BioQuakes

AP Biology class blog for discussing current research in Biology

Page 6 of 83

Cracking Down on Long COVID

By

On December 15, 2023

In Student Post

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

By

On December 15, 2023

In Student Post

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?

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

By

On December 11, 2023

In Student Post

-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?

By

On December 11, 2023

In Student Post

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.

Fphar-11-00937-g001.jpg

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?

 

Unmasking Covid: A Rollercoaster of Well Being

By

On December 11, 2023

In Student Post

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?

 

COVID CHANGES THE IMMUNE SYSTEM!?!

By

On December 11, 2023

In Student Post

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.

undefined

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?

 

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

By

On December 11, 2023

In Student Post

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!



 

 

Blood Clotting Proteins Predicting Signs of Long COVID

By

On December 11, 2023

In Student Post

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

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.

What Are The Current COVID-19 Variants in November 2023?

By

On December 11, 2023

In Student Post

In the United States, there are currently more than 10,374 patients hospitalized per week who tested positive for COVID-19. 15% of these patients are in the ICU (Intensive Care Unit). As of November 4, the test positivity rate is 8.5%. When the test positivity is above 5%, this indicates that transmission is considered uncontrolled.

Due to the fact that many people are using home tests that are not reported through public health or are not testing at all, the official case counts underestimate the actual prevalence of COVID-19.

SARS-CoV-2 without background.png

The dominant variant nationwide currently is HV.1, with 29% of cases, followed by EG.5, with 21.7% of cases and FL.1.5.1, with 9.3% of cases. HV.1 was documented by the Centers for Disease Control and Prevention (CDC) in low numbers during the summer. However, now that the strain has the highest prevalence of any, it claims responsibility for more than a quarter of new coronavirus cases in the U.S. as of late October.

This strain is still a sub-variant of omicron, as is every strain that is in circulation. This strain is a descendant of EG.5, which is the second most common variant in the U.S.

HV.1 is highly infections. The emergence of HV.1 shows how the SARS-CoV-2 virus, which causes COVID-19, is able to mutate and cause new, highly transmissible variants. The symptoms of HV.1 are very similar to those caused by recent variants of omicron.

Omicron S exhibits a heightened dependence on a significantly elevated level of host receptor ACE2 for effective membrane fusion compared to other variants. This characteristic may elucidate its unanticipated cellular tropism. The mutations not only reshape the antigenic configuration of the N-terminal domain of the S protein but also modify the surface of the receptor-binding domain in a manner distinct from other variants. This alteration aligns with its notable resilience against neutralizing antibodies. These findings imply that Omicron S has developed an exceptional capacity to elude host immunity through an abundance of mutations, albeit at the cost of compromising its fusogenic ability.

The Omicron variant of the SARS-CoV-2 virus introduces a distinctive challenge to the immune response system, primarily through mutations in the spike protein. These alterations in the antigenic configuration of the spike protein have raised concerns about the potential impact on the effectiveness of the immune response, particularly with regards to neutralizing antibodies generated from prior infections or vaccinations. The unique genetic makeup of Omicron may allow the virus to partially evade recognition by existing antibodies, potentially leading to breakthrough infections. Moreover, the variant’s influence on cellular immunity, mediated by T cells, is still under investigation, but T cell responses may play a crucial role in controlling infections even if antibody responses are compromised. The evolving nature of the virus underscores the importance of public health measures, including vaccination campaigns and booster shots, to adapt to the changing landscape of the pandemic and reinforce the immune system’s ability to respond to new variants like Omicron. Ongoing research is essential to comprehensively understand the implications of Omicron on the immune response and to inform effective strategies for mitigating its impact on public health.

Omicron stands out with approximately 50 mutations, surpassing the mutation count of any prior SARS-CoV-2 variant. Among these, 32 alterations are within the spike protein, the primary target for most vaccines aiming to neutralize the virus. As of December 2021, numerous mutations in Omicron were novel and distinct from those observed in earlier variants. By April 2022, the variant exhibited 30 amino acid changes, three small deletions, and one small insertion in the spike protein when compared to the original virus. Notably, 15 of these changes were situated in the receptor-binding domain (residues 319–541). As of December 2022, the virus featured additional modifications and deletions in various genomic regions. For instance, three mutations at the furin cleavage site, crucial for its transmission, were identified.

