Sunny day

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?

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? Hand with surgical latex gloves holding Coronavirus and A Variant of Concern text

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.

Sanger Sequencing Example

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.

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