AP Biology class blog for discussing current research in Biology

Tag: #COVID (Page 1 of 3)

How is Omicron still a problem?

Covid-19 under a microscope


Allow me to take you back to the early days of the Covid-19 pandemic. Alpha, and Delta were the primary variants.

And then Omicron stumbled in, and unlike the others, never left.

Unlike the others, who had viciously ensnared others to their deaths, Omicron was more akin to a hard cold, or the flu. Whilst it shared flagship symptoms like parosmia (loss of smell/taste) and other respiratory symptoms, they resulted in less hospitalizations. In addition, we were going stir crazy and had started to unlock the lockdown. 

And Omicron, unlike the others, was a rapidly evolving virus, one variant one second and another the next. The rapid mutations in the epitopes (the spike protein that the immune system uses to distinguish it from other viruses) made vaccines, which are designed to emulate the epitopes so the body can recognize it (hence the potential fever- your body is learning the epitope’s shape so it can catch the real thing faster), next to impossible to settle on. Trying to get a working vaccine for it was like trying to hold a tiny fish in the rain- it just kept slipping away. 

And now again, descendants of Omicron are dominant again.

HV.1 is a descendant of Eris (EG.5) but isn’t really that different from Eris. Vaccines that are designed to target XBB (another offshoot) still work on both of them. HV.1 is only dominant for minor mutations, as vaccines still work.

The real worry is BA.2.86, which has been determined to evade the immune system. It, in comparison to say, EG.5.1 or XBB.1.5, resulted in a lower concentration of neutralizing antibodies, meaning one infected would be infected for longer.

Its descendant, JN.1 might be even better at it. It can be transmitted at low levels due to its highly mutated spike protein, and still evades the humoral response more effectively than its predecessor.

I, for one, think that Omicron isn’t going away. It mutates too quickly to truly be caught. But I think a monovalent vaccine is possible per each set of dominant strains. And to that, I mean it will likely become another vaccine to get annually in the fall.

How COVID-19 Robs Us of Our Sense of Smell

Led by researchers from NYU Grossman School of Medicine and Columbia University, the study with the pandemic virus, SARS-CoV-2, found that the infection caused by SARS indirectly dials down the action of olfactory receptors (OR), proteins on the surfaces of nerve cells in the nose that detect the molecules associated with odors. This new study not only sheds light on the reason for loss of smell, but also sheds light on the effects of Covid-19 on other types of brain cells, and on other lingering neurological effects of COVID-19 like “brain fog”, headaches, and depression.SARS-CoV-2 without background

The study involved analysis of olfactory tissue from human autopsies and experiments on golden hamsters, a species highly reliant on their sense of smell. The researchers observed that the virus triggers an increase of immune cells, which release cytokines altering the genetic activity of olfactory nerve cells. They suggest that that if olfactory gene expression ceases every time the immune system responds in certain ways that disrupts interchromosomal contacts, then the lost of sense of smell may act as an early signal that the COVID-19 virus is damaging brain tissue before other symptoms presents, and suggest new ways to treat it. However, these cells are not infected by the virus directly. These findings could have broader implications than it first seems. The persistence of immune reactions in the nasal cavity may influence cognitive functions and emotions because these olfactory neurons are connected to sensitive brain regions. The team’s next steps include creating treatments to protect the “nuclear architecture” of these cells and prevent long-lasting implications. This study aligns with many core topics in AP Biology, such as proteins, the immune system’s role in disease response, and the immune system’s interaction with neurons. It offers insight into the understanding of how cells communicate and respond to pathogens. It also delves into gene expression which illustrates how factors like viral infections can lead to changes in a cell’s genetic activity. This study represented a significant step in understanding the broader effects of COVID-19 and opens options for new treatment strategies. The Study also provides valuable insights into the functions of the immune system and neurons during a COVID-19 infection. The increase of immune cells and the release of cytokines in response to SARS-CoV-2 can alter the activity of olfactory nerve cells. This not only affects our sense of smell but also has more affects on brain function. The immune reaction in the nasal cavity could impact cognitive functions and emotional states because of the connection of olfactory neurons to sensitive brain regions. This understanding of how COVID-19 effects immune responses and neuronal changes is crucial as it helps scientists find new ways for treating the long term effects of COVID-19. Now this brings the question of if this study gives insight into how to treat patients with long term issues from Covid and how they will be treated.


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 ghost of COVID: COVID-19’s affect on people years after they contracted it

In early 2020, the entire world suddenly stopped due to COVID-19. Even as time passed and the deadly rampage of the disease slowly died down, its effects could still be felt. In 2021, Jayson Tatum, a star basketball player for the Boston Celtics, admitted that COVID caused him to use an inhaler before games so he could open up his lungs, even months after he actually had it. Being a big Jayson Tatum fan, I wondered what caused that, but there wasn’t much research on the long-term effects of COVID at the time. Now, a recent ScienceNews article shows that even 2-3 years later, COVID-19 can affect those who contracted it during the height of the pandemic. This phenomenon, called long COVID, could lead to fatigue, blood clots, and even heart disease.Jayson Tatum

The study shown in the article used the health records of 140,000 veterans who were infected with COVID-19 during the height of the pandemic and compared it to about 6 million people who were not reportedly affected by COVID-19. The researchers in the study found that people with past battles with COVID were more at risk of contracting other diseases or having health complications. Though research on why this happens isn’t conclusive yet, recent researchers have discovered that people who experience long COVID tend to have traces of the Sars-CoV-2 in their poop even months after having the virus, which suggests that some of the virus still remains in their guts. This triggers the immune system to act, specifically the innate cellular defenses, which (in this case) is unnecessarily activated due to the detection of the strains of COVID-19 in the gut. This may explain the symptoms felt due to long COVID because as the immune system works, histamine is released, which causes expansion of blood vessels and swelling of fluid/inflammation, explaining many of the symptoms of long COVID, such as trouble breathing, are related to inflammation in the body. On top of this, the strains of Sars-Cov-2 lead to long COVID because the interferons, which are another part of the innate cellular defense, reduce the absorption of an amino acid called tryptophan. Without tryptophan, the body can’t make neurotransmitters like serotonin; the lack of serotonin and other neurotransmitters is what scientists currently believe causes long COVID symptoms.

Novel Coronavirus SARS-CoV-2

Long COVID is a severe problem that has affected billions worldwide. As of now, there is no way to cure it, so it’s essential to try your best to avoid getting COVID-19. People who have underlying health conditions, have been seriously harmed by COVID-19, or don’t have any vaccinations against COVID-19 are the most likely to contract long-term COVID. Another way to avoid long COVID is to stay up-to-date on COVID vaccinations. Many people don’t even know what long-term COVID is. Did you know about long COVID? If not, write about what you learned in the comments.

