AP Biology class blog for discussing current research in Biology

Tag: COVID-19 (Page 1 of 5)

Is COVID-19 Linked to Diabetes?

COVID-19 Virus diabetesToday’s children are being born into a world much different than what we once knew. The new reality of our world involves grappling with the effects of COVID-19. However, it seems that some children are experiencing greater effects than we could have imagined. As it was recently discovered, after a child is infected with COVID, he or she may have a heightened risk of developing Type 1 Diabetes. This adds another complicated layer to the pandemic that we thought we had mostly seen the end of. This article will detail the facts of the research while also providing insight from my AP Biology studies.

Over the past three years, we have become all too familiar with SARS-CoV-2, known as the virus that causes COVID-19. We have seen its effects in many different ways in our own lives and the lives of those around us. Now, as research improves, new discoveries have been made about COVID’s link to Diabetes in children. This article from NewScientist by Chen Ly highlights these studies. The article mentions that inside the pancreas are these structures called islets of Langerhans. These islets are groups of pancreatic cells that are responsible for producing insulin and glucagon, the two hormones that are crucial for the regulation of our blood sugar. The body can develop an autoimmune response to these islet beta cells and then fight against them with autoantibodies. If enough autoantibodies are created, they can trigger the onset of type 1 diabetes after killing too many islets in the pancreas. In a research study conducted by Annette-Gabriele Ziegler at The Technical University of Munich in Germany, it was concluded that children who had COVID antibodies were twice as likely to develop islet antibodies than those who have not been infected. This information provides insight on the relationship between COVID antibodies and diabetes. If children’s bodies can create these autoantibodies that kill the islets, the insulin production in young children can be weakened by COVID infection.

As stated in this article from the University of Minnesota, diagnoses of Type 1 Diabetes increased as a result of documented COVID infections. The incidence rate of T1D was 29.9 from January 2020 to December 2021. This was a jump up from the 19.5 incidence rate recorded in 2018 and 2019. This jump suggests that COVID infection is correlated to an observed increase in T1D. In an article by the CDC, it was reported that people under the age of 18 were more likely to receive a diabetes diagnosis after 30 days from COVID infection. This highlights the importance of COVID prevention strategies in order to additionally prevent other chronic diseases. In addition, this PubMed states that during the pandemic, we observed an increase in cases of hyperglycemia, diabetic ketoacidosis, and new diabetes. Th alludes to the possibility that COVID may trigger or unmask T1D.

Recently in our AP Biology class, we have been learning about the immune system and cell communication. This can be related to the research mentioned above in that we have covered the topic of blood sugar regulation and studied the pathway of insulin and glucagon throughout our bodies. Insulin regulates our blood sugar by helping to store the excess glucose in the liver when there is too much of it in the bloodstream. Glucagon does the inverse of this by taking the stored glucose from the liver and bringing it to the bloodstream when blood sugar levels are low. Both of these hormones seek to maintain homeostasis. In addition, we have focused on how our bodies react to viruses, and the different kinds of cellular responses that are necessary to fight infections. This is related to my research for this article because it dives deeper into the concepts of immune responses and blood sugar regulation. Getting to read about these topics in relation to the COVID-19 pandemic has further enhanced my understanding of them. 

I chose to write about this topic because of the impact that both COVID-19 and Diabetes has had on my family, which helps me to connect with these topics and heightens my curiosity. I welcome any comments regarding these topics and how they may have affected you or someone you know. What are your thoughts on these findings?

From Individual to Environmental: COVID-19 Antigen Testing Expands

Until recently, testing for COVID-19 has focused on the individual rather than on the environment. However, newly introduced technology promises to expand the scope of COVID-19 detection. Researchers at Washington University in St. Louis have developed an apparatus to detect the presence of the covert virus in SARS-CoV-2 without backgroundenvironmental settings. Previous attempts at this technology have been limited by the volume of air tested. Without adequate air quantity, the sensitivity of the technology is negatively impacted. The current system, however, is capable of concentrating up to 1000 m³ of air per minute, compared to the two to eight cubic meters assessed in previous attempts. The result is a system that increases viral detection sensitivity while maintaining specificity.

The newly introduced apparatus functions by using centrifugal force to approximate viral particles to a liquid matrix adherent to the wall of the test chamber. Within the matrix are found nanobodies, bioengineered antibody fragments derived from llama antibodies. As we discussed in class, the human immune system is composed of humoral and self-mediated factors. Antibodies fall into the humoral category. While human antibodies consist of a light chain and a heavy chain, llama antibodies are composed of two heavy chains. By isolating heavy chain llama antibody fragments sensitized to the COVID-19 spike protein and then splicing multiple sensitized heavy chains together, researchers were able to amplify the viral signal, in a manner similar to PCR.

While the device has yet to be approved, cleared, or authorized by the FDA, it holds promise for meaningful real-world application. For example, prior to a large public event, indoor spaces could be screened for the presence of COVID-19. If the virus were detected, remediation could be performed and the environment retested prior to the public event. In doing so, countless potential COVID-19 infections could be avoided.

This novel technology diverges from current efforts at viral detection in that it does not rely on the existence of an infected individual but rather focuses on environmental detection thereby constituting primary prevention. In the future, the technology could be applied to prevention of other infectious diseases, both viral and bacterial. Further work is needed to explore the potential application of this method.

I urge readers to respond to the above and offer opinions.

The “Slow but Steady” Increase of yet Another COVID-19 Variant: What are the Implications?

Globally, there has been a slow but steady increase in the proportion of BA.2.86 reported, with its global prevalence at 8.9% in epidemiological week 44” (WHO)

Another variant? Since the beginning of the epidemic, we have seen a few strains of COVID-19 arise, notably the Omicron, Delta, and Alpha variants. You may ask, how do these mutations keep on materializing?

Like all viruses, SARS-CoV-2 — the virus responsible for COVID-19 — goes under, and will continue to go under, several mutations.

File:SARS-CoV-2 without background.pngAs a coronavirus, SARS-CoV-2 uses protein spikes (visualization on right) that fit into cellular receptors, in order to infiltrate our cells. Upon entry of the virus, the invaded cell begins to translate the viral RNA into viral proteins, which leads to the production of new viral genomes. According to Akiko Awasaki, PhD, this is where mutations often arise, stating that, “When viruses enter the host cells and replicate and make copies of their genomes, they inevitably introduce some errors into the code.” While these introduced errors may be inconsequential, they can also be of benefit to the virus, increasing contagiousness. These successful mutations may change how the virus behaves in the future, becoming the foundations of new evolutionary steps.

