BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: #COVID (Page 1 of 2)

COVID-19 Puts the AGE in TeenAGEr

A new study from Stanford UnBrain 090407iversity suggests that stress from the COVID-19 pandemic may have changed the brains of teenagers, resulting in their brains appearing years older than the brains of pre-pandemic teenagers. The pandemic resulted in increased anxiety and depression among teenagers, but this new research indicates that the effects may not just stop there.

Scientists know that traumatic childhood experiences can accelerate changes in brain structure. Research conducted by Katie McLaughlin, associate professor of Psychology at Harvard University, and her team led to the conclusion that adversity was connected with reduced cortical thickness. This is a sign of brain aging because as people age, their cortices naturally thin. 

Marjorie Mhoon Fair Professor of Psychology Ian Gotlib originally designed a long-term study to research the effects of depression during puberty. He had been conducting brain scans on 220 children, ages 9-13, but he was not able to continue due to COVID-19. After the pandemic, Gotlib resumed his study, and the results were shocking. Researchers discovered that the deveDiversity of youth in Oslo Norwaylopmental process of cortical thinning had been accelerated for the teenagers compared to normal brain development. According to Gotlib, “Compared to adolescents assessed before the pandemic, adolescents assessed after the pandemic shutdowns not only had more severe internalizing mental health problems, but also had reduced cortical thickness, larger hippocampal and amygdala volume, and more advanced brain age.” It remains unclear to scientists whether or not the teenager’s brain age will eventually catch up to its chronological age.

Scientists speculate that the increased anxiety, depression, and overall mental health issues teenagers are experiencing following the pandemic may be linked to cortical thinning. Researchers speculate that cortical thinning may be linked to the expression of certain patterns of genes associated with different psychiatric disorders. Additionally, from studying children who suffered childhood trauma prior to the pandemic, researchers already know that negative childhood experiences can increase the risk of depression, anxiety, addiction, and other mental illnesses. The risk of physical conditions, such as cancer, diabetes, and heart disease, increases as well. 

Jason Chein, professor of psychology and neuroscience and the director of the Temple University Brain Research & Imaging Center, found the research intriguing, but he cautioned against accepting the conclusion that children’s brains definitely aged faster. “It’s pretty interesting that they observed this change,” he said. “But I’m reluctant to then jump to the conclusion that what it signals to us is that somehow we’ve advanced the maturation of the brains of kids.”

 

AP Bio Connection 🙂

I chose this topic because I was interested in the effects of the pandemic on people in my age group. This topic connects to AP Bio because brain aging has been linked to increase stress hormones. The stress hormone corticosteroid activates an intracellular receptor which results in the changed gene expression. Due to the fact that corticosteroids activate intracellular receptors, they must be nonpolar molecules in order to enter the cell membrane. Feel free to comment down below if you enjoyed the article!!

SARS-CoV-2 Is Making My Heart Ache??

New research from the University of Maryland School of Medicine’s (UMSOM) Center for Precision Disease Modeling identifies the specific protein in SARS-CoV-2, the virus responsible for COVID-19, that causes damage to heart tissue.

Protein Structure Gif

Some experiments they did were performed on fruit fly hearts. When Nsp6 is present in a fruit fly heart, the heart shows structural defects compared to a normal heart without the viral protein. However, when fruit fly hearts with the viral Nsp6 protein are treated with the drug 2DG, the hearts begin to resemble normal hearts more closely.

In their latest study, researchers found that the Nsp6 protein is the most toxic SARS-CoV-2 protein in the fruit fly heart. They also discovered that the Nsp6 protein hijacks the fruit fly’s heart cells, activating the glycolysis process and disrupting the mitochondria, which produce energy from sugar metabolism. When they blocked sugar metabolism in fruit fly and mouse heart cells using the drug 2DG, they found that it reduced the heart and mitochondria damage caused by the Nsp6 viral protein.

Dr. Han, the lead researcher, says this about the protein : “We know that some viruses hijack the infected animal’s cell machinery to change its metabolism to steal the cell’s energy source, so we suspect SARS-CoV-2 does something similar. The viruses can also use the byproducts of sugar metabolism as building blocks to make more viruses,”

 

Drosophila melanogaster under microscope

Thus, the University of Maryland School of Medicine’s research identified the specific protein in SARS-CoV-2 that causes damage to heart tissue and has found a potential treatment for it. The protein, called Nsp6, activates the glycolysis process in heart cells and disrupts the mitochondria, which are responsible for producing energy through glycolysis and oxidative phosphorylation. By blocking the processes  with the drug 2DG, the researchers were able to reduce the heart and mitochondria damage caused by Nsp6. This discovery aligns with the topic of glycolysis and ATP generation in AP Biology as it highlights the importance of proper metabolism in the functioning of cells and the potential consequences of disruptions to this process.