Astronomy tools used to detect COVID-19 !?

Would you ever expect a laser designed for outer space to analyze your health? If you answered yes, get ready to learn why! If not, pay close attention because what you’re about to learn is incredible! This laser is called an “optical frequency comb.” These lasers emit light waves, initially for researching outer space and accurate timekeeping. Because of the COVID outbreak, researchers have found a more promising use of this frequency mechanism. 

The Optical Frequency Comb received its name from the way it functions. These FrequencyComb-measurement
rapid bursts happen in a specific order across different colors of light, ranging from infrared to ultraviolet. When these frequencies are on a graph, it creates peaks that are said to look like the “teeth” of a comb. Now, researchers are exploring the possibility of utilizing this tool to identify specific molecules associated with COVID, and the comb can potentially identify these molecules by recognizing the absorbed colors. It would make most sense that the laser seeks out particular proteins on the virus. As evaluated in our AP Biology class, we know proteins are extremely important in terms of viruses. Proteins in viruses play a vital role by building the virus’s structure and helping it interact with the host’s cells. They enable the virus to enter cells, replicate, and avoid the host’s immune response. Viral proteins also manipulate the host’s cellular functions/processes, ensuring the virus’s survival and spread in the host organism.

Because specific molecules absorb distinct colors of light. The comb can recognize certain molecules in an air sample by identifying the absorbed colors. Because of the severe global pandemic, scientists have found a way to utilize this tool to diagnose patients with COVID in a less “nosy” technique (literally)! Rather than sticking a swab up your nose, all you have to do is exhale. Easy!

Researcher Qizhong Liang mentions that it is best to take the typical PCR test for a more precise result. Because this new COVID testing method is new and still under evaluation, it is best to double-check the test results. Nevertheless, this researchSARS-CoV-2 without background offers a promising future for detecting diseases, such as COVID-19, in a quicker, less effortless way! I find it incredibly fascinating how a group of scientists could take an astronomy tool and use it medically to help diagnose patients. Would you trust this method to diagnose you?

Covid Brain Fog

COVID BRAIN? That’s a thing? Yes. Within the metaphorical shadow of an ice sheet, “brain fog” has evolved into a comprehensive label, encompassing the intricate cognitive, psychological, and emotional struggles intertwined with long COVID.3D medical animation coronavirus structure

The referenced article shares the story of Kenton Kaplan, a senior in the Edmund A. Walsh School of Foreign Service at Georgetown University, showing signs of COVID-related brain symptoms. Ken’s year-long battle with severe memory loss, extreme fatigue, and immunosuppression highlights the diverse experiences enclosed by this term. Despite its recognition as a federally acknowledged disability, individuals reporting “brain fog” face disbelief, hindering their access to necessary accommodations. 

Emily Mendenhall, a medical anthropologist, explored the varied manifestations of long COVID symptoms beyond the popular definition of mild forgetfulness. Interviews with 22 sufferers revealed debilitating episodes, with individuals describing struggles with daily tasks during “brain fog” episodes. These individuals spoke of debilitating days where routine tasks became overwhelming: chronic nerve pain, severe headaches, episodes of dizziness, nausea, and fainting. The disparity between how healthcare professionals perceive “brain fog” and the actual experiences of those affected emphasizes the necessity for clear categorizations that can more effectively address the range and intensity of symptoms. 

Faced with difficulties in securing accommodations, Ken’s ongoing struggles with sporadic memory loss emphasize the importance of acknowledging the complexity of a cloudy consciousness. Clearer names and understanding the various aspects of symptoms could help make medical leave and accommodations more accepted. This support would be beneficial for those dealing with the continued effects of long COVID in their everyday lives.

When the immune system encounters specific pathogens, such as the COVID-19 virus, it relies on the binding action of B cell antigen receptors or antibodies to epitopes on the pathogen for recognition. This recognition serves as a trigger, setting off a cascade of events that activate B cells and stimulate the production of antibodies. These antibodies play a crucial role in safeguarding the body against the virus. This shows how important a strong immune system is in dealing with complicated conditions like long COVID, especially when it comes to cognitive challenges like “brain fog.”

A couple of weeks ago, my mom tested positive for COVID, marking the first time she had ever faced the virus since the beginning of the pandemic. Despite being up to date on all her vaccines, including mRNA shots, which introduce genetic material into cells to prompt the production of viral proteins and trigger the immune system, she still experienced a severe case. Unfortunately, COVID hit her hard, unleashing a wave of symptoms ranging from chills and fever to body aches, a runny nose, and a persistent cough. As if that wasn’t challenging enough, she started experiencing heightened anxiety as she struggled with memory lapses, struggling to recall the day she tested positive, losing track of time, and questioning how long she had been in quarantine. It was a tough period for her, navigating not only the physical toll of the illness but also the mental strain of uncertainty. So, how can we collectively raise awareness about the diverse experiences encapsulated by the term “brain fog” and advocate for better understanding and support?

Cracking Down on Long COVID

In a study funded by the National Institutes of Health (NIH), nearly 10,000 Americans, including COVID-19 survivors, became the researcher’s focus, attempting to figure out the complexities of “Long COVID-19”. This condition leaves individuals fighting with lingering symptoms even after the virus has been vanquished, which presents various challenges, ranging from persistent fatigue to cognitive fog and prolonged dizziness. Nature Reviews Microbiology further examines the ongoing challenges in “long COVID” symptoms, emphasizing the necessity for consistent research efforts. This exploration acknowledges the need for continued studies to understand and address the complexities of the condition. It urges a proactive approach, encouraging the scientific community to stay observant and work together to enhance our understanding of long COVID. By prioritizing continuous research,  strategies for diagnosis and management can adapt to the evolving nature of this condition. As part of the NIH’s 1.15 billion dollar “recover initiative,” the study revealed vital insights, showing that the severity of “Long COVID” is higher in individuals infected before the emergence of the 2021 Omicron variant. SARS-CoV-2 illustration (17)

The research identified 12 key symptoms, establishing a comprehensive scoring system that not only aids in diagnosis but also classifies patients into distinct subgroups, hence refining our understanding of the condition. Health Affairs jumps into the global impact of long COVID, stressing the significance of collaborative international efforts in research and treatment. Furthermore, the study described the influence of vaccination status and the timing of infection, compared with unvaccinated individuals and those infected pre-2021, demonstrating a higher susceptibility to severe forms of long COVID-19.
In the context of our AP Biology class, this study aligns with our exploration of infectious diseases and the biological responses to pathogens. The study advances our scientific understanding of the complexities between our immune system and the evolving nature of viral threats. B and T memory cells are formed during vaccination when specific immune cells are activated in response to antigens present in the vaccine. These memory cells, produced by both B and T cells, retain a “memory” of the encountered antigens. Upon exposure to the same pathogen, these memory cells enable a quicker and more effective immune response, contributing to long-term protection through vaccines. Throughout the year, we have learned the biology behind vaccines, and this study reinforces our learning by demonstrating that vaccines play a crucial role in preventing individuals from experiencing ‘Long Covid’ symptoms. The reason behind this is the vaccine’s ability to prime the immune system, effectively fighting the virus and reducing the risk of prolonged symptoms. Decoding the mysteries of “long COVID” through collaborative initiatives like NIH’s “RECOVER” not only fuels my scientific curiosity but also emphasizes the real-world impact of scientific research on global health.