Health officials are not concerned with the latest variant. This is because it appears that HV.1 is very similar to EG.5, also known as “eris.” They are so similar that the World Health Organization (WHO) does not separate the two in its estimates. Globally, Eris is the most prominent strain, accounting for 46% of global cases as of late October, according to the WHO. This estimate also includes cases from HV.1 and another similar strain, HK.5.

HV.1 does not appear to cause more severe illnesses. However, it is expected that it brings the same high transmissibility that eris has. More cases will cause more variants with more mutations to occur.

Dr. Perry N. Halkitis, the dean of Rutgers School of Public Health, says that “the concern about the multitude of mutations is that it is likely and possible that there are versions of the virus that will be more evasive to the immunity that people have.”

However, the fact that HV.1 is so similar to EG.5, the updated coronavirus vaccines are expected to work on the new strain.

However, the shots’ advantages are limited by low uptake so far. Only about 7% of U.S. adults and 2% of children got the new COVID-19 vaccines during the first month it was available, according to national surveys. Despite the rollout being hampered by availability and insurance issues, U.S. health officials say those problems have been mostly resolved.

Surveys also found that almost 38% of adults and parents said that they probably or definitely will not get the shot for themselves or their children.

Hesitancy and vaccine fatigue are surely large parts of the uptake problem. When it comes to COVID-19, there is a general lack of urgency now that vaccines and treatment are widely available.

Halkitis says, “we’ve opened a window of opportunity for people who are resistant to vaccination to begin with to say, ‘Well, it doesn’t look so bad anymore, so I’m just going to bypass it.’ Just like how they react to the flu.”

According to CDC data, COVID-19 weekly hospital admissions have been decreasing or stagnant for nearly two months. However, these numbers remain elevated at more than 15,700 new admissions for the last full week in October, more than double summer’s low of about 6,300 in June.

With the upcoming cold winter months approaching, scientists are anticipating more COVID-19 infections as cold temperatures push people indoors.

Halkitis says that, “I expect there to be more rapid spread as is the case with any respiratory virus in the winter months.”

The CDC is predicting that a moderate COVID-19 wave will sweep over the U.S. according to its respiratory disease season outlook.

The CDC said in an update to its respiratory disease season outlook published last month that, “COVID-19 variants continue to emerge but have not resulted in rapid disease surges. We continue to anticipate a moderate COVID-19 wave, causing around as many hospitalizations at the peak as occurred at last winter’s peak.”

Scientists anticipate that the variants circulating in the U.S. will continue to change as the virus spreads and adapts to its environment.

Halkitis says, “The more we spread it to each other, the more it’s going to keep replicating in people’s bodies, the more likely it will be that mutations are going to occur.”

Based on these findings, I am not very concerned about COVID-19 mutations and variants. Having recently received the COVID-19 booster, I feel great and confident in the effectiveness of the vaccination. In my view, the pandemic no longer appears to be a national emergency. What are your thoughts on this? Do you believe the government should continue to declare the U.S. in a state of emergency due to COVID-19?

Personally, I commend the government for its handling of the pandemic. The implementation of vaccination campaigns, testing protocols, and treatment plans has been commendable. The availability of booster shots is a testament to the ongoing efforts to curb the spread of the virus and protect public health. I believe these measures have played a crucial role in mitigating the impact of the virus.

While I acknowledge that COVID-19 mutations and variants are still a consideration, the fact that I feel well after receiving the booster is reassuring. I think it’s essential to strike a balance between vigilance and a sense of normalcy. What’s your perspective on the current state of the pandemic and the government’s response?

 

COVID-19: Multiple Doors and Multiple Species

By

On December 11, 2023

In Student Post

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?