 

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.

 

 

 

Why Nearly Every Human on the Planet Has Contracted Covid-19

While some have only heard the term ‘Coronavirus’ starting in 2020, the drama around this type of infectious disease is not new. This type of virus brings on illnesses that you have most likely contracted long before the start of the pandemic in March of 2020. For example, the common cold. But of course, Coronavirus is not responsible for just that– they also bring on SARS (severe acute respiratory syndrome) and MERS (middle eastern respiratory syndrome). With SARS-CoV-2 being the virus that causes COVID-19,  this extremely contagious disease is, in fact, a strain of SARS. 

But if the Coronavirus has been around long before now and there are so many types of it, what makes SARS-CoV-2 special? The answer to this is its relationship with a particular enzyme, ACE-2, whose shape, function and location opens doors right up for COVID-19 to enter and infect our healthy cells. 

While other types of SARS also attached to this enzyme, the ingenious design of the SARS-Cov-2 protruding spike protein is what makes this virus particularly contagious; Throughout the evolution of this virus from other versions of SARS, the shape of their spike protein has become more refined and specific through compaction of its structure to better mimic the shape of the receptor dock of a naturally-occurring enzyme called ACE-2. This mutation allows the virus to strengthen the grip that they can have on human’s cells, making their infection rate much more high and effective. 

The function and location of ACE-2 also practically facilitates the infection of SARS-CoV-2 within us. These enzymes play a critical role in the renin-angiotensin system (infection-fighting system), and while this virus utilizes them as an entrance to the body as a means to infect, it is reducing the function of the very cells that are supposed to be fighting it. Additionally, this suppresses the rest of the functions of our immune system. 

In the human body, one way in which our immune system works is by the release of T lymphocytes, or T-cells, along with macrophages and monocytes to fight off infections. However, with SARS-CoV-2 having already hijacked ACE-2 at the time when T-cell release is activated, the immune system becomes dysfunctional; the three aforementioned immunity cells are released via a positive feedback loop in a much greater magnitude than usual/ than with other illnesses. Lastly, ACE-2 positive cells are present in over 70 types of our bodily cells, and are especially abundant in oral, nasal, and nasopharynx tissues, which are hot spot entrances for this virus (and many others).

With the involvement of just one enzyme within our bodies, SARS-CoV-2 throws all aspects of our immune system into a disarray.  With the many adaptations and evolutions of SARS viruses, infectious diseases such as these are just getting smarter and smarter each time they sweep through the human population.

Coronavirus. SARS-CoV-2

SARS-CoV-2 Spike Protein

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!

The Covid Complacency Craze!

In the pandemic’s early days, countries reported their COVID-19 levels daily. However, that isn’t the case now. In 2022, countries most often report their COVID-19 infection and vaccination levels only five days a week. Despite this, there are still outbreaks of the virus. China, however, has a strict zero COVID-19 policy which results in lockdowns when too many cases are reported. This means that Chinese citizens often find daily life disrupted by the presence of COVID, an experience that we Americans have left more or less in the past.SARS-CoV-2 without background

This begs the question, which course of action should be adopted by countries worldwide? Of course, a middle ground would be ideal, however, that may be unrealistic as governments are trying to find a “new normal” (as the UK put it). Despite this hope to live with COVID, many people are outraged at what seems to be complacency coming from international governments, as citizens say that more needs to be done. What more is there to be done, though? Besides going back to the early ways of the pandemic, reporting cases and deaths daily, governments worldwide are doing everything possible to keep people informed on both COVID and its effects.

People's Republic of China (no claimed territories)

China’s lockdowns, while effective, are very extreme by international standards. There is a call from citizens in China asking for the COVID-19 protocols to be lessened, as the lockdowns are affecting people’s livelihoods. There are small wins, as the Chinese government has slightly repealed COVID-19 protocols, as citizens no longer need to show a negative covid test to use public transport. A study showed that when intrusive protocols are introduced, people overall show “non-compliance in applying health protocols” meaning that while China’s health practices may be effective for now, they may mean trouble in the long run as people stop following them. This supports the idea of a happy middle ground between the United States’ and China’s current protocols.

Fears of a Winter COVID-19 Surge

         In March 2020, our planet was invaded, as we were threatened by the very initial strain of the SARS-CoV-2 virus. This event was commonly referred to as the Coronavirus pandemic. Little did we know then that there would also be several increasingly virulent variants facing us in the immediate future. This highly infectious and adaptive virus forced virtually everyone on Earth to quarantine and patiently wait for a worldwide team of multi-disciplined scientists and medical practitioners to develop an approvable and effective vaccine. For at least a year, we sat before our TV sets and awaited the daily numbers of the newly infected, hospitalized, and deaths. Populations throughout the world were being sent to hospitals in an effort to survive this dangerous virus. The hospitals and healthcare workers across the globe were stretched way beyond capacity, and the untold emotional effects on care providers, in itself, reached epidemic proportions.