Symptoms of coronavirus disease 2019 4.0

(Post includes edits made through Grammarly)

Unlocking Omicron’s Secrets: Breakthrough in COVID-19 Research Reveals NSP6 Protein’s Key Role

While in a global battle against an invisible enemy, a team of spirited scientists have found a remarkable discovery that could change the course of the pandemic and challenge everything we thought we knew about the elusive Omicron variant! The study, led by Boston University and involving international researchers, investigates the Omicron variant of the SARS-CoV-2 virus. SARS-CoV-2, short for Severe Acute Respiratory Syndrome Coronavirus 2, is an RNA virus belonging to the Coronaviridae family, known for its distinctive spike proteins that facilitate entry into host cells. This virus, causing the COVID-19 disease, primarily targets the respiratory system and spreads via aerosolized droplets, leading to symptoms ranging from mild flu-like manifestations to severe respiratory distress.

Respiratory system complete en

It identifies mutations that enable Omicron to evade prior immunity and introduces a new protein, NSP6, as a key factor in its reduced disease-causing potential. This study refutes earlier misconceptions about its findings and offers new insights for vaccine and therapeutic development. Hopefully, we can create a vaccine that will finally rid us of COVID for good.

SARS-CoV-2 (CDC-23312)

Mohsan Saeed, the study’s senior author, highlights the minimal role of the spike protein in Omicron’s lower pathogenicity. We learned in AP Biology this year that a spike protein is a surface protein found on certain viruses, including the coronavirus, that facilitates their entry into host cells. These cells recognize foreign proteins, including viral spike proteins, and help orchestrate the body’s defense by binding to these proteins and signaling other immune cells to respond. This knowledge enhances our understanding of viral mechanisms and immune responses, highlighting the significance of proteins other than the spike protein in viral pathogenicity. It binds to receptors on the host cell’s surface, triggering a process that allows the viral genome to enter and infect the cell. Instead, mutations in the NSP6 protein are crucial in Omicron’s pathogenicity. This discovery opens new possibilities for future vaccines and treatments. The research, which will also be published in print, is a collaborative effort between various universities and research centers, emphasizing the need to explore non-spike regions of the viral genome.

The study began when researchers noticed the fast spread but reduced severity of Omicron. The initial focus was on the spike protein, as it was the primary differentiator between Omicron and the original virus. However, experiments showed that while the spike protein contributed to Omicron’s characteristics, it was not the sole factor. The National Institute of Health says that another reason for quick spread is several mutations of Omicron, which promote its ability to diffuse worldwide and its capability in immune evasion. It always amazes me how something so microscopic can have so many different factors at play!

Researchers adhered to strict protocols to avoid enhancing the virus’s strength, a concern known as “gain of function.” Comparing the chimeric virus (combining Omicron’s spike with the original virus) with the original strain revealed that the chimeric virus was weaker but not as weak as Omicron, indicating other factors at play.

Further research led to the discovery of the role of the NSP6 protein. This protein, previously understudied, was found to significantly reduce viral replication and infection severity. This finding shifted the focus from the spike protein to NSP6, revealing its importance in the virus’s ability to cause disease.

Understanding the role of NSP6 opens new avenues for combating COVID-19. It highlights the importance of examining genetic differences between variants to develop new treatments and vaccines. The research team plans to further investigate NSP6, potentially leading to more effective pandemic control strategies. Now that you’ve got the scoop on what’s happening with COVID-19 if you were hesitant about the vaccine, did this blog make you think differently? If it did, how so?

Unmasking Covid: A Rollercoaster of Well Being

Covid for many of us, is a villain. It tore society away from each other. Making us hide inside and distancing ourselves because we were scared. Covid also had many effects on us because it attacked people with health issues such as diabetes, fatigue, or blood clots.

SARS-COV-2 Impfstoff (50745105642)

A study based on the health records of about 140,000 U.S. veterans. shows the risk people with health issues such as diabetes, fatigue, or blood clots can have even with COVID being around for 2 years.  The study compared veterans who were infected with SARS-CoV-2 early in the pandemic with those who did not test positive. Even two years after their infections, individuals who had COVID-19 were at a higher risk for various health problems, including heart disease and gastrointestinal issues. Hospitalized patients during their initial COVID-19 cases were more likely to experience these issues, but those with milder infections were also at higher risk for certain medical problems. The study highlights the long-term risks and burden of disease associated with COVID-19, even for individuals with mild cases. However, the study has limitations, including its reliance on electronic health records. The use of electronic health records is a limitation in the study because electronic health records or EHRs, contain data that is available within the healthcare system. They may not capture information about symptoms or conditions that patients experience outside of the healthcare setting. EHRs may focus on medical events and diagnoses, potentially missing information about the broader impact of long COVID on patients’ daily lives and well-being. The study’s reliance on EHRs from a veteran population may introduce biases. For example, the data may be skewed towards men, as about 90 percent of the veteran records included in the study were from men. This may not fully represent the experiences of women, who are also affected by long COVID. People with health issues are much more vulnerable because certain health conditions do increase the risk of complications and severe illness if infected with the virus.Diabetes, can weaken the immune system, making it more challenging for the body to mount an effective defense against the virus. Diabetes, especially uncontrolled diabetes, can impair the function of various immune cells, including neutrophils and macrophages. These cells play a crucial role in recognizing and eliminating pathogens, such as bacteria and viruses. Diabetes also affects T cells,  which are a type of white blood cell that plays a central role in the immune response. In diabetes, there may be a reduced activity of T cells, which can compromise the body’s ability to identify and destroy infected cells.

Primary immune response 1

In AP Bio we saw the process in Pathogen Specific Recognition which is a part in the Immune System. First a pathogen would appear and the macrophage would ingest the pathogen, allowing the lysosome to come and kill the pathogen. Then the macrophage would present a antigen fragment with MHC proteins to helper T cells. This then causes the helper T cell to bind with the antigen fragment allowing it to produce interleukin. The interleukin would then either trigger cell-mediated response with T cells or humoral response which include B cells. The difference between the two types of response are with cell-mediated response T-cells make killer T-cells which kill infected or cancerous cells and  humoral response secrete antibodies which bind to and neutralize pathogens. How has the journey with COVID-19 unfolded within your family over the past two years? What challenges have you faced, and what lessons or changes have emerged from this unique experience?