As we learned in AP Bio, the sequence of amino acids plays a heavy role in the primary structure of the spike protein. When the sequence is altered, hydrogen bonds will be corrupted or created, affecting the stability of the secondary structures like alpha helices and beta pleated sheets. This changes will in turn affect the tertiary structure, ultimately morphing the three-dimensional shape of the spike protein.

Given this knowledge of how SARS-CoV-2 invades cells, and how it may lead to evolution and mutation, what is the significance of this newest variant, and how can it be fought?

BA.2.86 was discovered over the summer with cases from Denmark, Israel, the United Kingdom, and the United States. Later on, it spread to various countries all over the globe, being discovered in wastewater in countries such as Spain and Thailand. As weeks passed, the new strain did not seem to pose a threat compared to its predecessors. However, months later, BA.2.86 on the rise. On November 11th, the CDC estimated that 3.0% of cases came from BA.2.86. November 28th’s estimate, 8.9%, is shockingly almost triple of the earlier estimate just two weeks prior. This is apparently garnering the strain some sort of reputation, now being labelled a “variant of interest” by the World Health Organization.

While the percentage may seem scary, the rise of the strain has not brought a disproportionate growth in infections or hospitalizations. Rather than posing new or threatening danger, it seems to be much better adept to escaping our bodies’ defense systems. The improved ability to slip past antibodies, compared to previous variants, likely comes from its large number of mutations, 30, on its spike protein. Antibodies, which serve to fight these invaders, may find difficulty recognizing and defeating the new strain.

Due to the strain only taking the notice of researchers recently, there are still many things to be uncovered. Some researchers have affirmed their support in newer vaccines against BA.2.86 and future variants. As always, it is best to wear masks when necessary, wash your hands, quarantine if you are experiencing symptoms, and receive the latest vaccine.

File:Janssen COVID-19 vaccine (2021) K.jpg





What is the difference between the Pfizer, Moderna and Novavax vaccines?

After the COVID-19 outbreak, various vaccines were developed to fortify our immune response against the virus. However, questions have arisen regarding the distinctions among the three prominent vaccines: Pfizer, Moderna, and Novavax. Despite the emergence and spread of new COVID-19 variants, these vaccines continue to be recognized as effective measures in preventing severe disease.

The Pfizer vaccine is a messenger RNA (mRNA) vaccine, meaning that a small piece of mRNA will instruct the host cell to produce copies of the spike protein

Novel Coronavirus SARS-CoV-2from a harmless version of the COVID-19 virus. The immune system will then identify the viral protein and will begin to produce antibodies that will attach to and mark the pathogens for destruction. Isn’t the immune system so amazing! The immune system then deploys B memory cells to prevent reinfection by remembering the antigen so your immune system can quickly fight it in the future. Common side effects of the Pfizer vaccine include pain, redness, and swelling at the injection site, as well as tiredness, headache, muscle pain, chills, fever, or nausea throughout the body.

Similarly, the Moderna vaccine employs mRNA technology. It instructs host cells to replicate the spike protein, leading to the immune system generating antibodies that identify and target the foreign viral protein. B memory cells are then employed to prevent reinfection by remembering the antigen which allows your immune system to quickly fight it in the future. The side effects of using the Moderna vaccine are also pain, redness, swelling in the area where the shot was administered, and tiredness, headache, muscle pain, chills, fever, or nausea throughout the body. The key distinction between the Pfizer vaccine and the Moderna vaccine lies in storage requirement.  Pfizer vaccine needs to be shipped in a special freezer that reaches very cold temperatures compared to Moderna that can survive in less extreme conditions.

In contrast, Novavax is the only non-mRNA vaccine available in the United States. It is a protein adjuvant vaccine. A protein adjuvant vaccine contains pieces of a harmless version of the COVID-19 spike proteins and pieces of an adjuvant. The immune system identifies the spike proteins as foreign bodies and the adjuvant aids in antibody production and activation of other immune cells to combat the spike proteins. The B memory cells are then used to prevent reinfection by remembering the antigen so your immune system can quickly fight it in the future.

Isn’t the way our bodies are able to fight off infection really amazing. Feel free to leave a comment and one fun fact you learned from this blog post!

Is Long COVID-Induced Brain Fog Also Related to Blood Clots?

-As learned in AP Biology, the virus that causes COVID-19 is the SARS-CoV-2 virus. It has spike proteins attached to it that bind to the ACE2 receptors on our healthy cells which allow the virus to fuse with them. The viral envelope attaches to the membranes of our cells and then releases its genetic information to the inside of them. Its RNA hijacks the cells and instructs its machinery to create more virus particles, causing it to further infect the body.

Novel Coronavirus SARS-CoV-2

Shown above: SARS-CoV-2 virus with spike proteins attached.

After suffering from COVID-19, many people have experienced a condition called long COVID. Long COVID is a condition that causes either new or previously experienced symptoms from the COVID-19 virus to develop and linger for weeks, months, or even years after recovery. While scientists are constantly discovering more about the condition, they are still not completely sure what causes it. The variety of symptoms in addition to the lack of understanding regarding this topic result in the inability to properly treat the condition as a whole. Instead, doctors usually treat the symptoms individually and specifically to the patient. Some symptoms include chronic pain, shortness of breath, chest pain, intense fatigue, and brain fog. New research shows that long COVID-induced brain fog could possibly be linked to blood clots.

Data were collected from about 1840 unvaccinated adults in the UK who were hospitalized due to severe COVID symptoms. The patients provided blood samples when initially hospitalized, 6 months after hospitalization, and 1 year after hospitalization. They also completed cognitive tests and filled out questionnaires.

Blood clotting is a process that prevents uncontrolled blood loss when a blood vessel is injured. A type of blood cell called platelets combine with proteins in the plasma to form a clot over the injury. However, sometimes blood clots do not dissolve naturally or they can form when there is no injury, which can be very dangerous. Fibrinogen and D-dimer are two proteins involved in blood clotting, which were also later predicted to be linked to brain fog. Fibrinogen is created by the liver and is one of the main components in the formation of blood clots. D-dimer is a protein fragment that is released when the blood clot breaks down. People with more severe COVID cases and higher levels of fibrinogen proved to have worse memory and attention skills and overall rated their cognition more poorly on surveys. People with higher D-dimer levels also rated their cognition as poor and showed to have more trouble going back to work six to 12 months after recovery.

Figure 16.4.4 : Blood Clot

These proteins have already been linked to COVID-19 and fibrinogen has been linked to cognitive issues but scientists are still not completely sure how the proteins cause brain fog in long COVID. Dr. Maxime Taquet, a clinical psychiatrist at the University of Oxford, suspects that the blood clots could be blocking blood flow to the brain or directly interacting with nerve cells. Scientists wonder whether medicines used to treat blood clotting, such as blood thinners, could possibly reduce brain fog and other cognitive issues.