 

Enhanced efficiency with Reduced Dosage: Advancement’s in Moderna’s mRNA Covid-19 Vaccine

By

On December 7, 2023

In Student Post

Moderna has rolled our many versions of vaccines to fight against Covid-19 since the pandemic began in 2020. One of their latest versions of the Covid-19 vaccine is a streamlined version of its mRNA Covid-19 vaccine, called mRNA-1283. For those who don’t know, mRNA vaccines are vaccines that work by introducing a piece of mRNA that corresponds to a viral protein, usually a small piece of a protein found on the virus’s outer membrane. What is interesting about the mRNA-1283 vaccine and makes it seem quite efficient is that it is more effective at lower doses and lasts twice as long when stored in a refrigerator. This is likely due to a very unique feature of the mRNA-1283 vaccine: it does not include mRNA that corresponds to all parts of the famous SARS-CoV-2 spike protein—a protein on the SARS-CoV-2 virus that allows the virus to penetrate host cells and cause infection. Instead, it includes mRNA that corresponds to just two specific key parts of the spike protein.

Everything About COVID-19 Vaccines

Many studies have shown that the most effective antibodies to fight against Covid-19 are those that bind to one of the two key sites of the spike protein that protrude from the virus’s surface. For instance, one of these two key sites is the region on the spike protein responsible for attaching to human cells and assisting the virus in entering the human cell. Therefore, antibodies that bind to this key site will block the spike protein from attaching to the human cell and entering the cell.

A majority of the current existing Covid-19 vaccines, including other existing Moderna vaccines, contains the entire spike protein. This causes the immune system to create antibodies against all parts of the spike protein, meaning that many of these antibodies are ineffective because not all parts of the spike protein are responsible for entering or harming human cells. On the other hand, Moderna’s mRNA-1283 vaccine consists only of mRNA coding for the two parts of the protein that contain the two key sites of the spike protein that are harmful to human cells, which means all of these antibodies are effective.

When the the first human trial of mRNA-1283 was given, it revealed that even when people were given a tenth of the full dose for one of Moderna’s original Covid-19 vaccines, called mRNA-1273, they produced an antibody response that was just as strong as a full dose of this original mRNA-1273 vaccine, according to a trial released in October 2022.  

Additionally, the mRNAs in the mRNA-1283 vaccine are shorter than those in the mRNA vaccines coding for the entire spike protein, reducing the chance of mRNA breakdown and allowing the vaccine to last longer. When stored at temperatures between 2 and 8 degrees Celsius, the mRNA-1283 vaccine takes a year for 40 percent of the mRNAs to degrade, while the mRNAs in mRNA-1273 take only six months to degrade at these temperatures.

This connects to what we have learned in AP Bio class as in AP Bio we learned about the process of adaptive immunity. We learned that an adaptive immune response occurs when all the first and second line defenses of the body, such as skin or mucus, are unsuccessful in preventing a virus, such as Covid-19, or bacteria from spreading in the body. An adaptive immune response is then needed to target the virus or bacteria. Adaptive immune responses rely on two types of lymphocytes: B cells and T cells. B cells are the cells that take on the invading Pathogen, so in the case they would take on the SARS-CoV-2 in the body directly, while the T cells target the cells that were already infected by the virus. The adaptive immune response begins when the Macrophage cells of the body engulf the antigen through phagocytosis and then the vesicle formed for the antigen once engulfed inside the Macrophage fuses with a lysosome to break down the antigen. As the lysosome breaks down the antigen, it preserves the foreign antigen (epitope) which is the little part of the antigen that is recognized by the immune system. The epitope is then displayed on the outside of the macrophage membrane on the MHC protein. The T-helper cells see this displayed foreign antigen on the MHC protein and use their receptors to identify and recognize this foreign antigen. Once the T-helper Cell recognizes these proteins, it is now activated and releases interleukin which signals the start of the process to fight the foreign invader (the key sites on the spike protein) and activates the B and T cells. In the Humoral Response, the B cells bind to the foreign antigen that the T-helper cell recognized and once recognized by the B-cell, the T-helper cells help create the B-plasma cells. These B-plasma cells create antibodies to bind to and neutralize the foreign antigen.