File:SARS-CoV-2 (CDC-23311).png

In 2019, a new strain of SARS-coV-2 took the world by storm, sending millions of people into quarantine. While the past few years have seen the virus’s spread ultimately be controlled, the people continue to be infected today—I know this personally as last month I got COVID. Luckily my COVID was very mild, but for many people, the same can’t be said. Unfortunately, in addition to the terrible symptoms that one might have during their Illness, recent research has found that severe COVID-19 could cause long-term immune system changes.

This recent research found that severe COVID-19 causes long-term effects on specific cells responsible for our immune system. They found that a chemical, IL-6, changes how genes are expressed and impacts how cells work as a result. The cells called hematopoietic stem and progenitor cells (HSPC), undergo lasting changes in their characteristics and how their genes are regulated (epigenetic programs). These changes persist for months to a year and result in altered activities of transcription factors (proteins that control gene expression), modifications in how inflammation is regulated, and increased production of certain immune cells (myelopoiesis). The altered HSPC makes so many changes because HSPC, or stem cells, are the only type of cell that can differentiate or repair specialized types of cells.


This research is related to AP BIO because the article talks about COVID-19 influences epigenetics (how genes are turned on or off because of environmental factors) and in AP BIO we talked about how proteins are able to be made because of the information on the DNA. In protein synthesis in a cell, the first step is transcription where information on the DNA is transcribed onto mRNA. The mRNA then is sent to the Rough Endoplasmic Reticulum where it is received on the cis face. Then the ribosomes of the rough ER, the protein is synthesized. The type of protein that is synthesized here is determined by the information of the mRNA. Then the protein is sent to the Golgi where, based on the information from the mRNA, molecules are added to the protein to determine its final location.


This AP BIO information relates to the research because the research is about how a chemical changes how DNA is expressed, this information from AP BIO explains why DNA is important.

Wow! That was so interesting! Reading about epigenetics has made me wonder: what other conditions can influence how DNA is expressed?


Blood Clotting Proteins Predicting Signs of Long COVID

Many individuals experience sickness after they have already been cured of COVID. This is called long COVID, symptoms include cognitive problems also referred to as brain fog. Having these issues leads to a decreases in memory and concentration making it harder to function in everyday life. Now imagine still feeling sick even though you really are not sick with the virus, not a good feeling. These symptoms are now believed to come from blood clots triggered by the virus. The blood clots leave behind proteins in the blood so researchers are able to find and diagnosis patients who think they have symptoms after they have had COVID.

A study by Nature Medicine found that blood tests could point signs of long COVID. 15 % of people who contracted the virus develop long COVID symptoms. Symptoms of long COVID could last for months and possibly even years. This condition is difficult to treat and diagnose due to the wide range of symptoms it causes. These symptoms include brain fog, chest pain, dizziness, and joint pains. We all know what it is like having these pains so are able to understand how difficult it is to go through your everyday life with long COVID. Scientists are still trying to figure out if the virus stick around in the body or if it leads to other reaction, like having an autoimmune response.

The lead researcher Maxime Taquet, along with others from the University of Oxford, conducted an experiment in the United Kingdom. They tracked over 1,800 hospitalized COVID patients between the years 2020 and 2021. After six and twelve months the scientists conducted cognitive assessments and took blood samples. These are tests you still want to do good on. The blood tests revealed that the patients dealing with brain fog had specific proteins in their blood, proteins that we all have in common. The first protein is called D-dimer, which is present when blood clots breakdown. The patients with this protein did not do poorly on their cognitive tests so their memory and concentration is in tact. On the other hand these patients experience shortness of breath. This could be a sign the blood clots are taking place in the lungs causing the brain to not get enough oxygen levels. The second protein found in some patients is called fibrinogen. This protein is synthesized in the liver and stops bleeding. The patients who had this protein complained about memory impairment and sadly they also did not do well on the cognitive test.


D-dimer Formation

Another test was conducted, analyzing around 50,000 people in the United States looking for D-dimer and fibrinogen. Higher D-dimer levels were only found in people who previously had COVID, while high levels of fibrinogen correlated with brain fog whether or not a person previously had COVID. This indicates that fibrinogen is involved in other cognitive conditions.

Human fibrinogen structural scheme

Human Fibrinogen

Although scientists know there is a relationship between blood clots and long COVID, there still needs to be more research done. Even the blood in your body could help research! Research is currently being done on how the SARS-CoV 2 spike protein affects the fibrinogen protein, and research treatments for clot dissolving medications. This is challenging though since the symptoms and diagnosis of long COVID is still difficult to spot. Scientist will continue studying blood samples and patients suffering from long COVID to better understand the sickness.

The research being conducted can be related to the AP Bio class about the role of the immune system is response to the virus. The immune system is very responsive when COVID is introduced to the body and when it is gone in long COVID patients. A study was conducted and it was found that participants with long COVID had higher levels of non-conventional monocytes and activated B lymphocytes. They had lower levels of type 1 conventional dendritic cells and central memory T cells. The B cells are responsible for attacking pathogens that are free floating, and T cells are responsible for attacking pathogens in infected cells. The dendritic cells break down pathogens and present the antigen on its surface for it to then be found by the T helper cells to pass on the information. These participants’ antibody responses is also stronger against the SARS-CoV-2 spike protein. Those who do not have long COVID do not have responses as strong. Long COVID participants also are more susceptible to other diseases. Other disease, once in the body can trigger the body to have more and worse symptoms. All these specific parts of are immune system all work together in all of our bodies to form the way we each combat infections. We should all be grateful for processes our bodies go through to help us get through our everyday lives.

Subvariant EG.5 is on the rise and dominating the U.S!

Since COVID’s peak in 2020, what has been going on? Is it still on the rise? According to a recent article from LiveScience, the omicron subvariant of Eris, or EG.5.1, has been the leading cause of new COVID-19 cases in the U.S. In this research article, the data from a model of the Centers for Disease Control and Prevention (CDC) , from July 23 to August 5 of 2023, EG.5 was 17.3%  of the new cases of COVID-19, which had previously only been 11.9% two weeks prior. Personally, seeing that jump in percentage within two weeks worries me about what harm this subvariant could cause. Additionally, more recently, EG.5 had a higher percentage of infection than any other omicron subvariant in the XBB lineage!