While I have not gotten an official diagnosis, I am very curious about long COVID because I experience many of the symptoms. I’ve had a lasting cough, brain fog, and reflux. Do you or have you ever experienced long COVID symptoms?

What Impact Can Covid-19 Have on You? How Long Will It Last?

The University of Melbourne conducted a study, from January 2020 to October 2022 that involved over 12,000 participants. The study examined long COVID’s ability to last, and its correlation with different SARS-CoV-2 variants. The results showed a clear trend, where nearly 40% of individuals who had contracted COVID-19 had reported persisting symptoms associated with long COVID. The study observed a lessoning likelihood of COVID-19 causing lasting symptoms as the pandemic advanced. It was also revealed that individuals infected by the more recent Omicron variant were less prone to developing long COVID, with only 12% reporting persisting symptoms.


The study also revealed some demographic factors that influenced long COVID risk. Notably, women, individuals aged 40-49, and those with a history of chronic illness, anxiety, depression, or severe COVID-19 were identified as being at a higher risk for long COVID. In addition, the decrease in long COVID with newer strains did not appear to be solely attributed to vaccination rates, suggesting the involvement of other contributing factors. This new understanding of long COVID could pave the way for further exploration, offering insights into immunological and autoimmune mechanisms, and potentially shaping broader health research. Furthermore, the impact of long COVID, has caused 36 million people to still feel unwell up to weeks, months, and even years after contracting COVID-19.

Overall, the study underscores the widespread impact of long COVID, emphasizing the need for refined strategies in prevention, treatment, and support for individuals grappling with lasting symptoms after a COVID-19 infection. The evolving nature of the virus and its varying impact on different demographic groups highlight the importance of ongoing research to enhance our understanding and response to the long-term effects of COVID-19.

In AP Bio, we recently learned about the body’s immune system. The immune system is a complex network of cells that work together to protect the body from harmful pathogens. When a virus enters the body, phagocytic cells, like macrophages and dendritic cells, engulf the virus particles through phagocytosis.
Then, the virus is broken down into small peices. These pieces are presented on the cell surface as antigens. Those viral antigens are then presented to the helper T cells and once the helper T cells bind to the viral antigen, they become activated. Then the activated helper T cells release cytokines which starts the immune response and activated the other cells. The newly activated cells are helper B cells, cytotoxic T cells, and Memory B and T cells. The helper B cells have receptors that are specific to the viral antigens so they can directly recognize the virus. These cells begin to multiply. The cytotoxic T cells are able to directly kill the already infected cells, stopping the spread of the virus. They do this by releasing perforin into the cell, which tells the cell’s lysosomes to burst so the cell gets destroyed from the inside out. In addition there are plasma B cells which prevent the virus from infecting anymore cells. Then the memory cells remember the virus’ specific antigens so if the same virus infects again in the future, a faster response can be launched.

The immune system’s ability to recognise, combat, and remember viruses is what allows us to survive.

I chose this topic because one of my math teachers said he had long COVID and it was absolutely miserable so I wanted to learn more about it.

What is changing in the immune system that allows COVID-19 systems to persist in some and not others?


How HLA-B*15:01 Gives the Immune System a Head Start Against SARS-CoV-2

In the article I came across, it discusses how researchers have come across an ally within our immune system’s genetic coding. Human leukocyte antigen (HLA), otherwise known as the protein markers that signal the immune system, has been discovered to hold a secret that may revolutionize our approach to combating COVID-19. A specific mutation in the antigen, HLA-B*15:01, has emerged as a key player in asymptomatic infection of SARS-CoV-2. How did scientists stumble upon this discovery, and how does this mutation in the antigen actually allow infection without the presence of sickness?

Research conducted at the University of California, San Francisco (UCSF), led by Dr. Jill Hollenbach, didn’t hesitate to dive right into the genetic phenomenon, finding the very answers to those questions outlined above. Using a national marrow donor database and the COVID-19 Citizen Science Study (CSS) app, they tracked nearly 30,000 individuals through the first year of the pandemic, providing insights into genetic factors influencing COVID-19 infection and immune system-related reactions. In the end, the researchers revealed that a staggering 20% of asymptomatic individuals carried at least one copy of the mutated antigen HLA-B*15:01. Moreover, it was found that those with two copies were over eight times more likely to avoid falling ill.

SARS-CoV-2 (CDC-23312)

The secret of these genetic guardians is actually quite simple, and, through collaboration with researchers from La Trobe University in Australia, the UCSF team focused on the memory T-cell – a key element of the immune system’s ability to remember previous infections. Through their exploration, the researchers found that individuals with HLA-B*15:01, even without previous exposure to SARS-CoV-2, demonstrated T-cell responses to a specific viral peptide (the NQK-Q8 peptide). The researchers then concluded that exposure to a kind of seasonal coronavirus, which carries a strikingly similar peptide to SARS-CoV-2 called NQK-A8, enabled T cells in these individuals to quickly recognize Coronavirus and mount a faster, and, overall, more effective immune response. This led to minimal – if any – presence of symptoms within the study.  

Let’s link this research to what we’re currently delving into in our AP Biology class. In this unit in particular, we’ve been discussing and exploring the functions of cell signaling, as well as the ins and outs of the immune system. Thus, there are obvious associations between bodily response, antigens, and the immune system with SARS-CoV-2 to what we are currently uncovering in class. We learned how Helper-T cells kickstart the immune system by releasing cytokines that trigger mitosis in B – plasma B cells (which produce antigens) and memory B cells – and T cells – cytotoxic and memory. Knowing that this mutation in the antigen appears similar to SARS-CoV-2 NQK-A8 peptide, we can understand how this may have triggered an immune response in the past, and that a secondary infections would have been easier to take care of considering the memory B and T cells were already present in the body.

Can you see how it connects to what we’ve been learning in our AP Bio class? Isn’t our immune system fascinating? Let me know how you feel about this discovery!



COVID-19: Multiple Doors and Multiple Species

An article published in August of this year identifies how the Coronavirus is able to jump from one species to another. Since the discovery of the COVID-19, the disease caused by the virus SARS-CoV-2, in 2019, many scientists have wondered how SARS-CoV-2 infiltrates cells by hijacking a protein called ACE2 which is found on human cells. At first, many believed that the ACE2 protein was required for infection, but recent discovery from the Virginia School of Medicine reveals that SARS-CoV-2 can use multiple pathways to enter cells. A good example to describe this discovery is a house. To the virus, ACE2 is the front door, but if the front door is blocked, the virus can use other proteins to enter the cells which can serve as a back door or windows in the “house.” This is concerning as SARS-CoV-2 is able to adapt to different proteins that serve as the doors into cells of other species. 

