BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: antibodies (Page 1 of 2)

Could Sharks be the Solution to Ineffective SARS-CoV-2 Antibody Treatments?

Sharks are often associated with gruesome stories of attacks and horror. However, lead researcher at the University of Wisconsin-Madison School of Medicine and Public Health, Dr. Aaron LeBeau believes sharks deserve to be recognized in a more positive light– due to their potential for creating advanced neutralizing antibodies (NAb) therapeutics for treating SARS-CoV-2.

Ginglymostoma cirratum bluffs

Neutralizing antibodies have demonstrated efficacy in treating SARS-CoV-2 in previous trials. In the recent past, the FDA authorized two NAb therapeutics for emergency use for SARS-CoV-2. However, the effectiveness of these two treatments has been complicated by the development of new variants with highly mutated target antigens. These naturally occurring mutations in the target antigen result in insufficient neutralization of the virus when using those current therapeutics derived from classical human antibodies. 

This is news for concern as genome sequencing exposed the virus to create two single-letter mutations each month

As we learned in our AP Biology class, mutations to proteins such as SARS-CoV-2 antigens occur within the amino acid chains in the protein’s primary structure. These changes in chemicals could alter the kinds of covalent or ionic bonds in the protein’s tertiary structure. This, of course, changes the antigen’s three-dimensional shape. This is why the original NAbs have experienced diminished performance as new variants emerged. The antibodies from the treatments simply could no longer recognize the virus’ new antigen structure.

Therefore, there is a dire need for the development of new, more specialized NAbs, that can recognize the newly mutated epitopes that are currently incompatible with current neutralizing antibody therapeutics.

Dr. Aaron LeBeau believes that key findings for creating more efficient NAb treatments could be derived from the likes of nurse sharks! Within the immune systems of sharks, antibody-like proteins called Variable New Antigen Receptors (VNARs) were found to be highly effective at neutralizing coronaviruses, according to his recent publication in the Nature Communications journal.

Due to the small and highly specialized structure, VNARs are able to access and bind to epitopes that human antibodies normally couldn’t. This superior ability allows VNARs to reach deep into pockets and grooves within the target antigen, allowing for a better fit and neutralization. Dr. LeBeau’s research team concluded that their data suggests that VNARs would be effective therapeutic agents against emerging SARS-CoV-2 mutants, such as the Delta and Omnicron variants. 

With the help from researchers from the University of Minnesota and the Scottish biotech company, Elasmogen, the team hopes to develop the shark antibodies for therapeutic use within 10 years.

Do you think this is promising news? How do you feel about using shark “antibodies” in place of our own for serious cases of SARS-CoV-2? Assuming it’s safe, effective, and accessible to you, would you accept this treatment if you contracted a serious case of SARS-CoV-2? Please leave your thoughts in the comments.

Optimus Prime, Megatron, Proteins? The New Transformer Vaccine Candidate!

Amid the global outbreak of COVID-19, with no end in sight after nearly two years, the future wellbeing of humans is in danger. Coughs, fevers, and shortness of breath have lent way to millions of deaths across the globe. As thousands of researchers relentlessly work to find solutions to this virus, multiple vaccine candidates have emerged. Specifically, in the United States, millions of Americans have received doses of the Pfizer-BioNTech, Moderna, and Johnson & Johnson’s Janssen vaccines. However, scientists at Scripps Research recently recognized a new, self-assembling COVID-19 vaccine as a potentially more efficient and effective way to fight this worldwide battle.

 

Primarily, it is critical to understand how vaccines function as they help protect the immune system. The COVID-19 vaccines currently in effect are mRNA-based; in other words, the messenger RNA signals one’s body to produce a harmless viral protein that resembles the structure of a spike protein. The body, with the help of T-Helper cells, recognizes this structure as a foreign invader as B cells bind to and identify the antigen. The T-Helper cells will then signal these B cells to form B-Plasma cells and B-Memory cells. When getting the vaccine, the B-Memory cells are especially important as they prevent reinfection. This is a process known as adaptive immunity. Here, in the event of future infection with the spike-protein COVID-19, the memory cells would help carry out the same response more quickly and efficiently. Essentially, this process acts as the body’s training in case of any future infections.