Map of countries with confirmed SARS-CoV-2 Omicron variant cases

But the real question is, what is EG.5? How is it a subvariant, and why is it dominating the U.S.? Well, EG.5 was derived from a branch of omicron, an XBB variant. Yet, how it differs from omicron is what makes it EG.5 and what is allowing it to become so prevalent. EG.5 has a mutation in its spike protein that helps evade the body’s immune system. This spike protein called S:F456L may not only be able to escape our immune system, but the mutation in its subvariant Eris, EG.5.1, has an additional spike change, S:Q52H, that can be beneficial for the virus itself. To further the idea that the virus is harmful, the World Health Organization currently lists the variant as “under monitoring.” The article says that the genetics of the virus, EG.5, can theoretically boost its transmissibility, meaning that this virus is more easily spread than past variants. This article, to some relief, does not have enough evidence of it yet. Still, according to Johns Hopkins, the mutation is known to avoid the immunity you get after infection or vaccination. I think the idea that the virus is benefiting itself while infecting millions of people is, to say the least, cause for worry. Knowing that this immune system-bypassing virus could infect my grandparents or fellow students is unthinkable.

Spike omicron mutations top

After hearing that, I wanted to know what that means. Is there going to be another outbreak? But there is no need to worry. In this article, using the Washington Post, it is displayed that EG.5 is only different because it has more ability to enter the cells and does not seem to be more lethal than other variants. Dr.K Srinath Reddy proposed that it had the same effect on the human body. As of July 2023, a variant XBB.1.16 was still more prevalent globally than EG.5, and the subvariant only accounted for 11.6%, previously 6.2% in June 2023, of the sampled SARS-CoV-2 sequences. Even though EG.5 is only 11.6%, it is still on the rise and will still infect more people in every country, so it is essential to know your options. According to YaleMedicine, updated vaccines such as Pfizer and Moderna are not a perfect match for eradicating this subvariant and that the vaccine was aimed for a close relative called XBB.1.5. But, the CDC states that the updated vaccines, since XBB.1.5 and EG.5 are so similar, should give a reasonable degree of protection and that the genetic code among omicron subvariants allows for cross-protection.

COVID-19 Vaccine vial and syringe - US Census

Now, as an AP Bio student, this change of structure in COVID is something we have talked about a lot recently. We discussed how the SARS-CoV0-2 virus comprises five main parts: spike proteins, membrane proteins, viral genome, nucleocapsid protein, and envelope protein. To explain these briefly, the spike proteins, membrane proteins, and envelope proteins are on the virus’s surface. The nucleocapsid protein protects the RNA, the viral genome. For this particular variant, I want to speak about the spike proteins and how, in AP Biology, we learned that these spike proteins recognize membrane-bound proteins of human cells and bind to them. Since this is an omicron variant, it follows a Receptor-Mediated Endocytosis pathway, a form in which receptor proteins on the surface capture and encapsulate specific molecules. This makes it more infectious. Once the omicron virus senses the membrane-bound protein of ACE2, it can enter the cell. This works because the omicron variant uses the ACE2 protein to become an endosome, enter the cell by endocytosis, and then break through Receptor-Mediated Endocytosis.

Contrary to the more extended version for SARS-CoV-2, how a transmembrane protease serine 2 cuts the spike protein in a specific location to which the protein will then undergo changes to insert itself into the cell membrane, the omicron version skips these steps to be able to go straight into the cell. The ability to skip these steps also connects to my article because it says the EG.5 subvariant can enter cells even more quickly. At this faster rate, this process can be hazardous and can spread much more quickly, causing more death and destruction. Therefore, learning this in AP Biology and how this process works allowed me to realize how bad this variant can be if the cross-protection is insufficient! But, please, if you are an AP Bio student like me, let me know what you think. Do you think this is more dangerous than portrayed? What do you think we should be doing!?

The Revolutionary mRNA COVID Vaccines

Biochemists Katalin Kariko and Drew Weissman have won the 2023 Nobel Prize in medicine/physiology. Why? Because they were the people behind the vaccines that just allowed us to control the worldwide COVID pandemic.

Usually, vaccine development takes about 5 to 10 years. However, more resources were put into the urgent battle of fighting the rapidly spreading COVID-19 than ever before: in record time, after the genetic sequence of the SARS-CoV-2 virus was discovered, several pharmaceutical companies, namely Moderna and Pfizer, created messenger RNA vaccines. Then, for the first time ever, the FDA approved mRNA vaccines.

Covid Vaccine

Typical vaccines consist of weakened viruses or bacteria that provoke the immune system to make antibodies to protect against future infections:

As I learned in AP Bio class, once those weakened pathogens are allowed to get through the body’s innate defenses (skin, mucus, tears, saliva, etc.), macrophages and dendritic cells engulf the antigens of the foreign pathogens (the spike protein for coronavirus) through phagocytosis, which the phagocytes can display on the outside of their plasma membranes on MHC proteins, while simultaneously releasing chemical messengers called cytokines. Activated by the cytokines, certain T-helper cells then recognize the antigens displayed on certain MHC proteins and call for an appropriate response. If this process is in a cell, T-helper cells activate cytotoxic T cells and T-memory cells. However, if it is in the blood, T-helper cells activate B-plasma cells and B-memory cells. B-plasma cells are the cells that create antibodies, which effectively neutralize pathogens and B-memory cells remember how to create those antibodies significantly more effectively for better future protection.

However, it is a very costly and tedious process for scientists to get loads of the coronavirus and weaken it for vaccines. The way Pfizer and Moderna created working COVID vaccines so quickly, based on the research that Kariko and Weissman began in 2006, is by creating vaccines with mRNA that tells cells how to create weakened coronavirus proteins; this process is instead of scientists manually putting weakened proteins into vaccines and is significantly more efficient since our bodies are already good at making proteins based on DNA/RNA code.

The reason why mRNA vaccines have never been FDA approved before the COVID vaccines is because pumping mRNA into the body releases cytokines itself. As mentioned previously, in AP Bio we learned that cytokines trigger helper-T cells. If helper-T cells are triggered when they shouldn’t be, that could create many problems. So, to fix this problem, Kariko and Weissman slightly altered the structure of the RNA to lessen cytokine triggering. Additionally, they encased mRNA in bubbles of lipids. As I learned in AP Bio class, lipids are nonpolar, meaning they can travel through cell plasma membranes. This lipid bubble, therefore, allows the mRNA to travel directly to and inside the nuclei of cells without causing harm elsewhere. Then, the mRNA can tell ribosomes to create the certain weakened coronavirus proteins that trigger the immune response of creating antibodies as previously described.

With the help of the research of the very deserving 2023 medicine/physiology Nobel Prize winners, Weissman and Kariko, the problems with mRNA technologies have finally been resolved (for now). Thus, this more efficient and may we call it, revolutionary mRNA technology is now being looked at to potentially defend other viruses and even cancers. The opportunities for this technology seem extraordinary, but what other challenges will scientists and researchers face when trying to explore these opportunities?

I would argue it is time for them to explore and find out.

