AP Biology class blog for discussing current research in Biology

Tag: Immune System (Page 1 of 3)

Is COVID-19 Linked to Diabetes?

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

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

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

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

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

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

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


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

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

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

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

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

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


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?


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!

The cause of Asymptomatic COVID-19 cases: A Gene Mutation

Novel Coronavirus SARS-CoV-2 (50047466123)

What is the cause of asymptomatic COVID-19 cases?

The study led by researchers at University of California San Francisco, published in Nature on July 19, 2023, provides the first evidence of a genetic basis for asymptomatic SARS-CoV-2 infection.  Individuals who contract COVID-19 but remain symptom-free are more than twice as likely to carry a specific gene variation. The genetic mutation, HLA-B15:01, common in about 10% of the study’s population, doesn’t prevent virus infection but remarkably prevents the development of symptoms. The research identifies the HLA-B15:01 variant as a key factor in solving the mystery of asymptomatic COVID-19 cases, with 20% of asymptomatic individuals carrying it compared to 9% with symptoms. The study, focusing on unvaccinated donors, finds that risk factors for severe COVID-19 don’t play a role in asymptomatic cases. The HLA-B*15:01 gene’s ability to recognize and respond to COVID-19, facilitated by T-cell memory, suggests potential targets for drug and vaccine development. The collaboration with La Trobe University delves into the concept of T-cell memory, highlighting the immune system’s ability to recognize SARS-CoV-2 due to exposure to similar peptides in seasonal coronaviruses. The research opens avenues for promoting immune protection against SARS-CoV-2 in future vaccine or drug development.

Recently in AP Biology, my class learned about the intricate mechanisms of the immune system.  This research directly connects to our learning of the immune system, more specifically memory cells which are highlighted in the article as a key piece of how the HLA-B15:01 gene functions.  T memory cells are cells which are responsible for recognizing and responding to all previous infections.  As previously mentioned, La Trobe University found that the HLA-B15:01 gene recognizes COVID-19 because of its similarity and to the more common coronaviruses people are regularly exposed to.  Once recognized the immune system has the capability to attack it with T-killer cells and potentially create and secrete antibodies through macrophages and plasma cells.

Since March 2020 I have been curious to the reasoning behind asymptomatic cases and I am happy to find a potential answer to this long unanswered question.  Why do you think this research has taken almost three years to find the answer to.  Comparatively, the COVID-19 vaccine was made in around 8 months from March of 2020. Of course there was significantly more incentive and money invested into the development of the vaccine, however the two findings are years apart and the vaccine is seemingly much harder to research and develop.

Does Lifestyle and Diet Affect Immune System Aging?

Have you ever heard of the thymus? If not, most people could probably say the same, despite the enormous role it plays in our overall health. The thymus is a small gland in the upper part of the chest that is crucial to the immune systems of children. After puberty, the gland was previously thought to become smaller, gradually turn to fat through a process called fatty regeneration, and lose its function. Through the use of CT scans, a recent study shows that contrary to prior belief, this organ can be significant in adults as well, and the state of it can be influenced by lifestyle, age, and sex.

Diagram showing the position of the thymus gland CRUK 362

The main function of the thymus is to develop all the body’s immune cells before puberty. In order to carry out this function, the gland produces the hormone thymosin. Cells called lymphocytes pass through the thymus where they are fully developed into T cells, with the help of the hormone. Once they are fully developed, they are transferred to the lymph nodes where they help the body fight off infections and prevent autoimmune diseases. Autoimmune diseases occur when an immune system attacks cells from its own body. Have you ever touched your neck when sick and felt a small swollen part? Those are your lymph nodes! When you have an upper respiratory infection, more T cells rush to your lymph nodes to help your body fight off the illness. This is just one example of your immune system in action.

When you think of proteins, what is the first thing you think of? As presented in the AP Biology curriculum, proteins are not just a food group we eat everyday, though they are still very important to ingest! They are part of every cell in our bodies and therefore are crucial to the immune system and the thymus. Immune cells have receptor proteins attached to them that bind to foreign and potentially harmful substances, also called antigens. When the proteins bind to the substance, they trigger the body’s immune system to fight off the antigen. There are two types of immune systems: the innate immune system and the adaptive immune system. The innate immune system fights antigens mostly using killer cells and phagocytes (“eater cells”). The adaptive immune system makes antibodies that are made to fight off specific germs that the cell recognizes.