 

While the Scripps Research COVID-19 vaccine would evoke a similar immune response to that described above, it differs from other candidates in how it assembles in the human body; this new vaccine would be comprised of proteins that are able to self-assemble. On their own, these nanoparticle proteins would transform into a sphere protein structure surrounded by smaller proteins, mimicking the coronavirus’s shape. Here, the self-assembled spike proteins are more sturdy and stable than in an mRNA-produced structure. Thus, it more accurately prepares the body for future infection with COVID-19. In fact, multiple tests found that mice who were given the experimental vaccine were able to fight off not only SARS-CoV-2 but also SARS-CoV1 along with the alpha, beta and gamma variants.

 

Nonetheless, influencing the public to get a newer vaccine instead of the well-trusted vaccines already in production requires proof of the candidate’s benefits. Primarily, as mentioned, early results find that this new candidate would perform well with many different strains of COVID-19. Additionally, researchers assert that this vaccine would be relatively simple to produce on a mass scale. Lastly, scientists found that this vaccine may well be more protective and long-lasting than current vaccine candidates. Although the process of vaccine approval is lengthy and often difficult, I am hopeful for the future of the Scripps Research vaccine if it is put into production. Moreover, I believe that such experimentation with self-assembling nanoparticle proteins transcends the current pandemic. The benefits of this field present a wide array of opportunities, and I look forward to seeing what its future may hold.

 

What do you think? Are these transformer-like self-assembling particles a gateway to the future of medicine or an unnecessary distraction from effective treatments already in circulation?

We’ve Been Programmed to Fight Coronaviruses since 6 Years Old

It was previously thought that after initial infection your body creates antibodies tohelp your immune system in the future. But did you know that a common cold you had at a young age can affect how your react to covid today? Depending on the specific spike protein, your body may have a positive or negative response to future variants. An article by Rachel Brazil describes this as “original antigenic sin”(OAS) and has been linked to the differing immune responses to COVID-19.

THE HISTORY BEHIND OAS.

In 1960, Thomas Francis Jr, a US epidemiologist, noted that the immune system seemed to be ‘permanently programmed’ to produce specific antibodies against the first strain of flu it encountered. These antibodies would then reactivate when a flu virus shared similar epitopes to that of the first strain. Relating to SARS-CoV-2, the varying coronaviruses cause different immune responses from person to person. Similar to this, we learned about memory cells in AP Bio. Once the adaptive immune response takes place memory B, helper T, and cytotoxic cell are created to support future immunity to that specific virus.

child sick

Microbiologist at the University of Pennsylvania in Philadelphia, Scott Hensley, spoke with the author of the original article about his team’s work with OAS. “Much like flu, most of us are infected with these common coronaviruses by the age of five or six,” says Hensley. It’s surprising to learn that a coronaviruses have been around for many years before the pandemic. What’s even more surprising is that a simple cold we had as a kid can affectus even today. Hensley and his group analysed blood serum samples taken before the pandemic. Their findings were that the samples had antibodies that defended against a ‘common cold’ coronavirus called OC43. These antibodies could also bind to the SARS-Cov-2 spike protein. Hesley’s group then took samples from before and after SARS-Cov-2 infection for testing. Results showed that infection boosted the production of the antibodies that bind to OC43. They also found that these OC43-binding antibodies bound to the S2 subunit of the SARS-CoV-2 spike protein(due to its similar structure to that in OC43). On the other hand, the antibodies did not bind to the S1 region of the SARS-CoV-2 spike and were unable to stop the virus entering cells.

IS THIS A GOOD OR BAD THING?

Hensly’s group once again were studying OAS, but focused on its effects during the 2009 H1N1 pandemic. Their study showed that past infection to other historical flu strains provided protection against the H1N1 virus. While this may seem good, OAS also has drawbacks. The body may produce antibodies that could be used for other virus strains, but they may not be the best fit for the specific virus. As a result of this the ill equipped antibodies bind to the antigens preventing the body from creating more protective response. 

In her article Brazil mentions Aldolfo García-Sastre, director of the Global Health and Emerging Pathogens Institute at the Icahn School of Medicine at Mount Sinai in New York City. García-Sastre observed the levels of the OC43 binding antibodies in patients hospitalized with COVID-19 in Spain. He found an increase in levels of OC43 binding antibodies along with antibodies for HKU1(another betacoronavirus). García-Sastre claimed that, “We looked for a correlation between people mounting higher [levels of] antibodies against these conserved epitopes versus having less protective immunity against SARS-COV-2, and there was a slight correlation”.