Clot Chronicles: Decoding the Intricacies of Proteins and Vaccines in COVID-19 Immunity

Are you vaccinated for COVID-19? Well, the article titled, Protein interaction causing rare but deadly vaccine-related clotting found, discusses a mechanism that has led people to deadly clots. These scientists identified that some individuals developed these clots after receiving certain COVID-19 vaccines. The research explains  Vaccine-Induced Immune Thrombocytopenia and Thrombosis (VITT) which is a condition where the body produces blood clots. When a patient has this condition antibodies attach to a protein called Platelet Factor 4 (PF4), forming immune complexes. 

Protein PF4 PDB 1f9q(PF4)

Additionally, Platelet Factor 4 is a small cytokine in the CXC Chemokine family. Cytokines are small proteins that are released by macrophages to attack a virus.  Platelet Factor 4’s most prominent function is to promote blood coagulation; but, it is also involved in innate and adaptive immunity

The Immune System, as discussed in depth in my AP Biology class,  protects the body against pathogens such as bacteria and viruses. COVID-19 is an example of one of these viruses that infects the body through its various openings, most generally, the nose and mouth. Innate and Adaptive response are the two parts of the immune system. The innate response is something everyone is born with, works immediately upon infection, and is nonspecific which contrasts the adaptive immune response which is slower and more targeted. 

Returning to the vaccines, these complexes activate platelets and immune cells and lead to clotting and inflammation. Inflammatory responses are a result of the mast cells locating the “invader” and releasing histamine as an “alarm” to the body. Histamine causes inflammation in the body and an inflammatory response which is typically painful. When I had COVID I remember taking anti-inflammatory medications to reduce the pain I felt from the inflammatory response I was experiencing such as my high fever.

In summary, the ongoing research wants to find people who might be more likely to get VITT with future vaccines, so we can understand and manage the risks better, making vaccines more effective. 

After reading this article and doing outside research I believe this study to be highly important because researchers understand how to make vaccines safer for the future. As someone who has not been vaccinated it is valuable for me to know the risks and rewards of the vaccine. So … COVID-19 vax worth it or not? Let me know what you think in the comments!

COVID-19 Vaccine Going Retro?

Bottle with Coronavirus Vaccine and syringe with Novavax logo on white background
Have you ever wondered why the world started to use mRNA vaccines all of a sudden ever since the COVID-19 pandemic? Where did the traditional methods of vaccination go? This sudden shift in vaccine technology didn’t just happen by chance but was a result of years of scientific research and experiments. As the world faced an unprecedented pandemic, the traditional method of vaccination, while reliable, was slower and less effective to adapt to mutating virus than the mRNA vaccines, which is faster and more flexible when combating COVID-19 viruses. However, the traditional methods have returned! The new Novavax COVID-19 vaccine is an old-fashioned, protein-based approach to vaccination, a contrast to the mRNA technology used in Pfizer and Moderna vaccines. The Novavax vaccine especially targets the SARS-CoV-2 variant XBB.1.5, which is a descendent of Omicron. 

Novavax’s Differences: A Protein-Based Approach
Unlike the mRNA vaccines, which use modified viral genetic materials to cause an immune response, Novavax relies on a more traditional approach which injects proteins that resemble SARS-CoV-2 directly into the body. This method has over 30 years of application in vaccines such as the Hepatitis B Vaccine. The Novavax Company also uses insect cells, such as moth cells, to produce SARS-CoV-2’s unique spike proteins. The reason why Novavax researchers use moth cells is because of its efficiency in producing spike proteins. They first select the desired genes that create the spike proteins, and then they put these kinds of genes into a baculovirus, which is basically an insect virus. The baculovirus will then infect moth cells and replicate rapidly inside them creating lots of spike proteins. Finally, the researchers will extract and use the spike proteins for vaccines. Additionally, Novavax’s formula also includes Matrix-M, a compound from Chilean Soapbark Trees, which will further enhance our immune system’s response to the spike protein.

Targeted Variants and Efficiency:                                                                    Novavax vaccines are developed specifically for the XBB.1.5 variant, and they are not optimized for the newer Eris and Pirola variants. However, vaccinologist Gregory Poland notes that all vaccinations, including Pfizer and Moderna, have all been “chasing the tail” of the emerging variants all over the pandemic, so Novavax is not alone in this situation. Additionally, all of the vaccine boosters seem to be able to provide some protection against new variants, but protein vaccinations are way slower to adapt to the new variants than mRNA vaccines. In terms of efficiency, according to infectious disease researcher Kirsten Lyke, Novavax stands on par with other mRNA vaccines. It is 55% effective in preventing COVID-19 symptoms and 31% effective at preventing infections, and this is very similar to the mRNA vaccines.

Protein Synthesis Elongation.png (mRNA coding protein)

Side Effects and Availability:
When it comes to side effects, the Novavax booster demonstrates a lower risk of myocarditis(inflammation of heart muscle) or pericarditis(inflammation of the outer lining of the heart) compared to mRNA vaccines, but of course, it is not entirely risk-free. It also tends to have fewer side effects like muscle fatigue and nausea post-vaccination. A huge advantage of the Novavax vaccine is its availability, it can be stored in a typical refrigerator, making it considerably more accessible than mRNA vaccines, which require subfreezing storage. The Novavax booster is now available in pharmacies across the country, with the CDC recommending having two doses that are eight weeks apart for unvaccinated people.

Which one should I get?
Both the protein vaccines and the mRNA vaccines can help you fight against the SARS-CoV-2 virus, and neither is better than the other. The mRNA vaccine has a faster efficiency in preventing COVID and has a higher adaptability to new variants, while the Novavax vaccine uses a more familiar technology, has a more accessible storage requirement, and has a lower risk of side effects post-vaccination. But no matter which kind of vaccine you think is better, Lyke suggests that the most important thing is to “pick one and get it.”

Novel Coronavirus SARS-CoV-2 (SARS-CoV-2)

Connecting to AP Biology:
In AP Biology, we’ve learned about how our bodies fight bacterial and viral infections and specifically talked about how the spike proteins on SARS-CoV-2 work to attack our bodies. When our body first recognizes the SARS-CoV-2 virus, white blood cells like Macrophages and Dendritic cells will engulf the virus, breaking it down into small pieces and displaying it to Helper T cells on their MHC proteins. The Helper T cells will then release Cytokines which will trigger both the Cell-mediated response and the Humoral response of your immune system. These responses will ultimately kill most of the bacteria/viruses in your body. Additionally, your immune system will then remember the SARS-CoV-2 virus, and if you ever get affected again, your immune system will immediately respond to it. Understanding how vaccines help your body defend against real viruses links directly to our studies on the human body’s defense mechanisms against foreign pathogens.