Coronavirus. SARS-CoV-2

After discovering that SARS-CoV-2 has the ability to enter cells using proteins other than ACE2, scientists conducted further research to determine the necessity of ACE2 in the infiltration fo healthy cells. As a result, it was revealed that SARS-CoV-2 can bind to and infect cells without ACE2 being present at all. You may be wondering what proteins besides ACE2 COVID-19 and SARS-CoV-2 use to enter and infect cells. Here is one example. 

An article published in the same month identifies TMPRSS2 as an endothelial cell surface protein that allows the spread of COVID-19 and SARS-CoV-2. The definition is similar to that of ACE2 as TMPRSS2 is simply another door or window that SARS-CoV-2 can use to enter healthy cells and infect them. TMPRSS2 is commonly found in the respiratory and digestive tracts which is a supporting factor to why the Coronavirus may encounter this protein. For example, someone infected with COVID-19 may sneeze near you resulting in you breathing the virus into your respiratory tract. 

In addition, an article published in the summer of 2022 explains an experiment done in order to determine the structure of the TMPRSS2 protein. The results section of the article confirms that TMPRSS2 is composed of three domains and three subdomains. An image of the protein shows tertiary protein structure surrounding the protein which is integrated into the membrane. The experiment allows us to see how similar TMPRSS2 is to ACE2 and how an antigen is able to bind to either protein and enter the membrane, but, how can this be prevented?

Although SARS-CoV-2 can enter cells in our body and infect them by entering protein channels such as ACE2 on the cell membrane, cells can create antibodies that attach to their cell membranes. In AP Bio class, we learned that in adaptive immunity, B-cell antibodies bind to foreign antigens while also inhibiting B cells to divide. B cells are then able to create B Memory Cells which recognize a foreign disease such as COVID-19 if it enters the body multiple times. B cells which are activated by B-Cell antigens, can protect our cells and prevent SARS-CoV-2 from infecting our cells by entering through ACE2 channels. 

I agree that these new findings have helped us understand how SARS-CoV-2 enter healthy cells allowing them to jump species, but I also believe there is more to discover about both of these diseases such as the question of whether or not a variant of SARS-CoV-2 can be created that is able to bi pass antibodies and enter cells at the same rate it would before vaccination or first infection. ACE2 and TMPRSS2 have been around for a while but we are just now discovering how proteins like them allow diseases to jump species. What do you think?


Long Term Health Risks From COVID-19 Infection

A recent study examining the health records of 140,000 U.S. veterans suggests that risks of health issues such as diabetes, fatigue, or blood clots may persist for at least two years after a COVID-19 infection. 

As learned in AP Biology, the fundamental method in which SARS-CoV-2 virus enters the cells involves the interaction between its spike protein (S-protein) and the angiotensin-converting enzyme 2 (ACE2) receptor present on the surface of human cells. Upon initial contact, the S-protein of the virus binds to the ACE2 receptor. This binding triggers a series of events that hijacks the host cell’s machinery to release viral RNA and replicate itself, finally generating new viral components. COVID-19 can also trigger an excessive immune response known as a cytokine storm, which might lead to T cell obliteration.

The study compared veterans who had been infected with the virus to nearly 6 million others who did not contract COVID-19, analyzing new diagnoses, lab results, and prescription records. The research identified health problems that emerged from a month after individuals contracted the virus.

The research team discovered that patients hospitalized during their initial COVID-19 cases had a higher likelihood of facing subsequent health problems. But those with milder initial infections showed a higher risk for approximately one-third of the medical issues analyzed compared to those who didn’t test positive for the virus. This group, comprising mostly milder COVID-19 cases, could potentially strain the healthcare system more, according to Ziyad Al-Aly, a clinical epidemiologist at the Veterans Affairs Saint Louis Health Care System.

The most prevalent issues observed align with commonly known long COVID symptoms found in other studies. These include fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems. Furthermore, patients initially hospitalized were approximately 1.88 times more likely to experience acute gastritis (stomach inflammation) two years after infection compared to those without a COVID-19 record, while non-hospitalized patients had a risk factor of 1.44 times.

Finally, Al-Aly and colleagues determined that among every 1,000 individuals infected with the virus, there was a collective loss of 150 years of healthy life due to persistent symptoms in these patients. This stark revelation underscores the severe impact of long COVID, highlighting its destructiveness, as noted by McCorkell. Other studies, such as the U.S. Census’ Household Pulse Survey, have similarly noted how COVID disrupts the day-to-day lives of many patients.

Ultimately, with recent increases in COVID-19 transmissions, I strongly advocate for maintaining our vigilance and adhering to health guidelines, such as practicing good hand hygiene, and staying updated on vaccination recommendations. As a fellow germaphobe myself, I will certainly take heed of these practices. These measures remain crucial in curbing the spread of the virus and safeguarding both individual and community health. As the article mentions, even a mild COVID-19 infection could potentially lead to health issues in the months or years following the initial illness.

Let’s all do our part to keep our communities safe and healthy!

SARS-CoV-2 without background

The Long Term Effects of COVID-19 Hidden Behind the Fog

COVID-19 was one of the biggest pandemics in United States history. It changed everything including schooling and many other aspects of life, but do you ever seem to forget what life was like before COVID-19? You may be thinking am I just getting old? Why am I losing my memory? Well, findings in Nature Medicine have shown that you may be suffering from what they are calling “Brain Fog”. This Brain Fog can result in recurring memory and concentration lapses that can make it difficult to function every day. You may be thinking, how does this even relate to COVID? Well, It is believed that this brain fog is developed from blood clots triggered by COVID.

Before we get into the brain fog, I want to explain how the body first reacts to COVID-19 entering your cells. AP Bio we learned, that your body activates its innate and adaptive immune systems. First, the innate system releases mast cells which release histamine along with macrophages that secrete cytokines. Cytokines are small proteins that are crucial in controlling the growth and activity of other immune system cells and blood cells. When released, they signal the immune system to do its job. We then see natural killer cells take out any damaged or infected cells while cytokines attract smaller phagocytes called neutrophils and digest pathogens. Along with the Innate response we see the Adaptive response. The adaptive response relies on B lymphocytes and T lymphocytes. The B lymphocytes create the humoral response while the T activates the cell-mediated response. Both are just as important but different. When T-helper cells recognize the antigen it triggers both responses. In the cell-mediated response, the T-memory cells prevent reinfection while the T-killer cells go and kill any infected cells. In the Humoral response the B-plasma cells, secrete antibodies that bind to and neutralize the pathogen which is then engulfed by a macrophage, while B-memory cells also prevent reinfection. Even with all this protection people may still be left with long last symptoms including brain fog.