SARS-CoV-2 without background
The SARS-CoV-2 virus enters and attacks our lungs through our normal respiratory process. The virus causes our lungs to become inflamed, making it challenging for us to breathe. This can lead to pneumonia, an infection of the tiny air sacs inside your lungs where your blood exchanges oxygen and carbon dioxide. These viral effects made it difficult for middle-aged and older adults to cope and often left them vulnerable to the disease. Once the vaccines were advancing to a stage of government approval and being administered to the general population, we began to see statistically significant improvements in the overall ability of our immune systems to “take on” the virus and win the battle. As people were receiving the vaccine, most people were choosing the mRNA vaccines. These vaccines teach your cells to produce a harmless piece of the coronavirus spike protein that triggers an immune response to build antibodies. A spike protein is a specialized combination of amino acids designed to help the immune system know how to respond to the spike protein. In this way, one begins to build immunity to COVID-19, which results in mitigating the adverse effects of the virus or, in some cases, not succumbing to the effects of the virus. Once it does its job, the mRNA quickly breaks down, and the body clears it away in a few days.
All vaccines leave the body with a supply of T-lymphocytes and B-lymphocytes that will remember how to fight that virus in the future. Since COVID-19 is highly adaptive, as evidenced by the emergence of its numerous variants, biomedical researchers have to quickly produce a new vaccine to prevent a new SARS-CoV-2 virus variant from spreading.

Janssen COVID-19 vaccine (2021) F (cropped) 2
New concerns are now arising in the medical community with the threat of yet another new variant strand of SARS-CoV-2 emerging onto the scene as winter approaches. According to the Centers for Disease Control and Prevention, we could be looking at two new omicron subvariants becoming increasingly more dominant in the United States, raising fears that they could start another surge of COVID-19 infections. The new subvariants known as BQ.1 and BQ.1.1 are raising concerns because it appears to be proficient at evading the defenses of currently available vaccination formulations. According to the CDC, in recent weeks, BQ.1 and BQ.1.1 has quickly risen to 44% of all new infections nationwide and is approaching nearly 60% in some parts of the country, such as New York and New Jersey. Additionally, this viral landscape takes on even greater significance as we seem to be in a “viral trifecta” with the more common Influenza (flu) Virus and the Respiratory Syncytial Virus (RSV) taking the stage front and center this Fall and Winter season. Perhaps the best advice is to see your health care practitioner and see if a vaccination or booster shot is right for you!

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

 

Why does COVID-19 cause death in some people and no symptoms at all for others?

COVID-19 can have a variety of effects on the human body, ranging from no symptoms at all to death. Researchers have been investigating what factors such as demographics, pre-existing conditions, vaccination status, and genetics, may contribute to the severity of COVID-19 symptoms.

Researchers already know that older people and unvaccinated people are more likely to have complications. According to August data from the US Centers for Disease Control and Prevention, those unvaccinated and over the age of 50 were 12 times as likely to die than those who had received two or more booster shots.

Pre-existing conditions can have a significant impact on the symptoms COVID-19 can cause. For all ages, conditions like heart disease, kidney disease, chronic obstructive pulmonary disease, diabetes, and obesity can exacerbate COVID-19 symptoms. Cancer patients on immunosuppressants, however, are particularly vulnerable. Getting infected may cause a cytokine storm. In AP Bio, we learned that if a pathogen has managed to get past the barrier defenses, macrophages secrete cytokines as part of the innate cellular defense. Cytokines then attract other phagocytes called dendritic cells, as well as smaller phagocytes called neutrophils to digest pathogens and dead cell debris. A cytokine storm is harmful as it can trigger inflammation that damages organs and tissues. Fimmu-11-01648-g001

Scientists have also found that certain genes may predispose individuals to be more susceptible to COVID-19. Studies have shown that some genes from Neanderthals could protect against COVID-19, while other genes could raise the risk of developing severe symptoms. Additionally, scientists discovered that people with variations in the gene called toll-like receptor 7 (TLR7) are 5.3 times more likely to have severe symptoms from COVID-19. Proteins produced from this gene are involved with interferons to alert other cells to raise anti-viral defenses when a virus has invaded. Interferons essentially interfere with the virus. Conversely, having variations in another gene called TYK2 can protect against infection. TYK2 is involved with producing interferons. However, there is a genetic trade-off. Although having more interferons can help fight COVID-19, having more interferons when there is no infection may cause the immune system to attack its own body. Therefore, variations in TYK2 may also increase the chance of developing autoimmune diseases like lupus.