A new study performed in Sweden looked at the CT scans of 1000 people between the ages of 50-64, and examined the state of their thymuses. The people previously participated in the SCAPIS study which inspected their lifestyles and dietary habits. Results found that 6 out of 10 of the participants had a thymus that was completely turned to fat. It was more common in men and obese people. Dietary habits such as low fiber intake caused more fatty regeneration. People whose thymuses endured more fatty regeneration showed evidence of lower T cell regeneration. Ultimately, the CT scans showed the functionality of the thymus and the immune system. More studies must be performed to fully know whether or not the aging of the immune system affects our health, which is why this research will be expanded to the other 4000 participants of the SCAPIS study.

While people cannot change their sex and age, they can change their lifestyles. This study presents new information that can be used to help people improve their health. For example, I get the common cold once every few months and sometimes the grueling symptoms last for weeks. In the future, I will try to increase my fiber intake over a long period of time, which could possibly lower my chances of getting sick, feeling the harsh symptoms, or having them for a long time. I invite any and all comments to tell me whether or not this information could influence your lifestyle, and how.

This Immune Cell Might Be the Key to Getting Rid of Your Allergies

There is still so much to discover about the human body. Since we are made up of 100 trillion cells, we are constantly learning more and more each day about our cells, their functions, and the processes that they contribute to.

One such cell, known as an innate lymphoid cell, was discovered about a decade ago, but all we knew was that it functions similarly to T-cells. As we learned in AP Biology, helper T-cells cells play a large role in our adaptive immune system response, releasing cytokines, which activate more helper T-cells, cytotoxic T-cells, and B-cells to fight invading pathogens and infected cells. Innate lymphoid cells are also able to release cytokines but are a part of the innate immune system, hence why they are known as the innate counterparts of T-cells. Because of their overlapping functions, many scientists believed their function to be redundant and unnecessary… until now!

ILC Cell 3

Research from the Emmy Noether Independent Junior Research Group led by Dr. Christoph Klose in Charité has shown that group 2 innate lymphoid cells (ILC2s) are a vital part of the immune response. By using an animal model and single-cell sequencing, the scientists were able to determine the main functions of ILC2s. The team found that the presence of ILC2s relates to the development of eosinophils, disease-fighting white blood cells, which help promote the immune response of inflammation. Without ILC2 present, eosinophils were not fully developed and were unable to get involved in the inflammatory processes in the tissue. The scientists also discovered that ILC2s promote epithelial cells to produce mucus and expel parasites from the body. Without ILC2s, it became increasingly difficult to produce mucus in the tissue and to combat parasites. With this study, ILC2s have finally been recognized for their own roles in the immune response!

Dr. Klose took this study one step further by examining the relationship between ILC2s and symptoms of allergies. As inflammation and increased mucus production are common symptoms of allergies and ILC2s are linked to both, it is understandable the results demonstrated symptoms of allergies were improved when ILC2s were not present. Dr. Klose hopes to conduct further research on these cells and believes they may be the key to developing new allergy therapies. It is incredible to see how gaining a better understanding of one of our cells can unlock a door to new treatments, medications, and advancements in the field of medicine.




There’s A Fungus Among Us

Recent discoveries suggest that certain types of fungi that are responsible for severe lung infections have become more widespread in the United States. 

The first type of fungi, Histoplasma, responsible for histoplasmosis infections, was previously only found in the Midwest, and sporadically (no pun intended) found in parts of the East and South. 

Histoplasma pas-d

Medicare records from 2007 through 2016 reflect a serious cause for concern: 47 states and Washington D.C. have now reported a significant amount of cases of histoplasmosis. The second type of fungi, Blastomyces, which is responsible for the lung infection blastomycosis, has followed a similar pattern to Histoplasma

How do these infections occur? People inhale the spores from these harmful fungi, and they attack our immune systems. They do this by attacking B and T cells. The T and B memory cells ultimately remember the pathogen to prevent a repeated infection, and in the meantime, the cytotoxic T cells attempt to destroy the cells that the pathogen has already infected. The infection occurs if the immune system is unable to fight off the pathogens. 

Coccidioidomycosis is the third type of lung infection that has become more widespread. Coccidioides fungi used to only exist in the southwest, but have spread throughout the entire Western region of the United States. 

Letting these lung infections go undiagnosed can be fatal, so scientists hope that these recent discoveries will push doctors to test for fungi more frequently when confronted with patients that have lung infections.

Why is SARS-CoV-2 able to evade our immune system?

On December 1st, 2022,  Nature Immunology published an article based on discoveries, founded by University of Birmingham researchers, regarding why SARS-CoV-2 still continues to invade our bodies and harm our immune systems!