To find out if this brain fog really came from COVID, a psychiatrist from Oxford named Maxime Taquet took samples of over 1,800 people in the U.K. who had been hospitalized due to COVID-19 and made 6 six-month checks on their symptoms. When examining the blood, they found that people who still had “brain fog” tended to have elevated levels of at least one of two proteins. The first protein is called a D-dimer protein which is produced when a blood clot breaks down. Patients with high amounts of D-dimer tend to have memory problems yet the cognitive side seems to still be intact. Doctors believe these effects were caused by blood clots in the lungs, which lead to low oxygen levels in the brain. The second and seemingly more dangerous protein to find mass amounts of is fibrinogen. This protein is produced in the liver and causes clotting to stop bleeding. When patients have elevated amounts of fibrinogen during COVID-19, they seem to have memory loss along with scoring poorly on the cognitive test. These patients show signs of dementia. Taquet believes that fibrinogen may have caused blood clots in the brain or somewhere else that directly affects the brain.

SARS-CoV-2 without background

After hearing about the findings Resia Pretorius was very excited. From her own research, she has found connections between COVID and brain fog. She believes that the spike protein of COVID binds to the fibrinogen and causes it to change shape. But she believes this discovery can help determine ways to cure long COVID symptoms. So have you been affected by COVID’s brain fog or are you just getting old?

Aftermath Mysteries of COVID-19

Greetings, health explorers! Today, we’re diving into the twists and turns of a new study that unveils what happens in the aftermath of COVID-19. To put this into context, let’s picture this: you have now gotten rid of COVID from your body after suffering for a few days, but the health challenges still linger. A fresh study with 140,000 US veterans reveals how risks, from diabetes to fatigue, can play the long game for at least 2 YEARS! Crazy right? 

The research revealed that patients initially hospitalized during their COVID-19 cases were more likely to experience these health problems. However, even those with milder initial infections were still at a higher risk for about one-third of the analyzed medical issues compared to those who didn’t test positive. The most common problems align with long COVID symptoms such as fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems. The study found that for every 1,000 people infected with the coronavirus, a cumulative 150 years of healthy life is lost due to persistent symptoms, highlighting the significant impact of long COVID. 

The article notes limitations. Some of these limitations include relying on electronic health records and potential skewing due to the predominantly male and older veteran population analyzed. It also did not include individuals who may have been infected but did not receive a positive test result in the early stages of the pandemic when testing was limited.

Wow, the impact of COVID-19 on long-term health is truly eye-opening! What are your thoughts on how we, as a society, can better address and manage the challenges posed by Long COVID? Share your insights below!

To set the stage, the World Health Organization (WHO) defines Long COVID, also known as Post-COVID Conditions, as the persistence or development of new symptoms three months post-initial SARS-CoV-2 infection, lasting at least two months with no other explanation. The Centers for Disease Control and Prevention (CDC) expand on this, noting that Long COVID encompasses a large variety of health issues affecting various body systems, even emerging after mild cases or in those who never tested positive for COVID.

Delving into the ideas, Dr. Akiko Iwasaki of the Yale School of Medicine and director of the Yale Center of Infection & Immunity, underscores that Long COVID is NOT A singular disease. Her research puts forward 4 hypotheses, suggesting that persistent virus remnants, autoimmunity triggered by B and T cells, reactivation of dormant viruses, and chronic changes post-inflammatory response may all contribute. SARS-CoV-2 without background

In AP Biology, we learned about the immune system and B and T cells. The immune system plays a crucial role in identifying and eliminating pathogens, but in some cases, remnants of the virus may persist. This situation involves the adaptive immune response, where B and T cells are responsible for recognizing and responding to specific pathogens. Autoimmunity is triggered by B and T cells. The immune system is designed to recognize and target foreign invaders. Sometimes, it can mistakenly attack the body’s own health cells, leading to autoimmune disorders. B and T cells are crucial to the adaptive immune response. 

How have your studies or interests in biology influenced your understanding of topics like the immune system and the function of B and T cells? Share your insights! Fimmu-11-579250-g003

Some statistics addressed in the Yale Medicine article, address the question of Long COVID’s trajectory, the Household Pulse Survey in the U.S. shows a potential decline, with reported symptoms dropping from 19% in June 2022 to 11% in January 2023. The true prevalence remains elusive, with estimates suggesting 65 million affected globally, potentially underreported due to the rise in at-home testing since 2022. 

Now, let’s connect this to the study involving 140,000 US veterans. The article  showcases the persistent health risks associated with COVID-19, unveiling that even individuals with milder initial infections face a higher risk of enduring medical issues. Some problems at the top of this list include: fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems.  

For every 1,000 people infected, the cumulative loss of healthy life due to persistent symptoms amounts to a staggering 150 years. While the study acknowledges limitations, like reliance on electronic health records and potential population skew, it underscores the importance of protecting ourselves from COVID-19, given its potential long-term health consequences, even from seemingly mild infections. 

Long COVID demands continued attention, research, and comprehensive strategies for prevention and management. As we reflect on these findings, it is evident that understanding and addressing Long COVID is crucial.

What are your thoughts on this?

Shifting gears, another article from The Centers for Disease Control and Prevention (CDC)  delves into new guidance for healthcare providers treating patients with post-COVID conditions. The term “long COVID” is introduced, emphasizing that these conditions can affect individuals regardless of their initial symptoms. The CDC highlights a broad spectrum of symptoms, including heart palpitations, cognitive impairment, insomnia, and post-exertional malaise (PEM). While primary care providers can manage many cases, the CDC warns against relying solely on diagnostic results. People with post-COVID conditions are advised to continue preventive measures, and COVID-19 vaccines are highly recommended. The guidance is subject to updates as more information becomes available.

The FAIR Health study mentioned in the CDC article, indicates that over 23% of COVID-19 patients experience post-COVID conditions, with pain, breathing difficulties, hyperlipidemia, malaise, and fatigue being common. Half of hospitalized patients developed post-COVID conditions, and there’s a higher risk of mortality following severe treatment, more so for hospitalized individuals. The American Academy of Physical Medicine and Rehabilitation admires the CDC’s guidance for improving healthcare responses for long COVID.

As I did my research surrounding a health challenge that stretches far beyond the initial impact of the pandemic, the significance hits close to home. It’s not just data; it’s the lived experiences of individuals moving through the long-lasting effects of COVID-19. This isn’t just a call to action; it’s a call for our collective attention, research efforts, and a compassionate response. This health issue isn’t confined to statistics; it touches the lives of millions worldwide, making it a cause that resonates deeply within us all.