Even with all this research, scientists can not determine the risk that one individual has of having complications with COVID-19. The only factor we can control is our own habits. We should continue to wash our hands, wear masks in crowded spaces, and stay up-to-date with vaccinations. I thought this topic was very interesting because many of us at school do not perceive COVID-19 to be a serious disease anymore. However, we should remain vigilant in preventing the spread of SARS-CoV-2 and other viruses as there are others outside our community that are vulnerable.

How Bats Turned Themselves and the World Upside Down

In a research article written in early-mid November of 2022, Smriti Mallapaty conducts and evaluates the bat ancestry in SARS CoV-2. Over the few years of COVID research, scientists discovered that COVID shares ancestry with bats more recently than they believed. However, recent findings suggest that finding that ancestor is unlikely.
In a recent presentation at the 7th World One Health Congress in Singapore, scientists compared portions of the coronavirus set of genes, which led to the discovery that COVID and bats shared genes as recently as 2016. In addition, it narrowed down the time between SARS-CoV-2 jumping from bats to humans. According to the Bat Conservation Trust, the reason for the transmission of COVID from bats to humans is due to deforestation and livestock farming on the cleared land brought wildlife into much closer contact with humans providing the opportunity for a spillover event.
Bat 03
This study conducted by Mallapaty highlighted the difficulty of finding the direct ancestor of the coronavirus. However, this led to research efforts in Asia. Many southeastern Asian scientists have come together to test the sequencing of viruses in different tissues to identify the ancestor. But, due to their struggle to find their ancestors’ people began to believe that the virus came from a Wuhan Virology facility. In the Wuhan Virology facility, according to the United States Senate, researchers and their collaborators collected virus expeditions on large scales to Southern China and Southeast Asia, where bats naturally harbor SARS-related viruses, on an annual basis from 2004 onwards. Scientists collected samples of bat blood, urine, and saliva. The bats and or samples from the bats transmitted covid to humans beginning of the COVID-19 pandemic.
This passage relates to the AP Biology Curriculum, specifically the Immune system and Adaptive immunity. In adaptive immunity, the body uses Pathogen Specific Recognition to target infected cells through a cell-mediated response. The MHC protein on macrophages and dendritic cells displays the foreign antigen and releases cytokine. The cytokines activate the T helper cells to recognize the antigen and start the cell-mediated response. The T helper cells stimulate other T cells to divide into Killer T and T memory cells. The T-killer cells kill infected cells, and T-plasma cells block off and remember the antigen to cause a faster immune response if exposed again. In addition, one can be further protected by receiving the mRNA vaccine. The mRNAs vaccine blocks the spike protein surrounding COVID cells so it can bind to the receptor on human cells that would allow it in.
 Novel Coronavirus SARS-CoV-2 (51240985843)
Overall, from their rigorous research, these scientists were able to find that SARS-CoV-2’s closest known relative is a bat virus found in Laos called BANAL-52, whose genome is 96.8% identical to SARS-CoV-2. In addition, another virus = is called RaTG13, which is 96.1% identical. They did this using a method of isolating viruses from bats and comparing their genomes. All these percentages reveal that the virus has undergone between 40-70 years of evolution. On the other hand, some researchers say that comparing whole-genome sequences ignores the role of recombination in virus evolution. Recombination is a description of DNA made by combining genetic material from 2 different sources. In this process, pieces of RNA could be very different from SARS-CoV-2, suggesting they are more distantly related, whereas other fragments that are much more similar imply a closer relationship. Therefore to account for recombination, researchers compared bat and pangolin genes and split them into segments and smaller nucleotide segments. At that point, each segment was evaluated with a subset to estimate how recently SARS-CoV-2 shared a common ancestor with a bat or animal virus.
This topic grabbed my attention because I was reflecting on my interactions with animals. Besides domesticated animals, the only animals I have had true interactions with are bats and birds. In addition, since the pandemic, I heard about the role bats play in the spread of COVID but never took the time to understand their involvement. In short, I took this opportunity to educate myself on these creatures that hang upside down and turned our world upside down.

Is the recently discovered hidden cavity on the SARS-CoV-2 protein a target for drugs?

Many of us have been vaccinated against COVID-19 and have had the virus, leading us to become used to the virus being prevalent in our lives during the past few years. Even though a successful vaccine has been rolling out for a while now, new therapies have not yet been discovered for future strains. Finding new therapies for the virus remains a major priority in the field of science, even if many of us have been protected already. This issue remains a priority because new variants and strains have been continuing to emerge, and some resist present therapy mechanisms.