In the case of covid-19, the foreign antigen, or small piece of the antigen that is recognized by the immune system, are the two key sites on the spike protein that we discussed.  The T-cells recognize these key sites when they are embedded on the MHC protein and activate which releases interleukin and signals the start to the immune response. One of these immune responses is the Humoral Response which activates the  B-cells to bind and recognize these key sites on the spike proteins as well. From here, the T-helper cells help create the B-plasma cells which create antibodies to surround and neutralize the two key parts of the spike protein (the foreign invader). Antibodies produced by covid-19 vaccines that are for the whole spike protein are producing some antibodies that are not going to surround and attack these two specific key sites of the spike protein/ the foreign antigen. On the other hand, the mRNA-1283 vaccine only produces antibodies that attack the specific key sites on the spike proteins (the foreign invader), so it is not producing any antibodies that are ineffective in fighting SARS-CoV-2. This makes the mRNA-1283 vaccine just as effective or more effective in smaller doses as other vaccines that produce antibodies for the whole spike protein are in larger doses because even though the vaccines for the whole spike protein are producing more antibodies, some of these antibodies don’t fight the specific foreign antigen that is preserved when the antigen is broken down by the lysosome in the Macrophage cell and needs an immune response, and instead try to fight the whole antigen (the whole spike protein) which is unnecessary.

As Covid-19 continues to evolve, more and more versions of Covid-19 vaccines are emerging, making it increasingly challenging for people like myself to decide which vaccine is truly ‘the best’ and should be taken. After delving deeper into the Moderna mRNA-1283 vaccine, it seems that, due to its exclusive focus on the key aspects of the SARS-CoV-2 spike protein, this version of the Covid-19 vaccine could indeed be at the top of the list for the most efficient Covid-19 vaccines. As someone who has fallen ill after receiving a Covid-19 vaccine in the past, the prospect of receiving a lower dosage of the Covid vaccine while still achieving the same or better effectiveness is definitely intriguing to me. When it is time for you to get your next Covid-19 vaccine, would you be interested in trying Moderna’s mRNA-1283 vaccine as your next Covid vaccination?

 

The Other Mental Side of Covid-19

By

On December 7, 2023

In Student Post

When thinking of Covid-19 most people think of a fever, cough, or lack of taste and smell. However, there is another symptom found in a recent study, a psychiatric symptom, that remains unknown to most people, yet is still quite dangerous. These aforementioned symptoms are paranoia, delusions, and suicidal thoughts, all of which were developed by teens in the midst of their Covid-19 infections. Luckily, scientists believe they were able to pinpoint the cause of these symptoms.

Scientists believe rogue antibodies, while trying to fight Covid, accidentally targeted their own brain. The antibodies were found in the patients’ cerebrospinal fluid (CSF), which is a clear liquid that flows in and around the hollow spaces of the brain and spinal cord. The rogue antibodies found do target brain tissue, however we can’t say for sure whether they are the direct cause of the newfound symptoms. This is due to the fact that the newly found antibodies target structures on the inside of cells, not the outside.

According to the study, Covid-19  may trigger the development of the brain targeting antibodies. The study also suggests that treatments that calm down the immune system could resolve the psychiatric symptoms. Both teens in the research underwent intravenous immunoglobulin treatment, which is utilized to reset the immune response in conditions related to autoimmunity and inflammation. Following this, the psychiatric symptoms of the teenagers either partially or completely disappeared. However, it remains a possibility that the patients might have shown improvement without any treatment, and due to the limited size of this study, this cannot be ruled out.

3 teens who were hospitalized due to Covid-19 at the researchers’ hospital were chosen for a new study. They tested positive with either a PCR or rapid antigen test. As taught in AP Biology, antigens are the foreign receptors on the surface of antibodies. Immune cells can transport a piece of the pathogen to T-cells for recognition once the pathogen is eliminated. T-cells play a role in triggering B-cells, which then produce antibodies targeted against that specific antigen. Of the 3 patients chosen, one had a history of unspecified anxiety and depression, and after being infected with Covid-19, they experienced delusion and paranoia. Another had pre existing anxiety and motor tics, and after getting Covid-19, they experienced mood shifts, aggression, and suicidal thoughts. The 3rd teen had no pre-existing condition, and after getting Covid-19 experienced insomnia, agitation, and disordered eating.

As part of the study, all 3 patients had a spinal tap which showed they all had higher than the normal amount of antibodies. However, only 2 of the patients carried Covid-19 antibodies, which created more uncertainty in the study. In conclusion, with this small a study, we can’t say for sure whether there is a causation between the antibodies and the psychiatric symptoms despite the evidence.