New Injection Provides Hope for Regaining Smell Following COVID-19 Infection

Did you or someone you know ever contract COVID-19 and lose your sense of taste or smell? This is called Parosmia. There are people on social media who have tried to theorize ways to regain the ability to smell normally. For example, burning an orange peel. However, if your nasal cavity is damaged, regardless of the strong orange aroma, it may be believed that you will not be able to regain your sense of smell.

So, how was your nose damaged in the first place? The olfactory system contains a zone that detects scents towards the top of the nasal cavity. When molecules diffuse up into the nose, they dock in receptor proteins which ultimately initiates a cascade to create a cellular response. Hence, we are able to smell aromatic molecules.

When someone is infected with the SARS-CoV2 virus, the olfactory epithelial cells are damaged. Doctors have analyzed singular cells following a biopsy in order to examine the effect of the virus on healthy cells.  They were able to conclude that the body ignited a innate immunity response, in which swelling occurred where the nerve endings are located. While in some cases the swelling decreased following the innate response, other times, the swelling remained and damaged the tissue.

Novel Coronavirus SARS-CoV-2

This can be explained by what we have learned in AP Biology. During an innate immune response, cells release histamines. These dilate blood vessels, while macrophages secrete cytokines. Cytokines attract phagocytes that allow the infected cells and pathogens to be destroyed. The proteins that attempt to interfere with the viruses cause more histamine to be released and overall more swelling. Therefore, the nasal cavity can remain damaged.

However, new research has found that an injection just might help patients with long COVID symptoms to regain their sense of smell. According to Dr. Adam Zoga, one way that patients have begun to smell again is by injecting stellate ganglion blocks into the neck on either side of the voice box. This reaches the stellate ganglia which contains nerve bundles that control your body’s fight-or-flight responses, known as the sympathetic nervous system. Patients also received a steroid injection to decrease swelling.

The patients that participated in the study did not all benefit from it. However, 22 of the 37 that followed up with administrators following the trial injection noticed improvements in one week. Dr. Leigh Sowerby analyzed this data and theorizes that this may work to treat Parosmia because the sense of smell is affected when the sympathetic nervous system is overactive. He believes that this injection “resets” the nervous system, allowing the nerve bundles to return to normal and patients to regain their sense of smell. However, because only 37 of the original 54 patients followed up after the injections, and there was no control group, researchers cannot further extended this claim.

Universal cure for all variants of Covid-19?


The main issue with COVID-19 since the beginning of the pandemic has always been the various mutations. Someone could get COVID-19 and develop some sort of immunity, but then a new variant would come around and the immunity would be less effective. Scientists at the Pohang University of Science and Technology are working hard to develop a cure for all variants of COVID-19

COVID-19 is a disease caused by the SARS-CoV-2 virus, which is a member of the coronavirus family. In AP Biology, we learned about viruses and how they infect and replicate within host cells. We learned about how COVID-19 is a prime example of how a virus can cause disease in humans. The SARS-CoV-2 virus enters host cells by binding to a receptor called ACE2, which is found on the surface of cells in the respiratory tract and other organs. Once inside the host cell, the virus uses its own enzymes to replicate and produce more copies of itself. This can lead to the death of the host cell and the release of new virus particles, which can then go on to infect other cells. The immune system plays a crucial role in defending the body against viral infections such as COVID-19. When the body is infected with a virus, the immune system recognizes the virus as foreign and mounts an immune response to try to eliminate it. This can include the production of antibodies, the activation of immune cells such as T cells and B cells, and the release of inflammatory molecules.

The reason COVID-19 has been so infectious and is able to mutate so much is because of the ability of the virus to change structure. This structure change increases the strength of its interaction with hACE2 receptors. An hACE2 receptor is the human version of the Angiotensin-converting enzyme 2, the enzyme that serves as the entry point for SARS-CoV-2. As we learned in AP bio, in order for a virus to enter the body, the antigen must bind to a receptor and then travel into the cell. SARS-CoV-2 binds to hACE2. First, the presence of SARS-CoV-2 produces the protein called, IgG. IgG binds to the spike protein on the SARS-CoV-2 cell and that IgG protein binds with the hACE2 receptors in human cells. This binding of IgG is what allows coronavirus to enter human cells.

Understanding this binding process has been key to developing cures for the virus. Most recently, a research team at Pohang University of Science has developed a revolutionary SARS-CoV-2 neutralizer that can adapt to mutations in the virus. This discovery is groundbreaking in the disease prevention world because the type of technology that is used for this specific example can be spread out across the field and used for other viruses. As Professor Seung Soo Oh described: “It is significant that we have developed the world’s first self-evolving neutralizer-developing platform that shows increasingly better performance with the occurrence of viral mutations.” He added, “We plan to develop it into a core technology that can respond to the next-generation pandemic viruses, such as influenza and Hantavirus.”

This neutralizer works by mimicking the interaction between the virus and the receptor, and than once that reaction is mimicked, its protein fragment and nucleic acids can stick to virus, preventing further interaction with the receptor, which eventually prevents the virus from entering the cells.

In all, a neutralizer that adapts with the virus in order to prevent infection and sickness is a groundbreaking discovery that could potentially change the way COVIS-19 (and viruses as a whole) are looked at.


Researchers Find Ways To Combat COVID-19

Ever since COVID-19 was discovered scientists had no idea how to stop this virus. After lots of research we were able to know that there were many different variants of  COVID-19. We understood that some variants were stronger than others according to research. There is an article that talks about how they can be able to stop all kinds of COVID-19 viruses and the different variants. In the article, Professor Seung Soo Oh had an idea on how to stop all kinds of variants in one go. He says that the virus can change its structure whenever. It will then bind to the angiotensin-converting enzyme receptor which is a receptor protein. His team developed a hybrid neutralizer that is able to bind to the virus which then cause the virus to not interact with the protein receptor. This neutralizer was able to be about 5 times more effective then what they first had when COVID-19 was discovered.

According to this article, Omicron which was found in November of 2021 in South Africa, is the most dangerous variant of COVID-19. It is a variant of COVID-19 and is one of the strongest variants. In December of 2019, sub-variants of Omicron began to appear. Some of the sub-variants include BA.5, BQ.1, and BQ.1.1. According to the article, the Omicron sub-variants were very effective and was more transmissible then the Delta variant. The neutralizer should be able to stop Omicron and the sub-variants.

According to another article, variants aren’t weakened by covid vaccines that were had a while ago. In order to help stop COVID-19, the article says that getting boosters will be more effective for any new variants that are discovered. This doesn’t mean they will 100% work. With this knowledge, the new neutralizer that was developed should be able to stop all these viruses from mutating and from entering the cell.