SARS-CoV-2

The most effective approach to attempting to combat the virus is addressing the proteins on the surface of therapeutic targets, known as spike proteins. The spike protein (S proteins) located on the surface of the virus leads to its spiky protrusions, and its mechanism to enter human cells. Like we learned in AP Biology class, the spike proteins of the virus latch to cells by matching with a specific receptor on a cell’s surface. The spike proteins of the virus have to latch on to the new cell to infect. Successful messenger RNA vaccines properly target this spike protein, which is the main goal when creating new therapies for viruses. 

                                             Spiky appearance of SARS CoV-2 virus

Luigi Gervasio, a chemistry and structural/molecular biology professor at University College London, and his team have been working towards addressing this issue. By partnering with the University of Barcelona’s research team, the two teams took the first steps to discover a possible mechanism for future drugs to detect and protect against the SARS CoV-2 Virus. Through thorough research and investigation, they uncovered a “hidden” cavity on the surface of a prominent infectious agent of the virus known as Nsp1. The team was able to make this discovery by testing small molecules that had the potential to bind to the Nsp1 cavity. The team identified one, 5 acetylaminoindane, which is essential for the development of new drugs against viruses. They concluded that this cavity permitted the calculation of the cavity’s atomically spatial arrangement, which will allow the development of these drugs.

The results of their breakthrough findings set the stage for developing new therapies that will be able to target the NSp1 protein against SARS-CoV-2 and present Nsp1 proteins in future coronavirus strains. Not only will this finding be impactful for targeting SARS-CoV-2 and future variants, but also new cavities on the surface of other proteins that have yet to be found by scientists. Finally, this research is monumental for both SARS-CoV-2 and virus treatment in years to come!  

 

Should EVERYONE Get Boosted? Young Men & COVID Vaccines

COVID-19 is perhaps the most politicized issue in medicine, yet the scientific community is generally in agreement that most, if not all, people should get vaccinated; however, recent studies have shown that for young people (specifically young men) the booster has some cardiac risks. These men are at risk for myocarditis, an inflammation of the heart muscle.

Scientists are concerned with the longHeart rotating.gif-term effects this has on young men, and they must weigh the risks of protecting people from COVID, and eliminating harmful long-term effects of the vaccine. Jane Newburger, a pediatric cardiologist at Boston Children’s Hospital has studied patients suffering from post-vaccine myocarditis. She says, “I am a vaccine advocate, I would still vaccinate the children.”

Conversely, Michael Portman, another doctor studying patients with myocarditis, is more skeptical. He said: “I don’t want to cause panic, but I crave more clarity on the risk-benefit ratio.” Although the rates of post-vaccine myocarditis are minimal, they are still concerning. The rate was 1 in 6700 for 12-15-year-old boys and 1 in 8000 for 16 and 17-year-old boys. For the vast majority of patients, short-term myocarditis resulting from the COVID vaccine was treatable. Scientists still don’t know why some people experience myocarditis after taking the vaccine, but they have some theories.

Jeremy Asnes, chief of pediatric cardiology at Yale Medicine and co-director of the Yale New Haven Children’s Hospital Heart Center gives insight on the topic: “Though rare, myocarditis can be caused by an immune response to a vaccine such as smallpox vaccine, which was the most successful vaccine in history.” The general consensus among scientists is that they don’t know the reason it’s happening, but the inflammatory reaction is concerning none the less.

Young boy receiving a vaccine (48545943301).jpgOverall, the medical community continues to recommend the coronavirus vaccine to people of all ages. A new study published in the American Heart Association journal indicates that the risk of myocarditis from COVID-19 is higher than the risk of myocarditis from the vaccine for the vast majority of people. Specifically, the risk from COVID is 11x higher than the risk from the vaccine.The exception in question is young men, but for now, scientists still believe that the safest choice for everyone is to take the vaccine; however, you should be aware of the rare side effects that can result from taking the vaccine so that you can stay vigilant after you take yours!! I encourage you to leave a comment on this post. I would love to read your feedback!

AP Bio side note 🙂

Myocarditis is related to AP Biology. Since Myocarditis is inflammation of the heart muscle, to determine the connection between AP Bio and this article, we can examine how myocarditis is resolved in patients. In order to fix inflammation, dying cells are engulfed in the coated by phagocytosis and later transOxford AstraZeneca and Pfizer BioNTech COVID-19 vaccine.jpgported by the vesicle to lysosomes that can digest them. This process is controlled by phagocytic receptors which signal to the cell that the particles can and should be engulfed.

I chose this topic to write about because I was interested in learning about the COVID vaccine. Coronavirus was such an integral part of my life experience, and the vaccine allowed my life to get closer to normal. I feel as if I owe the vaccine that changed my life and kept me safe the courtesy of learning about it.