Structural model of SARS-CoV-2 infection - Oo 422117

In an experiment funded by the National Institute for Health and Care Researcher, CD4+ T cells (which are a necessity for our immune systems to protect from viruses) were tested at the beginning of the pandemic in healthcare workers that were infected with COVID- 19. This experiment determined that T-cells were successfully able to identify epitopes in the spike protein of SARS-CoV-2 but as SARS-CoV-2 continued to  evolve and mutate, the T-cell recognition was impaired. Against certain variants of SARS-CoV-2 such as Omicron, it was shown through this experiment that the T-cell recognition was less effective against the Omicron variant. Due to SAR-CoV-2 constant mutation affecting the role of our T- cells, this causes a lack of protection from our immune system which effects our health. This relates to biology class where we have been learning about how our immune systems can fight and prevent viruses, such as SARS-CoV-2. We have discussed the central roles of T- cells and how “helper T- cells” recognize antigens and stimulate humoral and cell mediated immunity by releasing cytokines. Learning about how vital T- cells are to our bodies while fighting off viruses makes me understand why after 3 years we are still being affected by SARS-CoV-2 virus!  This is also interesting to understand why certain variants of SARS-CoV-2 can be more detrimental to our health than other variants.

Healthy Human T Cell

This study also makes it clear that while the current vaccines are still essential to protect us from COVID-19, researchers are continuing to develop new vaccines that are specific to other variants.


Next Time You Think Losing An Hour Or Two Of Sleep Won’t Hurt… Think Again.

We’ve all been there. It’s a busy week, it’s getting late, and you’re tired, but you still have a lot to do for tomorrow.

A Cartoon Man Sleeping At Work

You convince yourself that if you sacrifice your sleep during the week and make it up on the weekend everything will be okay. Right? Well, unfortunately, according to the Mount Sinai School of Medicine, quite the opposite is true.

Research completed by Mount Sinai Hospital demonstrates that reducing the amount of sleep you get each night can lead to an increased risk of inflammatory disorders and heart disease. The researchers monitored 14 healthy adults that normally sleep 8 hours a night and had them sleep 6-7 hours for 6 weeks. They then drew and analyzed their blood, finding an increased number of immune cells, many of which did not function properly to protect against infections. An increased number of immune cells may seem beneficial, but in reality, if the number gets too high, immune cells can overreact and create inflammation. The DNA structure of the cells was also altered, which provides evidence for their decreased ability to defend against illnesses.

The researchers continued the study with testing on mice and found that even after having sleep recovery time, the mice still had changes in their immune system. The mice’s immune cells were rewired and reprogrammed to function under the stresses of having disrupted sleep, producing more white blood cells, which put the mice at a greater risk of having inflammation or a disease. These results serve as evidence to prove that sleep recovery cannot reverse the effects of lack of sleep.

Diagram of a white blood cell CRUK 028

The cells experience this change due to limited time to repair injured cells. As we sleep, our bodies turn their attention to our immune system, repair damaged cells, and release growth hormones. When we have disrupted or limited sleep, our bodies are not able to carry out these functions, causing greater susceptibility to health problems. It is important that our cells are able to complete their tasks, and it’s even more important that we can remove and replace cells that cannot. As we learned in AP Biology, the lysosome plays a major role in helping damaged cells perform apoptosis (programmed cell death). If our bodies are not given the time to carry out apoptosis and replace old damaged cells with new immune cells, our bodies are at greater risk for metabolic abnormalities and replication errors, connecting sleep deprivation to disease risk. So the next time you’re thinking of sacrificing sleep to do work, I hope you remember the health consequences and reconsider your decision 🙂


A Vision For a Better Future

CRISPR is a world changing technology that is essentially used to edit genes. The discovery of CRISPR took place in the University of Alicante, Spain. Reported in 1993, Francisco Mojica was the first to characterize CRISPR locus. Throughout the 90s and early 2000s, Mojica realized that what was once reported as unique sets of repeat sequences actually shared common features, which are known to be hallmarks of CRISPR sequences. Through this finding, Mojica was able to correctly hypothesize that CRISPR is an adaptive immune system. In the year 2013, Feng Zhang, was the first scientist to successfully adapt CRISPR-Cas9 for genome editing in Eukaryotic Cells. Zhang was able to engineer two different Cas9 orthologs and he then demonstrated targeted genome cleavage in both human and mouse cells. They discovered that this system could then be used to target multiple genomic loci and could also drive homology directed repair.

CRISPR-Cas9 mode of action.png

How Does it Work?