THE VERDICT: THERE ISN’T ONE…YET

Because of the varying reactions that follow OAS, the debate on whether or not it is to be seen as beneficial is polarizing. Though th, scientists are still working to find ways to use it in potential vaccines. Comment below to let us know your opinion on the matter!

 

COVID-19 May Induces Cell That Produce Antibodies for Life

Once in our body, SARS-CoV-2, the virus that causes COVID-19, forces the body’s innate immune system to activate. However, the innate immune system response typically is deemed unsuccessful due to the complexities of the virus’s structural components, which then paves way for the body’s adaptive immune response to initiate. As we learned in Biology, adaptive immune response begins with a macrophage engulfing SARS-CoV-2 through phagocytosis. Then, the MHC proteins present on the macrophages, white blood cells that surround and kills microorganisms, remove dead cells, and stimulates the action of other immune system cells,” display the antigen on the surface, creating a ‘wanted’ poster for the immune system (Cancer.Gov). We also learned that eventually, a T-Helped cell comes along and binds to the displayed antigen, which activates the T-Helper cell which fosters the secretion of interleukin, a cytokine. Finally, both B and T cells are stimulated, which then begin the process of fighting off the virus, along with preventing reinfection. One of the cells that assists in the preventing reinfection are B-Plasma Cells, which are, “antibody-producing immune cells [that] rapidly multiply and circulate in the blood, driving antibody levels sky-high”(WashU School of Medicine).

Tingible body macrophageOne crucial step in determining a person’s ability to fight reinfection is testing to see if antibody secretion has either occurred or is currently occurring. While typical blood samples will suffice, “the key to figuring out whether COVID-19 leads to long-lasting antibody protection, Ellebedy [ PhD, and associate professor of pathology & immunology] realized, lies in the bone marrow”(WashU School of Medicine). The B Lymphocytes, which initiate a humoral response, mature in the bone marrow, and so, to determine the prevalence of antibody secreting cells, bone marrow samples must be received from past COVID-19 patients. To determine if antibody production increases after the body completes its fight against, Ellebedy collected blood samples and “As expected, antibody levels in the blood of the COVID-19 participants dropped quickly in the first few months after infection and then mostly leveled off, with some antibodies detectable even 11 months after infection” (WashU School of Medicine). However, people who exhibited mild cases of COVID-19, meaning that their body removed the virus after two to three weeks, antibodies continue to secrete antibodies, and will continue for an indefinite time period.

Covid-19 San Salvatore 09One problem introduced was rooted in the mainstream media, which spread a misinterpretation of data, being that “antibodies wane quickly after infection with the virus that causes COVID-19” (WashU School of Medicine). Ellebedy believes that this is a major misinterpretation of data, and actually means that antibody production is continuing inside of the bone marrow. Typically, antibody production plateaus after a certain period of time preceding infection, yet these numbers don’t go to zero.

Ellebedy concludes that this result is highly promising, especially for people who experienced a more severe infection from SARS-CoV-2, because an increased amount of circulating virus cells typically leads to a stronger immune response due to the body being required to secrete more antibody cells. Although she believes that more studies need to undergo in people who experienced moderate to severe infections, and show if they also have the same everlasting antibody production.

 

 

 

 

 

 

Is A Vaccine Update On Its Way?

On December 11, 2020, the Pfizer-BioNTech COVID-19 vaccine was approved for its first public use. Since that day, there have been multiple variants of the virus, varying in their mutations from the original strain. One of these strains, in particular, is the Omicron variant. This variant is a new strain of COVID-19 and was first identified on November 24, 2021, in Botswana. With the emergence of this new unknown variant, in addition to all of the past variants, has the time come for an updated vaccine that is tailored specifically to the variants? This question is explored in the Bloomberg article Third Pfizer-BioNTech Dose Is Ket To Fight Omicron’s Spread

Solo-mrna-vaccine-8

After researching the Omicron variant in relation to two doses of the COVID-19 vaccine, there was seen to be a 25% reduction in antibodies capable of fighting the virus. However, after a third dose of the vaccine, increased antibody levels close to that of those made for the original COVID-19 strain. With this information in mind, Pfizer stated that an Omicron-specific vaccine may be required. This new vaccine is projected to be ready for the public by March of 2022. The company also stated that their vaccine would change from a two-dose to a three-dose vaccine with the third shot being for Omicron. The third shot would be administered about three months after the first two doses have been given.