Leave a Comment!
COVID-19 is a years-long pandemic that still hasn’t ended today, I think it is really important for everyone to know how they can protect themselves through modern technologies and minimize the impact of the virus. I am also intrigued by how fast different vaccine technologies have evolved to help mankind to combat the virus. How do you feel about the re-introduction of protein-based vaccines like Novavax? Do you think this will change the public’s preferences on COVID-19 vaccines? Feel free to leave a comment below and we can discuss more about this topic! For more information on this post, go to for the latest research and updates.

COVID Always Spikes in the Winter!

Have you ever wondered why you always catch a virus when it’s cold outside? Perhaps why we have seen spikes in the disease, COVID-19 (caused by the virus SARS-Co-V-2) during the winter months compared to summer? Recent studies have been conducted on why viruses thrive in cold weather. Additionally, researchers have come up with ways to protect yourself during the cold season!

Novel Coronavirus SARS-CoV-2 (50047466123)

How We Catch Viruses

Viruses are caught by breathing in small droplets known as aerosols. As learned in AP Biology, when a virus is first detected, the innate immune system activates. The innate immune system is nonspecific and will attack anything. It consists of barrier defenses such as mucus and saliva to trap pathogens. Then, if a pathogen gets past these barriers, innate internal cellular defense is activated. The mast cells release histamine and macrophages secrete cytokines. Histamine dilated blood vessels to increase capillary permeability, causing the area to swell. The cytokines attract smaller phagocytes called neutrophils that digest pathogens and dead cell debris. The innate immunity response might induce a fever, for higher body temperatures enhance phagocytosis. However, if the virus (ex: SARS-Co-V-2) makes it past this, it will begin to infect the cells. The virus will latch onto the ACE2 receptors of a cell, allowing the viral genetic material to fuse with healthy human cells. The human host cells will then begin to replicate SARS-Co-V-2RNA to create the proteins that make up SARS-Co-V-2.


How Weather and Seasons Impact Viruses

To start, your location matters in regards to catching COVID. Researchers have found that being outside significantly decreases your odds of catching COVID from the SARS-Co-V-2 virus. The outdoors are well-ventilated. Viruses exhaled outside are diluted faster in the vast and clean outdoor air. This is relevant because we tend to be outside more in the summer than the winter. Inside (during cooler months), viruses can build up in the poorly ventilated space: such as schools and office buildings. 

Additionally, humidity plays a large role in the spread of SARS-Co-V-2 and other viruses. The droplets that the virus is in, such as saliva, dry slowly when it is humid. This could kill viruses like SARS-CoV-2 and influenza. However, the dry air of the winter is known to disarm people’s immune systems. Studies have found that dry air can trigger death of the cells lining the airways. These are the cells of the innate immune system. 

Evidence also suggests that the cold itself is a culprit for the spread of SARS-Co-V-2 and other viruses. When a virus is detected, sensor proteins signal the cell to produce bubble like structures called extracellular vesicles. These vesicles act as a sort of diversion for the virus. The virus will attempt to dock to the vesicle rather than the cell. The vesicle’s microRNA will then release in an attempt to kill the virus. Research states that compared to the standard 37° Celsius, cells in 32° Celsius released 42% less vesicles. They also packed 24% less microRNA than the vesicles in warmer temperatures. 

Face Mask used in Coronavirus pandemic COVID-19

How Can I Keep Healthy This Winter? 

While a humidifier may help, it can produce mold and rot. So, professionals are now leaning towards using exhaust fans, or even better, a HEPA filter to filter viruses in the air. Post Pandemic, we know a lot about mask wearing.. Did you notice that you did not contract as many illnesses while wearing a mask?  Well, masks act as shields to protect you from the aerosols an infected person may produce. Additionally, masks keep the nasal area warm and moist, boosting the immune system.

Unlocking Our Ancient Past: Exploring the Genetic Legacy of Extinct Cousins DNA

Have you ever wondered where we came from? Who we were? What genes truly lie within us, our mothers, fathers? According to a recent research article from ScienceDaily, Neanderthal genetics is one of them, and the genes still affect human life today. In this research article, the researchers from multi-institution teams, including Cornell University, have shown that Neanderthal genes comprise about 1 to 4% of the genome of present-day humans, mostly of those whose ancestors migrated out of Africa. These genomes are not surprising to the scientific community, but their effect on today’s society in human bodies is remarkable. Through a new plethora of computational genetic tools, researchers found the genetic effects of interbreeding between humans of non-African ancestry and Neanderthals that took place 50,000 years ago, as well as the effects on present-day human life. 

Close up of a Neanderthal in a museum

 In a study published in eLife, researchers reported that some Neanderthal genes are essential for specific traits in modern humans. Using an extensive dataset from the UK Biobank consisting of hereditary and trait information of nearly 300,000 Brits, the researchers examined more than 235,000 genetic variants likely to have originated from Neanderthals. They found that 4,303 of those differences in DNA play a vital role in modern humans and influence 47 distinct genetic traits. These genetic traits can include how fast someone can burn calories or a person’s natural immune resistance to certain diseases. Isn’t that unbelievable? How did something from so many years ago affect such a critical part of our lives? Even though they lived thousands of years ago, we all have a part of the Neanderthals in our genetics.

In another article by U.S.News, the idea of immune resistance through our body’s fight against COVID-19 is displayed. The results show that some people who have increased genes from their Neanderthal ancestors may have an increased likelihood of suffering severe forms of COVID-19. These genes, haplotype, increase the risks of hospitalization and not recovering from the virus, showing that having these traits while being able to burn calories fast may cause harm to us as well. As appealing as it might sound, I know it does to me that Neanderthal genes can help in various ways; it is also quite scary. The risk factors of diabetes, heart problems, and obesity can lead to death when mixed with the virus and the gene itself lingering within us. Since these genes are a part of our fundamental hereditary units and will continue to pass down from generation to generation, with all of these effects, this investigation commenced and evolved into an important and crucial step toward understanding where we came from and who we are. Therefore, these traits affect the lives of humans every day in COVID as well as provide multiple factors of traits that we live with every day, not even knowing where they came from.

Hospital HallwayNovel Coronavirus SARS-CoV-2

As an AP Bio student, in Unit 1, we talked about the parts of the cell along with the DNA that is within the cell. These cells are deeply related to what this topic is about, as the process in which genes work revolves around the cell that it is in. First, it starts with transcription, which is the process in which the genetic material is stored in DNA and replicated into a molecule of messenger RNA. The information goes from the DNA in the nucleus to the cytoplasm to carry out protein synthesis. In the cytoplasm, ribosomes make the proteins that create these specific effects mentioned above. Each gene carries instructions for the proteins that determine your features, such as eye color, hair color, height, and, in this case, immune resistance. These two must connect with each other to fully understand how these genes are still here thousands of years later. The answer is that the genetic material has been carried down for this time through each and every ancestor we have had. It’s pretty scary, if you ask me.