Can Mouthwashes Suppress SARS-CoV-2?

Various Listerine Products

SARS-CoV-2, the COVID causing virus, could spread from the oral and nasal cavities (mouth and nose). Along with infecting the cells of the respiratory tract, the virus also also infects the cells of the lining of the mouth and salivary glands.

A recent study led by Professor Kyoko Hida at Hokkaido University suggests that a component found in mouthwashes could have an antiviral affect on SARS-CoV-2. Low concentrations of the chemical cetylpyridinium chloride, a component of some mouthwashes, has an antiviral affect on SARS-CoV-2.

Mouthwashes contain antibiotic and antiviral ingredients that fight oral bacteria. It has been demonstrated that cetylpyridinium chloride (CPC) reduces the viral load of SARS-CoV-2 by disturbing the lipid membrane surrounding the virus. While there are other chemicals with similar effects, CPC has the benefit of being tasteless and odorless.

In this study, researchers were interested in studying the effects of CPC in Japanese mouthwashes. Japanese mouthwashes typically contain a fraction of the CPC compared to previously tested mouthwashes. Researchers tested the effects of CPC on cell cultures that express trans-membrane protease serine 2 (TMPRSS2), which is required for SARS-CoV-2 entry into the cell.

During this study researchers found that within 10 minutes of treatment CPC decreased SARS-capacity CoV-2’s for cell entrance and infectivity. They also discovered that mouthwashes that contain CPC perform better than CPC alone.

This study relates to AP biology because the chemical found in mouthwash helps breakdown the lipid membrane surrounding the virus just like the cells on your tongue produce lipase which helps break triglycerides down.

Omicron: The Most Infectious COVID Variant Yet

Omicron has become the most infectious variant of COVID yet, even managing to re-infect people who already had COVID. According to researchers in Botswana and Africa, omicron’s ability to spread so easily is due to its 60 genetic mutations, which include 42 changes to its spike proteins.

In class, we learned about a form of endocytosis called receptor-mediated endocytosis. Receptor-mediated endocytosis occurs when ligand bind to receptor proteins on the cell membrane that match their shape. This process triggers the cell to let in the virus in a coated vesicle. In this case, the ligands are the COVID spike proteins are the receptor proteins are called ACE2. The omicron spike protein is shaped like a claw machine. Most antibodies attack the claw fingers, however, omicron keeps its “knuckles” bent to hide the parts the antibodies target. Omicron can also stick out one positively charged finger to grab onto the negatively charged receptor. This electrical attraction in omicron is three to five times greater than that of the delta variant, greatly contributing to its ability to infect the cell.Coronavirus. SARS-CoV-2

Researchers also suspect that omicron uses a mechanism unlike previous variants to enter the cell. They believe that omicron uses a backdoor compartment called an endosomes, sorting organelles part of the endomembrane system, and a protein called cathepsin L to drop its genetic material. We discussed in class that the endomembrane system also included vesicles, nuclear envelope, the Golgi body, plasma membrane, and the ER. Through this method, omicron is able to enter the cell without killing it. This is particularly significant as the virus can use the host cell to create even more of the virus to spread. Another mutation that aids the virus is a sugar molecule on the spike protein. This modification makes it difficult for antibodies to attack the virus. For these reasons, omicron has managed to evade very effective vaccines. In one case, it was found that two doses of the Moderna vaccine was only 44% effective at preventing omicron infection between 14-90 days after getting the vaccine, and only 23.5% effective between 3-6 months after getting the vaccine.

I was interested in this topic because I’ve noticed that many of my classmates have gotten infected with COVID recently, even after receiving multiple vaccines or having already being infected with COVID. We can only hope that the next mutations will not lead to a more virulent form of the virus.

Why COVID-19 Messes With Smell and Taste

Have you ever wondered why only some people lose their smell when they contract covid-19? The answer to this question is more complicated then it seems. The real answer requires a deep dive into genetics and DNA.

Earlier in the pandemic we were told that if you were to lose taste or smell then this is a likely sign you have the virus. Now we are understanding that not all people have this “common” symptom. A study was done to show the true numbers behind this phenomenon. Out of 70,000 adults who contracted the virus, 11% of adults with a certain genetic makeup on chromosome 4 were more likely to lose their smell and taste. I then wondered how can one chromosome have an effect on losing taste?

I found my answer. As it turns out, the two genes: UGT2A1 and UGT2A2 are two genes that help people smell. These genes are located right next to chromosome 4 which is why these people are more prone to losing their smell when they contract the virus. Additionally, the actual pathways that cause our ability to smell and taste are over and under performing depending on the person. Similar to our Biology class, everyone has different sets of genes. Some genes can be closer to others. Therefore, only some people are affected by this lack of smell and taste if their UGT2A1 and UGT2A2 genes are closer to the location of the variant.