Based on the evidence presented, do you think there is a causation between the antibodies and they psychiatric symptoms of Covid-19 found in the teens?

Have you or anyone you know experienced these psychiatric symptoms or ones similar to those discussed in the study after getting Covid-19?(2020.05.08) Coleta De exames para Covi-19 (49870440091)

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

By

On December 7, 2023

In Student Post

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

By

On December 7, 2023

In Student Post

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.

Long Term Health Risks From COVID-19 Infection

By

On December 7, 2023

In Student Post

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

Sticky Viruses – How Strengths of Adhesion Influence the Transmission of COVID-19

By

On December 7, 2023

In Student Post

SARS-CoV-2 without background

Keeping track of each new SARS-CoV-2 strain and variant may feel like learning a new language. The myriad of Greek letters used to designate each one quickly turns science into classics, so it’s understandable how one may get lost in the confusing terms. But keep calm, these identifiers are crucial for understanding how COVID-19 evolves. They help scientists organize the virus’ different traits and open a window into understanding its behavior at the molecular level. A recent experimental study has just discovered how one of the determining factors that contribute to virulence could be the strength with which the virus binds to the host cell. In a joint effort between the University of Auburn, University of Munich, and Utrecht University, scientists analyzed the virus’ atomic structure.

The team observed how the different variants’ spike proteins interacted with the human ACE-2 protein and found that Alpha’s docking sequence is much stronger than those of Beta and Gamma. However, these latter variants appeared equally virulent as Alpha, leading researchers to conclude that it was their ability to evade immune responses that compensated for their relatively weak adhesion. The lead experimental scientist, Dr. Bauer, took an innovative approach by using force stability – essentially the net force with which the virus binds to the protein receptor of the host cell – as a means of determining the strength of adhesion.

Being a respiratory virus, the cells to which COVID-19 primarily binds are those along the path air takes from the nostrils to the lungs. After making contact with one of these cells, the virus begins a docking sequence that will allow it to assume control of the cell’s replicative mechanisms. In one of the universe’s most fascinating existential tricks, the virus is neither living nor dead: it is simply an envelope filled with genetic material. If it wants to replicate itself, it can’t do it alone. The virus binds to an ACE-2, a common receptor protein on the outside of the phospholipid bilayer. Once firmly connected, the host cell sends lysosomes to digest the envelope, revealing the virus’ genetic information, which enters the cell through a pinocytotic vacuole. Once inside, the virus then hijacks the existing cell structures to replicate itself. After assembling an army of fellow viruses, the host cell ruptures, releasing legions of viruses to neighboring cells in an attempt to repeat and amplify the process. This rupturing is often the source of the soar throats from which infected patients suffer.

As someone who has in the past gone toe-to-toe with COVID-19, I can say that it is a formidable opponent. It is clever, elusive, and stubborn. For a while I felt only the most bitter animosity towards this microscopic speck, but after developing an understanding of its behavior and anatomy, I can now respect its sophisticated biological processes that aid in its reproduction. I still view it as the most heinous and lowest “life” forms in the universe, but at least I understand its point of view. Let me know what you think about this groundbreaking research! Will it prove pivotal for engineering future vaccines for specific variants? How fascinating and haunting that the severity of the illness can be determined by how firmly the virus snatches at your cells!

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

By

On December 7, 2023

In Student Post

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?

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

By

On December 7, 2023

In Student Post

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!

Using Mosquitoes’ Greatest Asset Against Them

By

On December 7, 2023

In Student Post

What if mosquitoes were not a threat anymore? The most deadly animal known to man, harmless?

Aedes aegypti CDC-Gathany

Even today, even with deaths down 31% from 2010 to 2019, mosquitoes still kill around 1 million people a year. According to the CDC, in 2020 they killed over 600,000 to malaria alone. Excluding other viruses such as dengue or West Nile virus.

 

But scientists intend to turn their affiliation with viruses into an advantage. By implanting their own virus into mosquitoes, one that can limit the transmissibility of other ones.

 

Wolbachia. A virus preexisting in an abundance of other bugs to the point of it not harming the ecosystem. A virus that can suppress the transmission of viruses. A virus that will be passed down the generations.