This relates to what we have learned in class this year because we have learned cell structure. When COVID enters the cell, it must bind to a receptor. Once it enters the cell the RNA or DNA would then reproduce. This is similar to what we have learned about how other things enter the cell such as glucose and amino acids. In receptor mediated endocytosis, the ligands must bind to the receptor and then enter the cell. This relates to what we have learned in class because we have learned how molecules are able to enter the cell and how receptors work.


SARS-CoV-2 without background


Why are some people’s sense of smell unable to recover after COVID-19?

A recent finding published on December 21, 2022, in Science Daily, regarding the topic on why COVID-19 affects our ability to smell in the long run, was uncovered by the Duke University Medical Center. The biological mechanisms that are behind the loss of smell many people face who have had COVID-19, may also be the reason for some of the other symptoms of COVID-19 such as fatigue, shortness of breath, and brain fog.

SARS-CoV-2 without background


Although many people recover from the side effects of being infected with SARS-CoV2 within a few weeks, there are many cases where some people’s smell is still altered for several months after. An experiment at Duke University conducted by  Bradley Goldstein, M.D., Ph.D., associate professor in Duke’s Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology, collected 24 biopsies and examined the olfactory epithelial in each one. Using a single- cell analysis to examine the biopsies, it was discovered that multiple T-cells were heavily inflamed in the olfactory epithelium and that there was a loss of multiple olfactory sensory neurons. This is why many people have had a loss of smell even in the absence of SARS-CoV-2. 

In biology class when learning about the immune system and can fight and prevent viruses, such as SARS-CoV-2. We also learned about the importance of T-cells, which are a large group of lymphocytes that play an important role in the immune response. We also specifically touch upon the central roles of T- cells and how “helper T- cells” recognize antigens and stimulate humoral and cell mediated immunity by releasing cytokines. We have discussed how vital T- cells are to our bodies while fighting off viruses because they protect us from infection and Without T cells, every exposure of pathogens that we face daily could be life-threatening to us. This relates to why our smell could be altered for so long after being infected with SARS-CoV-2 virus because our T-cells aren’t able to properly function since they are inflamed in the olfactory epithelium.

Healthy Human T Cell
According to Goldstien, other COVID-19 symptoms might be caused by a similar inflammation that affected people’s loss of smell. 


A New Hope? Promising new research finds a way to treat COVID-19

Despite the recent decline in COVID-19 cases, researchers and public health officials struggle to treat and prevent new cases of the disease.  A 2022 article in the Washington post outlined the recent efforts by researchers to treat and prevent COVID-19, particularly examining monoclonal antibody treatment, a treatment that utilizes human-made antibodies to aid in the Body’s natural response.

However, according to researchers, new mutations are quickly arising which undermine the effectiveness of these treatments, making it difficult for the medical world to keep up with the virus, so biologists are turning to more novel methods.  One Quebec-based company, Sherbrooke, thinks they’ve found the solution, “We saw a sharp decline in viral loads,” says the company’s chief medical officer Bruno Maranda.

Traditional monoclonal antibody treatment has had trouble inhibiting the binding between the spike protein of the virus SARS-CoV-2 and human cells because the binding location of the spike protein is mutating quicker than researchers can adjust antibody treatment.  According to Andrés Finzi, associate professor at the University of Montréal, “there is a huge immune pressure on the virus,” indicating that it will likely continue to mutate in this way.  


Novel Coronavirus SARS-CoV-2 Spike Protein (49583626473)



However, scientists have noticed that certain areas of spike protein have remained rigid as the virus mutates; one such area is the stem helix.  Because of its lack of mutation, scientists believe that this area is essential to SARS-CoV-2 and if disrupted can limit its ability to mutate and cause harm to our bodies.  

Although the new drug from Sherbrooke uses 2 antibodies that attack the spike protein in a more conventional way, the new third antibody attacking the more rigid areas of the protein has proven effective in all trials that have been undertaken.

Another recent paper has also attempted to amend antibody treatment to target more stable sections of the spike protein: the fusion peptide.  According to the chief of the Antibody Biology unit of the National Institute of Allergy and Infectious Diseases, this structure “acts like a grappling hook and inserts into the human cell membrane, pulling the membrane closer to the virus membrane.”  Researchers hope to use these rigid structures to help develop more reliable treatments and preventions for COVID-19.

This system of antibodies protecting our bodies from illness is similar to what we are currently learning in Biology class.  In class, we learned that in the body’s humoral response to pathogens, B-plasma cells secrete antibodies that bind to pathogens, thereby neutralizing them, allowing them to be quickly engulfed by macrophages and destroyed.  Monoclonal antibody treatment leverages this function of antibodies, creating artificial antibodies to facilitate this interaction more strongly.

While these new developments in COVID-19 treatment are exciting, Finzi warned that “we shouldn’t underestimate the capacity of a coronavirus to mutate.”  Other scientists, including Harvard professor of pediatrics Bing Chen, believe that antibody treatment research should not take the place of other disease-fighting tactics; according to Chen “we need much more effective vaccines, for sure.”  But one thing remains true, and that is that SARS-CoV-2 continues to mutate, and will continue to be a serious problem if we fail or adequately treat and prevent it, and while the number of cases is decreasing, it still remains strikingly high for us to write off the disease as harmless.

The APOE Gene: little known secret to COVID-19 survival

I’m sure you all have heard it before – surviving COVID-19 is based on your age, sex, and pre-existing health problems – but what if I told you that another factor you should consider is your APOE gene.

A 22K fragment of APOE4 (APOE4) (IB68)

Apolipoprotein E, also known as APOE, is a gene that suppresses the spread of melanoma and is involved in anti-tumor immune responses. 60% of the population has APOE in its most common form, the APOE3 allele, but the other 40% of the population has APOE2 or APOE4. Unlike APOE3, APOE2 and APOE4 negatively impact the immune response against melanoma, and individuals with APOE4 are at greater risk of developing atherosclerosis and Alzheimer’s. These alleles can create such different responses by coding for proteins that differ by just one or two amino acids, which as we learned in AP Biology, can make a big difference in how a protein is structured and functions.

After studying APOE’s impact on the immune response against melanoma, Sohail Tavazoie’s lab at The Rockefeller University grew curious to research if APOE variants impact COVID-19 outcomes. By testing on 300 mice with a mouse-adapted version of SARS-CoV-2, they found that mice with the APOE3 allele were more likely to survive than those with the APOE2 or APOE4 allele. Mice with APOE2 or APOE4 had a less effective immune response, causing more virus to replicate in their lungs, more inflammation, and more tissue damage. The researchers further demonstrated APOE’s impact by analyzing 13,000 patients in the UK Biobank and discovered that patients with two copies of APOE2 or APOE4 were more likely to have died of COVID-19 than those with two copies of APOE3.