COVID-19 Icon

 

Pregnancy vs The Vaccine

Getting COVID as one person is already a risky and life-threatening experience, but imagine obtaining COVID while carrying another human inside of you! Though there are risks of getting the vaccine shots while pregnant, there are far more risks for the baby to be born unhealthy if the mother is unvaccinated. Why risk your baby’s life when there is an easily preventable way of avoiding the possibility of losing your child? 

The risks from developing COVID-19 when pregnant and unvaccinated were demonstrated in a recent study from Scotland. From December 2020 until the end of October 2021, a period when vaccines were available, there were 4,950 confirmed coronavirus infections among pregnant women. 77% percent occurred in those unvaccinated, along with 91 percent of the 823 hospital stays and all but two of the 104 intensive care admissions, researchers report January 13 in Nature Medicine.

209-pregnant-woman-2

Babies suffered too. The death rate for babies born within 28 days of their mother’s COVID-19 diagnosis was 22.6 deaths per 1,000 births, much higher than the rate for all newborns during the pandemic, 5.6 per 1,000. All of the babies who died over the course of the study were born to women who weren’t vaccinated when they got COVID-19, the researchers found. Scientists are still unraveling what’s happening behind the scenes during a SARS-CoV-2 infection in pregnancy, and why the delta variant was especially deadly for those expecting. The highest numbers of U.S. deaths for pregnant individuals, 40 in August and 35 in September, occurred during the delta surge. There aren’t details yet on how pregnant people fare after becoming ill with the now-dominant omicron variant. But experts don’t advise a wait-and-see approach. And the vaccines continue to offer protection against severe disease and death.

Pregnancy can be a risky time to get an infection in general. Influenza and malaria, for example, can be more severe in people who are pregnant than in those who aren’t. That risk is tied to changes in the immune system. “Pregnancy is a very complicated immune state,” says Andrea Edlow, a maternal-fetal medicine specialist at Massachusetts General Hospital and Harvard Medical School in Boston. The immune system needs to defend pregnant individuals and their fetuses against pathogens. If COVID is contracted by the mother while pregnant, then the baby in the womb will have to fight off COVID just as the mother has to. Learned in AP Biology, the mother has an advantage over the baby because the mother’s immune system has been exposed to more pathogens including bacteria, viruses, toxins, or other foreign substances that the baby hasn’t. In other words, the mother has adaptive immunity or acquired immunity, so after the first line of defense, known as innate immunity, is insufficient to control the infection, the adaptive response kicks into gear to try and fight off COVID. This puts the baby at severe risk of dying because its immune system is not fully developed yet, and hasn’t been exposed to any other pathogen before.  

There have been 169,407 cases of COVID-19 among pregnant individuals in the United States since the pandemic’s start, with a spike in late December of 2021 due to omicron. The counts for January 2022 are not yet complete. When the delta variant took over in the summer and fall of 2021, the risk of stillbirth grew, the study found. From March 2020 to June 2021, before delta, the risk was 1.5 times higher for pregnant women with COVID-19. From July to September of 2021, when delta reigned, there were 3,559 deliveries among women with COVID-19, of which 96, or 2.7 percent, were stillbirths. Of the 169,330 deliveries among those without the disease, 1,075, or 0.6 percent, were stillbirths. That’s four times the risk.

The first inklings that COVID-19 was especially dangerous for pregnant people came in the first year of the pandemic. Year two brought vaccines and plenty of research found COVID-19 vaccination was safe during pregnancy. More than 194,000 pregnant people in the United States have gotten COVID-19 vaccines as of January 31, according to the CDC. There have been no reported safety concerns. A study of close to 2,500 participants in a CDC COVID-19 pregnancy registry found no increased risk of miscarriage after vaccination, researchers reported in October of 2021 in the New England Journal of Medicine. Nor is there a risk of the baby coming too soon or too small, researchers report January 7 in Morbidity and Mortality Weekly Report. The U.S. study of over 40,000 pregnant women found no link between COVID-19 vaccination and preterm birth.

COVID-19 vaccines (2021) A

Even with the reassuring data on COVID-19 vaccination during pregnancy, it’s been hard to stamp out the uncertainty some feel about the shots. Other vaccines are routinely recommended in pregnancy, such as the influenza shot. But the COVID-19 vaccines were new, and pregnant people, as is standard practice, were excluded from the clinical trials that assessed the shots’ safety and efficacy. Excluding pregnant women from the trials can make it seem like “something must be wrong, this must be dangerous,” Edlow says. There were no safety issues among individuals who became pregnant during the trials, nor were there safety concerns in animal studies. Medical organizations said that COVID-19 vaccines shouldn’t be withheld due to pregnancy, but a forceful recommendation for vaccination didn’t come until July 2021.  