Fab fcfragment colors

While the public is waiting for the third dose from Pfizer, Pfizer says that people should use their current vaccine for a third dose, as it would give further protection against the virus. Then, once the Omicron vaccine comes out in early 2022, people should get a dose of that vaccine as well. This new strategy of getting the vaccine is due to new research from multiple labs on the effectiveness of the vaccine on the Omicron variant. An original observation saw a 25 times drop in antibodies, but two other labs found that there is actually a 40 times reduction with this variant. Globally, South Africa found a 41 times drop in antibodies, and a 37 times drop from a German lab. With this research, Pfizer is beginning to look into an Omicron vaccine but must find that it heavily increases protection against the new variant, and if not it will keep the current vaccine in circulation. There is also speculation about a yearly booster for the vaccine, but there must be research conducted on that as well.

The COVID-19 Vaccine: How, What, and Why

We have all seen the news lately – COVID, COVID, and more COVID! Should people get the vaccine? What about the booster shot? Are vaccines more harmful than COVID-19? Will my child have birth-defects? This blog post will (hopefully) answer most of your questions and clear up a very confusing topic of discussion!

Discovery of monoclonal antibodies that inhibit new coronavirus(Wuhan virus)

First off, what are some potential effects of COVID-19? They include, but are certainly not limited to, shortness of breath, joint pain, chest pain, loss of taste, fever, organ damage, blood clots, blood vessel problems, memory loss, hearing loss tinnitus, anosmia, attention disorder, and the list goes on. So, our next question naturally is: what are the common effects of the COVID-19 Vaccine? On the arm that an individual receives the vaccine the symptoms include pain, redness, and swelling. Throughout the body, tiredness, a headache, muscle pain, chills, fever, and nausea can be experienced. To me, these effects seem much less severe than COVID-19’s!

COVID-19 immunizations begin

Now that we have covered effects, you are probably wondering what exactly the COVID-19 Vaccine does – will it make it impossible for me to get COVID-19? Will I have superpowers? Well, you may not get superpowers, but your cells will certainly have a new weapon, which we will discuss in the next paragraph! The COVID-19 Vaccine reduces “the risk of COVID-19, including severe illness by 90 percent or more among people who are fully vaccinated,” reduces the overall spread of disease, and can “also provide protection against COVID-19 infections without symptoms” (asymptomatic cases) (Covid-19 Vaccines Work).

So, how does the vaccine work? Many people think that all vaccines send a small part of the disease into us so our cells learn how to fight it at a smaller scale. However, this is not the case with the COVID-19 vaccine! As we learned in biology class, COVID-19 Vaccines are mRNA vaccines which use mRNA (genetic material that tells our cells to produce proteins) wrapped in a layer of fat to attach to cells. This bubble of fat wrapped mRNA enters a dendritic cell through phagocytosis. Once inside of the cell, the fat falls off the mRNA and the strand is read by ribosomes (a protein maker) in the cytoplasm. A dendritic cell is a special part of the immune system because it is able to display epitopes on MHC proteins on its surface.

Corona-Virus

After being made by the ribosomes, pieces of the viral surface protein are displayed on the surface of the dendritic cell (specifically the MHC protein), and the cell travels to lymph nodes to show this surface protein. At the lymph nodes, it shows the epitope to other cells of the immune system including T-Helper Cells. The T-Helper Cells see what they’re dealing with and create an individualized response which they relay to T-Killer cells that attack and kill virus-infected cells. This individualized response is also stored in T-Memory cells so that if you do end up getting COVID-19, your body will already know how to fight it! The T-Helper Cells additionally gather B-Plasma cells to make antibodies that will keep COVID-19 from ever entering your cells. T-Helper Cells are amazing! As you can see, the vaccine never enters your nucleus, so it cannot effect your DNA! No birth-defects are possible!

You are now equipped with so much information and able to disregard many common misconceptions about the COVID-19 vaccine! Additionally, you can make an educated decision about whether or not you should get the vaccine. I think yes! If you have any questions, please feel free to comment them and I will answer. Thanks for reading!