“Clustered regularly interspaced short palindromic repeats,” also known as CRISPR, are repeats found in bacteria’s DNA. CRISPR-Cas9 was adapted by scientists from a naturally occurring genome editing system in bacteria. This bacteria captures parts of DNA from invading viruses and it uses them to create DNA segments known as CRISPR arrays. This DNA allows the bacteria to recognize and remember the virus’s. If the same virus, or a similar one, attacks again, the bacteria will consequently RNA segments in order to target the viruses DNA. After, the bacteria uses the enzyme Cas9 in order to cut the DNA apart, thus disabling the virus. Scientists in a lab will create small pieces of RNA that attach to a specific target sequence of DNA and also the Cas9 enzyme. In this process, the RNA is used to recognize DNA and the Cas9 will cut the targeted DNA. Once cut, researchers will utilize the cell’s ability to repair DNA in order to add or remove pieces of genetic material. It can also replace existing DNA with custom DNA in order to make changes.

How is it used?

CRISPR is a tool that can be used to fight cancer among other known diseases. The therapy involves making four modifications to T-cells. T-cells are cells that help fight cancer. CRISPR adds a synthetic gene that gives the T-cells a claw-like receptor. This receptor can locate NY-ESO-1 molecules on cancer cells. CRISPR is then used to remove three genes. Two of the removed genes can interfere with the NY-ESO-1 receptor and the third limits a cell’s cancer killing abilities.

Another way CRISPR is used is against Leber’s Congenital Amaurosis(LCA). LCA is a family of congenital retinal dystrophies that results in vision loss. Patients tend to show nystagmus, sluggish pupillary responses, decreased visual acuity and photophobia. The CRISPR trial focuses on one gene mutation that causes a severe form of degeneration. It is said that this mutation creates somewhat of a “stop sign,” and RNAs will target sequences on either part of the stop sign. The Cas9 enzyme will then cut them out, allowing the DNA to then repair itself.

Why Our Brain Wants Us to Adopt Routine Exercise in the New Year

In her article titled The Year in Fitness: Shorter Workouts, Greater Clarity, Longer Lives, Gretchen Reynolds outlines the many studies done that prove different ways that physical activity aids in our body’s overall health and well-being, even improving our brain power. 

Fitness news throughout 2021 revolved around the length of our workouts in connection to our health. Research has proven that short workouts are enough to improve strength in both college students and adults. This key evidence proves that in order to maintain your weight and health jAbdominal Exerciseust a few minutes of working out every day should do the trick if you don’t have enough time. On the other hand, we have learned that losing weight may be even harder than we think. Many studies have reinforced the idea that on days that we exercise we are actually burning fewer calories than when we don’t, making it harder to lose weight. Despite these findings, exercise helps us to maintain our weight and is essential in our overall health. 

Furthermore, exercise can also enhance our brain power and lend a hand to our creativity. From multiple experiments done this year scientists have found that “physical activity fortifying immune cells that help protect us against dementia; prompting the release of a hormone that improves neuron health and the ability to think (in mice); shoring up the fabric of our brains’ white matter, the stuff that connects and protects our working brain cells; and likely even adding to our creativity”. There was even a study done that showed that physically active people thought up more creative and inventive ways to use umbrellas and car tires than those who didn’t partake in as much exercise. In connection to what we have learned in AP Biology this year, the immune system protects our body against pathogens. Since physical activity strengthens our immune cells, it will in turn help our overall health and wellness in the long run, protecting us from various diseases. 

In preparation for the new year, Reynolds discusses a study that reported that those who were active had a much stronger sense of purpose in their lives. Reynolds discussed with the leading scientists of the study and found that “exercise amplified people’s purposefulness over time, while simultaneously, a sturdy sense of purpose fortified people’s willingness to exercise” creating almost a perfect symbiotic mutualism relationship towards one’s health and wellness. For me personally, exercise does just this. I find that on the days I workout I feel more productive, more efficient, and am eager to take on the rest of my day. 

Overall, taking in all of this year’s exercise research, we should prioritize exercise in the coming new year if we want to use our brains with continuing clarity and for optimSquatsal creativity in the coming years. I know that I will be continuing to prioritize working out every day, even if it is just a quick walk to start my day. My favorite workouts are strength training and walking outside. Comment below the workouts you’re going to carry into the New Year and if they have had any significant effect on your daily life, health, and brain power. 