Though there has been hesitation from amounts of pregnant women about receiving the vaccine, at the end of the day they are just trying to protect their children from this very harmful and deadly virus, and the more knowledge they get from their doctors the more they understand that the best way for their child to be protected and healthy is if they get the vaccine.

 

Jet Injectors: Getting Your Vaccine Without Needles

Typically, when you get injections at the doctors office, whether it is a flu shot or any number of vaccines that one is advised to take, it is usually injected via syringe/needle. However, there is an alternative way to give people the medication required that doesn’t involve a needle. This is achieved by using a Jet Injector, and this may be more favorable for people who have trypanophobia.

Before understanding and diving into the Jet Injector, we should take a look at how the traditional needle injections work. These injections are doing through syringes. Syringes are “pump[s] consisting of a sliding plunger that fits tightly in a tube.” These syringes, in the medical field, are filled with some vaccine or other fluid that is meant for injection into the body. The syringe was invented in 1853, and is still the main form of medical injections today. These have been so popular and efficient that some people label syringes as the “greatest medical device of all time.”

I’m sure many are no strangers to this syringe, especially with the increased use of them due to their importance in being the delivery system for the COVID-19 vaccine. The syringe is used to get the mRNA vaccine into the blood stream. As talked about in our bio class lessons, the vaccines contents need to be able to reach cells (in this case within the arm) in order to instruct them to produce antibodies  that latch onto the spike protein of COVID-19.

Despite the syringe being widely used and very efficient, it is just not suitable for everybody. For some people they just have trypanophobia and prefer not to use it, while others are better off without it. This is where Jet Injectors come in. Jet Injectors are an alternative to a syringe that do the same job. Jet injectors use a “narrow, high-pressure stream of liquid [that] penetrates the outermost layer of the skin to deliver medication.” These Jet Injectors are either powered by springs or compressed gas (varies based on manufacturer). These found good use in the military as it required less maintenance to use than changing out the needle after each injection. Although that was a use of the Jet Injector in the past, they are currently used as an alternative to the syringe for injection Flu Vaccination.

Luckily, the side effects of the Jet Injector is similar to that of the syringe: soreness, bruising, itching, and redness. So, if you are someone who is not too fond of needles, the Jet Injector could be the solution for you if your doctor has one.

Omicron Variant: How Will it Affect the Vaccinated?

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

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

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

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

 

 

14 Days or 14 Months?

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

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

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

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

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

Primary immune response 1

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

anti-idiotype antibody

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

LONG COVID

After the long sufferable weeks from catching COVID-19, you would think you are in the clear; until, that is, you feel some extra “health-issues”. The term for these health issues, specifically after COVID-19, are called Long Covid (post-covid). Generally “one in two [covid recovered people] experienced long-term COVID manifestations” and the symptoms included are a diverse field of sickness. Penn State investigators mentioned the trend of symptoms from 250,351 unvaccinated adults and children:

Loss of General Well Being (weight loss, fevers, fatigue)

Decreased Mobility (1 in 5 experienced a decrease in mobility)

Concentration Issues

Lung abnormalities (6 in 10 survivors tight chests and a quarter of patients had difficulty breathing)

Digestive Issues

What could be the reason that COVID-19 is still lurking around in our bodies when the sickness is gone? Researchers at Yale University studying long-COVID have found a pattern of patients having an “unusual level of cytokines” also known as a cytokine storm. Cytokines are a secreted chemical proteins released by cells for communication. In the Immune System process, after a Macrophage, large phagocytic cells, ingests an antigen it releases cytokines, signaling for a t-helper cell to come. After the helper t-cell recognizes the antigen, more cytokines are released and trigger the Cell-Mediated and Humoral Responses (B and T cells). I mention all this because researchers are saying that post-covid patients tend to have patterns of irregular, more-than average cytokines being produced as well as an “unusual pattern of activity by…t cells. The greater than average amount of cytokines suggests a “state of chronic inflammation” and “kill tissues and damage organs.” The unusual activity of t-cells suggests that COVID-19 could still be lurking in the body.

Cytokine Release

Cytokine release and the numerous amounts of it

The treatment for these conditions are mostly to take the vaccine but there are still many unknowns to this Long-Covid problem. These problems are mostly lying in the Immune System rather than other parts of the body that can be tested with machines; which is why solving this problem is very difficult. This problem can only be solved by a matter of time and hope the scientists can figure this out.

 

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