 

In Medellin, Colombia, a mosquito factory exists solely for this purpose. To breed enough of the Aedes aegypti mosquito, that will propagate this virus throughout the town. Rather than the insecticide trucks barrelling through the streets, spraying the air and killing the water, mosquito eggs are injected with incredibly fine needles, nurtured, then released. And there were results. Mosquitoes who picked up a virus were less likely to transmit it to humans. In Yogyakarta, Indonesia it worked too.

 

Whilst the A. aegypti mosquito originally originated from Africa, they escaped via the slave trade, and later, would follow the paths of troops in World War II. And now many communities are affected by it.

 

So the introduction of something to suppress these fatal diseases is good, right? 

 

This program is too new. The Wolbachia might work now, but it’s only a matter of time before these viruses mutate and harness the power of the increased number of mosquitoes. “Mosquito populations are increasing and additional methods are needed to control the mosquitos during their adult stage,” the EPA states in regards to the mosquito population in Puerto Rico. And they do not mention the added mosquito populations. If say, dengue mutates, changes even the slightest bit of its genetic code, and Wolbachia no longer works, then we have simply increased the problem, kicking that can down the road.

There is a chance that a virus will mutate every time it duplicates its RNA/DNA, and since it occurs quite frequently, there is a solid chance for a mutation that ignores Wolbachia to become prevalent in mosquitoes. If the epitope (the spike protein that antibodies recognize) in one of the viruses Wolbachia seeks to prevent changes significantly, Wolbachia’s gift will turn back into its weakness. Akin to how old Covid vaccines no longer work, but I digress.

I cannot say for certain that this may occur, but then viruses are like elusive fish: nearly impossible to predict or ensnare, yet still so prominent in its effects. 

 

Please tell me if you think this will work. These studies feel a little too optimistic, but I hope I’m wrong.

 

New COVID-19 Vaccine

By

On December 5, 2023

In Student Post

Did you know that different variants of COVID-19 can have SUB variants as well? Because the Omicron variant is now the world’s most prevalent strain, it has been able to mutate into different sub variants. The XBB sub variants stood out because they contain a high number of genetic mutations compared to other variants. These mutations or changes help the virus avoid the body’s immune response even if one has been vaccinated for COVID-19 already. Specifically the XBB. 1.5 sub variant (also known as Kraken) has a mutation that helps the virus bind to cells making it more contagious. Scientists believe that XBB. 1.5 binds “more tightly to cells in the human body that the predecessors” (Andrea Garcia). This was the dominant strain in June 2023. 

COVID-19 vaccines (2021) A

The updated COVID-19 vaccine is now being recommended by the CDC and has been approved by the FDA as of this September. It is a monovalent or single component version that specifically targets this sub variant of Omicron (XBB. 1.5). This vaccine is meant to broaden vaccine-induced immunity and provide protection from other XBB sub variants as well. This is similar to how the flu shot works in that the formula changes every year depending on which strain is spreading the most at the time. The vaccine will not prevent every version of COVID-19, however, unless there is a great change in the genetics of the virus, it should provide at least partial protection from other strains as well. The treatments for COVID-19 such as antivirals will still work against this new XBB. 1.5 sub variant. 

In AP Biology, we learned about the immune system and how memory T cells and B cells are made to fight the same virus in the future. A virus enters the body through a macrophage or dendritic cell. Viral antigens are then presented on the surface of the dendritic cells or macrophages and infected cells. The viral antigen then binds to the Helper T cell and causes cytokines to be released to stimulate B cells and cytotoxic T cells. This creates a memory helper T cell. B cells divide to create plasma cells and memory B cells. The plasma cells secrete antibodies for this virus. 

This process is why it is important to receive this vaccine even if one has already been infected by COVID before or if one has received the vaccine before because of the new variants such as XBB. 1.5 that are emerging. The previous COVID-19 vaccine does not necessarily protect against the XBB subvariants and having COVID-19 previously and getting those antibodies through the process described above does not mean you have the antibodies for the new strains.

I still got COVID after having the vaccine because it was a different strain of the virus than the one being targeted in the vaccine. This is very common but hopefully this vaccine means that there will be one less sub variant to worry about! 

Page 6 of 83

← Previous

Next →

Archives

Powered by WordPress & Theme by Anders Norén

Skip to toolbar