The Key to SARS-CoV-2 Survival

Can your chance of surviving SARS-Cov-2 be predicted? It sure can be due to recently combined research efforts by ISB, Fred Hutchinson Cancer Research Center, Stanford University, Swedish Medical Center St. John’s Cancer Institute at Saint John’s Health Center, the University of Washington, the Howard Hughes Medical Institute. It comes from studying your immune system and a special part of your endocrine system, your metabolism

The researchers sampled the blood of nearly 200 COVID-19 patients. They took two draws per patient during the first week after being diagnosed with SARS-CoV-2 infection, totaling 374 blood samples. The researchers then analyzed their plasma and single immune cells. The analysis included 1,387 genes involved in metabolic pathways and 1,050 plasma metabolites. 

“We analyzed thousands of biological markers linked to metabolic pathways that underlie the immune system and found some clues as to what immune-metabolic changes may be pivotal in severe disease,” says researcher and graduate student from Fred Hutchinson Cancer Research Center, Jihoon Lee. Well, what were these clues? The clue is the link between how certain metabolic changes regulate how immune cells react when it comes to disease severity and predicting patient survival. Basically, increased COVID-19 severity leads to increased immune-related activity. 

Image drawn by author

With these new discoveries, researchers used single-cell sequencing to further investigate. They found that each major immune cell type has a distinct metabolic signature. “We have found metabolic reprogramming that is highly specific to individual immune cell classes (e.g. “killer” CD8+ T cells, “helper” CD4+ T cells, antibody-secreting B cells, etc.) and even cell subtypes, and the complex metabolic reprogramming of the immune system is associated with the plasma global metabolome and are predictive of disease severity and even patient death,”  says Dr. Yapeng Su, a research scientist at Institute for Systems Biology.

Despite the need for more advanced single-cell multi-omic analysis, this research has proven to be very successful. It provides significant insights for developing more effective treatments against COVID-19. What do you think about this research being used for predicting survivability for other diseases to come? 

Needle in a Haystack

Immunization is defined as the action of making a person immune to infection by the process of inoculation. While the COVID-19 vaccine may be new, vaccines have actually been around for a lot longer than you may think. We’re used to getting vaccines through needles when we go to the doctors office, but what if I told you that that’s not the only way to receive one. Hundreds of years ago, Buddhist monks actually used to drink snake venom in order to build immunity to it. Though more formally, Edward Jenner is considered the founder of vaccinology after successfully inoculating a 13 year old boy in 1796 with a smallpox vaccine. The 13 year old actually demonstrated immunity and the first small pox vaccine was officially developed in 1798. While that may be just a brief recount of the history of vaccines, the significance of their revolutionary effects will follow humanity to the end of time. Through vaccines we’ve immunized viruses such as Chicken Pox, Polio, Influenza, Hepatitis A, Hepatitis B, HPV, Measles and many more. These viruses plagued the world in the past, but many of them are now obsolete.

While these vaccines may be different in nature, they all have one similarity… They are administered through needles. The “proper” term inoculation, however it is not specified how the virus needs to be administered. Monks used to drink snake venom and that was considered inoculation. So that begs the question… Does a needle really need to inject a vaccine? The answer is no.

The sterility of each batch of vaccine is tested before it leaves the laboratory. USPHS (United States Public Health Service) Rocky Mountain Laboratory, Hamilton, Montana 

Title and other information from caption card.Transfer; United States. Office of War Information. Overseas Picture Division. Washington Division; 1944.More information about the FSA/OWI Collection is available at note: owibatch1Film copy on SIS roll 1, frame 1090. 01/01/1942

How does the COVID-19 vaccine work?

The COVID-19 vaccine is considered an mRNA vaccine. Normal vaccines would put an inactivated germ into our bodies in order to build immunity. An mRNA vaccine uses mRNA that is created in a laboratory in order to instruct our cells on how to make a protein. The COVID-19 is administered through the upper arm muscle and it enters muscle cells. Inside these cells, the mRNA is assembled in the Endoplasmic Reticulum to form spike proteins. The mRNA that is injected is coded to constantly recreate the spike protein and it is displayed on the surface of the cell and our immune system will respond with antibody production.

What are other Methods of Vaccination?