Diagram of a gene on a chromosome CRUK 020

I am not the only one who believes that these causes of our ancestral genes are threatening. If you are like me and want to continue learning about this, reach out! As well as anyone with first-hand knowledge of the research or possible medical intervention, please comment! Share your knowledge with me. The custom software discussed in the ScienceDaily link from UCLA is available for free download and use by anyone interested in further research. So, if you are an AP Bio student like I am or just interested in the genes defining us, even though they are from thousands of years ago, join the conversation. These traits and genes are just being figured out, as most of the work started in September 2023. No matter what fears you may have, to leave you with a sense of comfort after a long list of possible effects, modern human genes are prevailing over successive generations. Therefore, this research, although evolving with us, must continue.

Genetic Variation the Savior

In the article “Genetic variation in the SARS-CoV-2 receptor ACE2 among different populations and its implications for COVID-19,” published in Nature Communications, the authors explore the genetic variation in the ACE2 receptor across different populations and its potential impact on COVID-19 susceptibility and severity. The ACE2 receptor is a key entry point for the SARS-CoV-2 virus into human cells. Its expression level and genetic variants may affect the virus’s ability to infect and replicate within the host. Therefore, understanding the genetic variation in ACE2 among different populations can provide insights into the different susceptibilities and severity of COVID-19 seen across the world. The authors analyzed genetic data from various global populations and found that there is significant genetic variation in ACE2 between populations. Specifically, they identified several ACE2 variants that are more prevalent in certain populations, including a “variant that is more common in East Asian populations” and may affect the receptor’s expression level.


The authors also conducted in vitro experiments – medical procedures, tests, and experiments that researchers perform outside of a living organism – to investigate the impact of these ACE2 variants on SARS-CoV-2 infection. They found that some variants, such as the one more prevalent in East Asian populations, led to reduced viral entry and replication, while others did not significantly affect viral infection. These findings suggest that genetic variation in ACE2 may contribute to the different COVID-19 outcomes observed across different populations. For instance, the higher prevalence of the ACE2 variant in East Asian populations may explain why these populations had a lower incidence of severe COVID-19 despite being initially hit hard by the pandemic. Furthermore, the author highlights the importance of considering genetic variation when developing COVID-19 treatments and vaccines. For instance, vaccines that were designed based on the original strain of SARS-CoV-2 may be less effective against strains that have evolved to better utilize ACE2 variants prevalent in certain populations. Overall, the article sheds light on the genetic variation in ACE2 among different populations and its implications for COVID-19 susceptibility and severity. The authors’ findings show the importance of taking genetic diversity into account when studying diseases and developing treatments and vaccines, particularly in the context of a global pandemic. In our recent DNA unit in class genetic variation was one of the topics of discussion, genetic variation is extremely important for the survival of a population as there is an easier chance that the species will be able to adapt and survive in different situations. Without genetic variation, many species can die out and therefore including the topic of genetic variation in viruses like covid-19 is extremely detrimental to the survival of humans when fighting this illness.

Can Your Lungs Work Against COVID-19?

Within the last two to three years there has been an immense focus in the field of science, COVID-19. This pandemic has sparked a myriad of research opportunities as well as brought up questions we didn’t even know we needed answered.

With this, recent research at the University of Sydney shows that our lungs contain a protein that blocks the COVID-19 infection and works to create a protective barrier within our body. The way it works is that a protein receptor found in our lungs sticks to the virus, and then pulls it away from the targeted cells. The protein is known as the Leucine-Rich Repeat-Containing Protein 15 or in short, LRRC15. For context, leucine is an essential amino acid for protein synthesis as well as many other biological functions. The protein is a built-in receptor inside of our bodies that binds to the COVID-19 virus and doesn’t pass on the infection.

Lungs diagram detailed

Initially, the research was published on February 9, 2023, in the PLOS Biology Journal. Led by Professor Greg Neely and his team members, the findings serve to open a new sect of immunology and COVID research, specifically around the protein, LRRC15. Moreover, it creates a path to develop new drugs and treatments to prevent infections such as COVID-19. Greely states that ” This new receptor acts by binding to the virus and sequestering it which reduces infection,” essentially the receptor is able to attach to the virus and “squish” it before it moves to infection. He also pushes the idea that the new receptor can be used to “design broad-acting drugs that can block viral infection or even suppress lung fibrosis.” Continually Dr. Lipin Loo, one of Greely’s team members, mentions, “We think it acts a bit like Velcro, molecular Velcro, in that it sticks to the spike of the virus and then pulls it away from the target cell types,” here he outlines the stickiness of both the receptor and the virus as well as the receptor’s nature to latch onto the virus and “hold” it. In addition, Loo states, “When we stain the lungs of healthy tissue, we don’t see much of LRRC15, but then in COVID-19 lungs, we see much more of the protein,” here he fronts the idea that COVID-19 lungs are far richer in the LRRC15 protein than normal lungs, this may be due to a result of the protein’s ability to immobilize the virus.

To outline COVID-19 infects us by using a spike protein to attach to a specific receptor in our cells. It mainly uses the ACE2 receptor to enter human cells. Moreover, our lung cells have high levels of ACE2 receptors, which is why being infected can often cause severe problems in our lungs. Similar to ACE2, LRRC15 is a receptor for COVID. But, LRRC15 does not support infection, instead, it sticks to the virus and immobilizes it. This prevents other cells from becoming infected. LRRC15 attaches to the spike of the virus and pulls it away from certain target cell types. The LRRC15 protein is widely present throughout our body, it is in the: lungs, skin, tongue, fibroblasts, placenta, and lymph nodes. However, the researchers observe that the lungs “light up” with LRRC15 after infection. They think the new protein is a part of our body’s natural response to combatting the COVID-19 infection. It creates a barrier that separates the virus from our lung cells most susceptible to COVID-19 infection


To connect to our AP Bio Class, we learned about adaptive immunity where we develop an acquired immunity after being exposed to pathogens, a specific response. I see some similarity here in that the LRRC15 protein is specific to immobilizing the COVID-19 infection. Additionally, in our Cell Signalling Chapter, we focused on signal transduction and its stages, reception, transduction, and response. Specifically in the reception stage, we focused on intracellular and transmembrane receptors. I think that LRRC15 would be transmembrane in order for it to efficiently bind to the COVID-19 Spike. With this, however, I would like to see more about the transduction component of the LRRC15 receptor. Lastly in our Enzyme Unit, we learned about how different factors can affect enzymatic activity; heat, pH, and even general surroundings. I wonder which factors work to hinder and work to stimulate the purpose of the LRRC15. I invite any and all comments with additional info relevant to the topics discussed.

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!!

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