With more studies done in the future, clinicians should prioritize that individuals with these alleles receive not only COVID-19 vaccinations and boosters, but also antiviral therapies if they get infected. If testing for which APOE allele you have sounds important to you, you can easily get genetic testing with a saliva sample or a blood test in a commercial lab.

Pockets Galore! Pockets of COVID-19 Antigens are Stuck in the Body and are Causing Long COVID

Do you know someone who has long COVID? It turns out that they may have pockets of SARS-CoV-2 hiding in their body! 

Researchers at University of Colorado’s Anschutz Medical Campus have found in a recent study that patients who suffer from long-term COVID symptoms (called PASC) have 100x more SARS-CoV-2 specific T cells than those who have recovered fully from the virus.  This discovery suggests that the virus itself lingers in the body, not that symptoms continue even after the virus has left.  

This evidence will allow doctors and researchers to shift the mentality surrounding treatment of PASC, as prevPaxlovidiously the only option was to treat exclusively the symptoms.  The shift has led them to antiviral medications (such as Paxlovid) and vaccines, both of which use adaptive immunity to their advantage.  The study found that the body’s natural adaptive immune response focused on systemic inflammation, pulmonary symptoms and reduced lung function because of the high levels of T-cells in the body.  The T-cells are very important in the primary stages of the infection because they help identify and destroy infected cells, however after controlling the infection, it creates longer symptoms, along with continued shortness of breath and lung damage.

About 20-30% of patients infected with COVID developed PASC.  Over the course of over 500 million COVID infections, healthcare systems are pressed to support 150 million patients with lasting symptoms, so a solution is a priority for physicians.  The upcoming solutions’ primary goal is to clear the virus from the body entirely so that T-cell levels decrease back to a normal level.  

In addition to identifying the higher levels of T-cells, the researchers found that the higher the level of SARS-CoV-2 specific T-cells there were in the body, the higher the inflammation levels there were in the body, showing that the T-cells play a role in creating lasting inflammation associated with PASC.  

The next step for the researchers is to continue to do research on the differences in lung cells between people with PASC and people who have not had COVID.  They claim that this research is vital because the “kitchen sink symptomatic treatments have not solved the problem” (Palmer).  

How Having Allergic Asthma Can Protect an Individual From COVID-19

Scientists have found that individuals with asthma are, in fact, less susceptible to COVID-19. One could question how a pre-existing health condition could actually aid in fighting off a virus? It is accurate to assume that an individual with allergy asthma would be at more risk than a perfectly healthy individual. 

Allergic asthma occurs when your airways tighten when an allergen is inhaled. The same immune system proteins that are involved with excess mucus production and the tightening of airways are used to form barriers around exposed airway cells (immune system mechanism for people with allergy asthma). This information is the basis behind the studies that explains the reasoning behind why people with asthma are less susceptible to COVID-19. 

Asthma attack-airway (bronchiole) constriction-animated

When a patient has asthma, usually the development viruses such as the Flu and Strep Throat are more dangerous for them, and still these patients with asthma are at more risk when they are infected with COVID-19. The difference lies between asthma and allergic asthma. Researchers were able to identify that people with allergic asthma were not showing major symptoms to COVID-19, which was not what one would expect. Why is that? 

Protein Protection

The differentiating factor that sets allergic asthma from regular asthma is a specific protein called interleukin-13 (IL-13). The normal function of IL-13 is to help fight off parasites. Normally, specific T-Cells release this protein. In response to the release of IL-13, the body produces a sticky mucus substance and compacts airways. This traps the parasite until the immune system finishes the job by killing the parasite. 

However, when an individual has allergic asthma, the body mistakes harmless matter such as pollen for a parasite, and uses IL-13 when it is not needed. The researchers now need to determine how, exactly, IL-13 is protecting patients from COVID-19.

Protein IL13 PDB 1ga3

No IL-13 Present Study

Researchers conducted a study in which they would compare how cells that haven’t  been treated with the IL-13 protein react when healthy and when infected with coronavirus. 

It was found that the healthy cells  grew in lawns that nearly resembled grassland. This area is made Bronchiolar epithelium 3 - SEMup of a hair-like substance called cilium. The cilia move in waves which aids in mucus movement and the excretion of anything stuck in the mucus.

On the other hand, the cells that were infected with the coronavirus had a much different reaction. The cilia lawn was no longer clear. The cilia was covered with mucus and many bald spots that seemed as if infected cells died. The infected cells were compressed out of the lawn of the cilia, and in that process they become inflated. This inflation occurs due to vacuoles in the infected cells getting blocked up with viruses. Once the infected cell gets filled up with viruses past its capacity, it explodes and releases all of the viruses that had been in the cell. 

Unfortunately, it is not as simple as this singular reaction, not all cells that were in the infected lawn were affected the same way. Researchers noticed that the cells that were attached to the cilia were infected with SARS-CoV-2, but the goblet cells, which are mucus producing cells, were barely affected. The researchers found that a protein called ACE2 is present on the surface of ciliated cells more commonly that goblet cells. With this finding, the researchers can assume that ACE2 is the protein receptor that allows SARS-CoV-2 to enter the cell. 

IL-13 Present 

Now the researchers conducted a second study in which they will coat the cell in  the IL-13 protein and compare how the cell reacts when infected with coronavirus. The celia lawn surface with the IL-13 present has a lot less inflated dying cells on its surface and the movement of the cilia was much less rapid. This decrease in movement indicates that the mucus is present in the cilia for much longer than when IL-13 is not present. It was made clear that the IL-13 protein acted as a protectant towards the infection. 

They later found out that untreated cells, once infected with SARS-CoV-2, release bursts of mucus. Whereas the IL-13 cells keep the mucus stored. Furthermore, it is known that IL-13 proteins produce a sticky mucus that has the ability to trap viruses before they get the chance to infect the cell. So, this excess mucus that is present in the treated cells can make sure the virus is out of the lungs before the damage has been done. Researchers also found A thick layer of keratan sulfate that was developed on the cell’s surface that was treated with IL-13, which protects them against SARS-CoV-2 from coming into contact with the cell.

In addition to protecting the cells, the IL-3 protein causes cells to produce less ACE2. And with less ACE2, not as many SARS-CoV-2 can come into the cell, since ACE2 is the SARS-CoV-2 receptor. 

There is so much unknown about IL-3, and researchers are still trying to determine specific properties of this protein. Scientists are eager to find out more about IL-13 as they think this protein can lead to new treatment findings.

This new information about how people with allergy asthma react to COVID-19 can be looked at as a positive because it’s one thing about having allergy asthma that actually benefited the individual!

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.

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