According to Victoria University, there is more than one way to administer a vaccine. While they’re usually administered with a needle, you could also administer one using Jet Injectors. These Jet Injectors date back to the mid 1860s. They penetrated the skin and administered the vaccine without a needle. The method included a spring-loaded injector where a spring is released to deliver the vaccine. Another method of administering the vaccine is a liquid jet injector that uses very small volumes of liquid that is forced through very tiny microscopic holes in your skin, also not requiring a needle. This method was used during clinical trials against HIV and it is also utilized in some influenza vaccinations. A third method of vaccination is a band-aid-like patch that contains 400 tiny needles. It is said that if the vaccine were administered through antigen-presenting cells in the skin than into muscle cells the chances of the DNA (A DNA based vaccine) entering the nucleus would increase. The researchers created a delivery system by attaching DNA sequences encoding SARS-CoV-2 spike protein on the surface of nano-particles. The tiny needles were then coated with the nano-particles. After this, the patch would then be applied onto the skin, painlessly penetrating it.

Jet injector gun.jpg


Can HCQ(Hydroxychloroquine) Prevent COVID-19 Infection and Help Recovery? The Research Says “No”

Have you ever wondered what chemicals and such are being used to treat and illness you have? HydroxychloroquineWell, for treatment of the COVID-19 vaccine, one of the chemicals used is hydroxychloroquine (HCQ), also known as Plaquenil. HCQ is a immunosuppressive drug and anti-parasite that can treat and prevent malaria, lupus, and arthritis.

HCQ was used as pre-exposure prophylaxis against COVID-19 infection in healthcare workers as a study. There were 1294 participants from ages 24-38 with 61% being women. 273 (21.1%) of the participants were healthcare workers but still 83 (6.4%) of them tested positive after duty. This showed that the use of HCQ had no effect on the prevention of the COVID-19 virus.

What made hydroxychloroquine an option used in preventing COVID-19 in the first place? Symptoms of coronavirus disease 2019 2.0There are typically four phases of a more severe version of COVID-19. The first phase would be the incubation period that has a median of 5.1 days. After that is the second phase which lasts around 5-10 days where flu-like symptoms arise. These include, fever, cough, muscle pain/soreness, fatigue, nausea, and diarrhea. Up until the second phase, the severity of the illness can be considered normal. After the second phase, there is normally a progression to a hyperinflammatory acute respiratory distress syndrome (ARDS). ARDS is a life-threatening lung injury that makes breathing difficult. As the second phase progresses onto the third phase, ARDS causes dyspnea, tachypnea, and sometimes hypoxemia making a person extremely out of breath and in need for hospital care. During this third phase, a person affected severely of COVID-19 will normally have high fevers with elevated inflammatory markers and progressive formation of organ failure. For some of these severe cases of COVID-19, effective treatments were desperately needed.

From data of previous epidemics, HCQ have been widely used around the world for Ebola, H7N9 influenza, and SARS virus infection. HCQ has been used to treat a number of auto-immune diseases by raising intracellular pH and affect endosomal activity. However, in the case of COVID-19, HCQ has no positive effect in preventing the coronavirus and may even cause more harm to our bodies.


As an immunosuppressive drug, it made sense to give HCQ to patients with early onset of COVID-19 and as a pre-exposure prophylaxis. HCQ impacts cytokine production and suppresses antigen presentation. The medication was used in various ways: as an oral medication by itself to take before contracting COVID-19, taking it after contracting COVID-19, and combined therapy with azithromycin. None of these ways had a surprising result in preventing COVID-19 or with helping a person recover. It was then believed that the impact of cytokine production and suppression of antigen presentation may cause immunologic consequences resulting in the hampering of the innate and adaptive antiviral immune response, possible making it more dangerous with patients with COVID-19. It has been determined that HCQ is not suitable for the treatment of COVID-19.

The process of proving HCQ effectiveness in fighting COVID-19 can be related to AP Biology because of the way the medication works with the immune system. Hydroxychloroquine is a medication that can raise intracellular pH and affect endosomal activity. Acidity of cell pH and endosomes are topics that we learned first quarter. In relation to the second quarter, HCQ is a immunosuppressive drug known to impact cytokine production and antigen presentation. Cytokines and antigens are part of the innate and adaptive immune system that we learned about recently.

SARS-CoV-2 and Our Evolving Immune Systems

A scientific study analyzed in a recent article by Monique Brouillette brings hope with the emergence of possibly more infectious COVID-19 variants. The study looks at the blood of people who are vaccinated, and people who recently have had COVID-19, to learn more about the cells in our immune system. Studying and seeing these cells create their own way to counteract mutations could mean the evolution of our immune systems in response to the variants. So the study poses the question: Along with our cells ability to respond to the initial SARS-CoV-2 virus invasion, do our bodies adapt so that those same cells can recognize the new variants?

An Immunologist at the Rockefeller University, Michel Nussenzweig, conducted a study along with his colleagues by testing the blood of individuals both one month and seven months after they had COVID-19. The scientists noticed that individuals had lower levels of antibodies, and equal or higher levels of memory B cells, seven months after having COVID-19 than one month after. This was expected as the virus had been fully cleared by the seven month mark, and memory B cells were created in response to the initial invasion of SARS-CoV-2.

Memory B cells are created by the humoral response. This is when macrophages or dendritic cells recognize a forign antigen (in this case SARS-CoV-2), and stay in the body near its lymph nodes with the ability to recognize the virus.

Memory B cell response

If someone were to get infected for a second time, these memory B cells would activate to quickly produce antibodies and block the virus. This is called the secondary immune response (pictured on the right).

The scientists then did another test in the study. They tested reserve B cells and antibodies someone produced in response to SARS-CoV-2 against a version of SARS-CoV-2 they created to be more like a new variant. The replica new variant virus was made to be more like the new variants by having a mutation in the spike protein, which is the part of the virus that binds to our cells. When they tested this, they saw that some reserve B cells produced antibodies that went and attached to the mutated spike proteins, showing that the reserve B cells and antibodies from SARS-CoV-2 were able to adapt and recognize a different or mutated version of SARS-CoV-2.

New COVID19 mutant (SARS-CoV-2 VOC-20201-01)

Example of SARS-CoV-2 Mutation

The SARS-CoV-2 variants have many similar elements to the original SARS-CoV-2, but also contain mutations in their spike proteins and receptor binding domains (for the most part), which allow them to usually go undetected by our bodies. This is why those who are vaccinated or have SARS-CoV-2 antibodies are not fully immune to the variants.  

Most recently, Nussenzweig and his team conducted the same experiment again, but with new and improved viruses that more closely resemble the COVID-19 variants. One of the replica variants is of B.1.351, which contains mutations K417N, E484K, and N501Y, was tested against cloned six month old (previously exposed to SARS-CoV-2) B cells. Although it has not yet been reviewed and confirmed, this test did show that some of the antibodies produced by these B cells had the ability to recognize and attach to these mutated variants engineered to be very similar to the viruses of the Covid variants. 

What these scientists discovered with SARS-CoV-2 is a process called somatic hypermutation. This is when the immune system adapts to recognize and attack forign mutations or viruses it has not seen before when they have previously fought off a virus with some similar elements. The occurrence of this process with SARS-CoV-2 gives us hope that after getting the vaccine or having had COVID-19, our bodies will have a better defense against the new variants, which will, hopefully, in turn, lessen the fear and stress surrounding the emergence of new SARS-CoV-2 variants.  




Omicron: The Latest Invader

As it has been for the past few years, COVID-19 is the talk of the town. However, just when things seemed to be dying down, a new variant made its way into our lives. It goes by the name “Omicron”.

Unlike the past two variants, Delta and Mu, Omicron presents a whole new dilemma in the fight against COVID-19. After Delta took the world by storm with significantly greater infection rates than Mu, seemingly nothing could get worse. However, over 30 mutations to the spike proteins of the virus now trumps Omicron above all other variants. Identified in South Africa on November 24, 2021, Omicron has already made its way to many other countries around the world, including the US.

The threat of Omicron derives from its ability to resist the effects of the antibodies of the vaccine due to the changes in the protein structures. As we learned in our AP Biology class recently, the vaccine works by stimulating the production of plasma B cells, which secrete antibodies to identify and neutralize the antigen of the COVID-19 virus by recognizing the spike proteins, as well as B memory cells that exist to prevent further infection of the virus. The many changes to the spike protein make the antibodies unable to properly detect and neutralize it, allowing for the virus to continue to spread throughout our bodies. Virologist Penny Moore warns of the reduced effects the vaccine will have against Omicron, as well as the exponentially faster infection rates that pose threat to the world.

6VSB spike protein SARS-CoV-2 monomer in homotrimer

A recent study from a South African virologist, Alex Sigal, isolates blood samples from 12 Omicron infected patients who have been vaccinated with the Pfizer vaccine. The study shows that the antibodies from the vaccine are nearly forty times less effective against Omicron than the other two variants. This uncovers that the vaccine may not be efficient enough to combat the new virus. Sigal’s experiment also found that people previously infected with the virus held stronger immunity to Omicron than those with the vaccination. This is due to the fact that natural B memory cells made are able to evolve for multiple months to help fight against COVID-19 while B memory cells from the vaccine only evolve for a few weeks. Though, the experiment was not done with enough patients to make a certain conclusion.

Although, there is a glimpse of hope to retain some immunity against Omicron using the booster shot. Pfizer-BioNtech research has indicated that the third dose of the vaccine can produce antibody levels against Omicron that closely resemble the antibody levels of only two shots against the prior variants. Scientists have begun to branch off from the traditional concept of stimulating production of plasma B-cells to create antibodies in hope to find a new way to trigger the immune system to adapt to new COVID-19 variants. Biologist Jesse Bloom suggests a deeper dive into the function of T-cells, particularly cytotoxic T-killer cells, and their ability to destroy cells already infected with the virus.

Omicron poses severe potential threats to the state of the world with its fast infection rate and immunity to the vaccine. The studies of the few infected patients with Omicron do not seem to promising, but not enough has been collected about Omicron to determine its true potential. The only thing we can do now is hope for the best!



How COVID-19 Antibodies Are Causing Long-Term Effects

The COVID-19 vaccine has been essential in flattening the curve of the pandemic, but there have been reports of various side effects derived from the vaccine. These side effects include allergic reactions, heart inflammation, and blood clotting. These symptoms have been commonly thought to be because of the patient’s immune system. But, this question as to why these immune responses to both the vaccines and responses to the virus itself have been possibly answered in a new article in The New England Journal of Medicine.

COVID-19 vaccines (2021) A

Various types of the COVID-19 Vaccine


William Murphy and Dan Longo, both Professors of Dermatology and Medicine respectively, believe that the Network Hypothesis by Niels Jerne contains insight as to why these side effects occur. In this hypothesis, Jerne details the process as to which the immune system regulates antibodies. This process is a cascade, in which the immune system launches antibody responses initially to an antigen. These antibodies can trigger an antibody response toward themselves, causing them to disappear over time. Anti-idiotype antibodies, also known as secondary antibodies, bind and deplete the initial antibody responses. They have the ability to act like the original antigen itself, which would initiate side effects to the person. 


SARS-CoV-2 spike protein, the protein responsible for binding to ACE2 Receptors

SARS-CoV-2, the virus that causes COVID-19, enters the body by binding its protein spikes to the ACE2 receptor, thus gaining entry into the cell. The immune system then reacts by producing antibodies for the virus, which neutralizes the effects of the virus. However, these antibodies can cause immune responses with the anti-idiotype antibodies. These secondary antibody responses clear the initial antibodies, which results in the depletion of the initial antibodies and a weakened efficiency for antibody production. 


Murphy states that “A fascinating aspect of the newly formed anti-idiotype antibodies is that some of their structures can be a mirror image of the original antigen and act like it is binding to the same receptors that the viral antigen binds. This binding can potentially lead to unwanted actions and pathology, particularly in the long term.” He and Longo also believe that these anti-idiotype antibodies can also target the same ACE2 receptors. 


In an article published by The Conversation, the ACE2 receptors play an important role in the immune response against SARS-CoV-2. The authors, Krishna Sriram, Paul Insel, and Rohit Loomba, write that the “SARS-CoV-2 virus binds to ACE2 – like a key being inserted into a lock – prior to entry and infection of cells. Hence, ACE2 acts as a cellular doorway – a receptor – for the virus that causes COVID-19.” Personally, this fact baffles me, since it’s truly both amazing and terrifying that non-living viruses are able to manipulate and finesse their way into infecting the host cells. 


Returning to the main article, the ACE2 receptors could be responsible for the long-lasting effects being reported to both the vaccine and the virus itself. These responses can also answer why these long-term effects can occur, even long after the infection has passed. 


These terms are apparent in our AP Biology classroom, specifically regarding the Immunity System. The immune response used to combat SARS-CoV-2 is Adaptive Immunity, which develops after exposure to pathogens including bacteria, viruses, toxins, or other foreign substances. Due to the complexity of SARS-CoV-2, Adaptive Immunity is used because it’s a specific but slower response to the virus. Both B Lymphocytes and T Lymphocytes are used in the response against COVID-19 but during different stages of the infection. When the virus first enters the body, the Immune System performs Humoral Response, in which B Cells bind to the antigen and secrete antibodies that are made by B-Plasma cells, and these antibodies are stored in the B-Memory Cells to prevent future infection. In the case that COVID-19 enters and infects a cell, the Cell-Mediated Response is used to kill off infected cells using T-Killer Cells and T-Memory Cells are created to prevent future infection.

How do you think this research will be implemented for the prevention of these long-term effects? Let me know in the comments below and stay safe!

14 Days or 14 Months?

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

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

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

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

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

Primary immune response 1

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

anti-idiotype antibody

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

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