 

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

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!

How Killer T Cells Could Increase Immunity Against New COVID Variants.

In recent news, there are concerns about the newly discovered COVID variant named Omicron. Preliminary evidence suggests an increased risk of reinfection with this variant, as compared to other variants of concern. Scientists are hopeful that T cells could provide some immunity to COVID-19, even if antibodies become less effective at fighting the disease.

Along with antibodies, the human body’s immune system produces a plethora of T cells which target viruses. Helper T cell’s stimulate killer T cells, macrophages, and B cells to make immune responses. T cells do not prevent infection because they kick into action only after a virus has infiltrated the body. But, they are important for clearing an infection that has already started. If killer T cell’s are able to kill virus-infected cells before they are able to spread to from the upper respiratory tract, it will affect how you feel and will be the difference between a mild infection and a severe one.

Studies by Sette and his colleagues have shown that people who have been infected with SARS-CoV-2 typically generate T cells that target at least 15–20 different fragments of coronavirus proteins. But, the protein particles that are targeted vary from person to person. This means that a variety of T cells will be generated, making it difficult for the virus to mutate in attempt to escape cell recognition. Research suggests that most T-cell responses to COVID variations or previous infection do not target regions that were mutated in recently discovered variants. If T Cells remain active within your immune system against specific variants, they might protect against severe diseases.

Ultimately, in my opinion, this is extremely important since researchers have been analyzing clinical-trial data for several coronavirus vaccines in attempt to find clues as to whether their effectiveness fades in the face of new emerging COVID variants such as Omicron. As of now, coronavirus vaccine developers are already looking at ways to develop next-generation vaccines that stimulate T cells more effectively. Antibodies only detect proteins outside cells, and many coronavirus vaccines target spike proteins, located on the surface of the virus. Since spike proteins are liable to change, it may be prone to mutating and raising the risk that emerging variants will be able to evade antibody detection. T cells, on the other hand, can target viral proteins located inside infected cells, and some of those proteins are very stable. This raises the possibility of designing vaccines against proteins that mutate less frequently than spike proteins, and incorporating targets from multiple proteins into one vaccine.

Biotechnology firm Gritstone Oncology of Emeryville, California, is designing an experimental vaccine that incorporates the genetic code for fragments of several coronavirus proteins known to elicit T-cell responses, as well as for the full spike protein, to ensure that antibody responses are robust. Clinical trials are due to start in the first quarter of next year. If approved, this vaccine could revolutionize how we approach the creation and experimentation of COVID vaccines in the future.

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. 

Antibody Concoctions: Possible COVID-19 Prevention and Treatment?

We all have heard the exciting news about Pfizer’s COVID-19 vaccine: a possible savior and source of hope for years to come. According to a LiveScience article by Nicoletta Lanese, “an antibody cocktail designed to prevent and treat COVID-19” entered late-stage trials over the summer. Scientists have been working to find an effective treatment that doesn’t have as many limitations as current findings. A treatment known as convalescent plasma therapy has been circulating clinical trials. It is not FDA-approved and therefore not available to the public. Antibodies are extracted from recovered COVID-19 patients and injected into sick patients in order to boost their immune systems. This method is too unreliable and unpredictable.  The plasma donors all have a variety of antibodies. Some have proven to be effective against the virus by not letting it enter cells in the first place. On the other hand, nothing is guaranteed and a patient could be injected with antibodies that have no effect against the virus. To reduce this risk, drug developers have noted the effective antibodies against SARS-CoV-2 and mass produced them in a lab.

This is a representation of what a spike protein would be under a microscope. The clinical trials are testing to see which antibodies can bind to the spike proteins and prevent them from entering/infecting healthy cells.

Another possible therapy called REGN-COV2 has also entered a late phase in its clinical trial. It supposedly has two antibodies that can prevent the virus from infecting healthy cells by binding to the spike protein. Hopefully the FDA approves the drug at the end of its current phase (phase 3), so short and long-term effects can be monitored. The Co-Founder, President, and Chief Scientific Officer of Regeneron, Dr. George Yancopoulos, released this statement: “We are running simultaneous adaptive trials in order to move as quickly as possible to provide a potential solution to prevent and treat COVID-19 infections, even in the midst of an ongoing global pandemic.” Many other pharmaceutical companies continue with their trials to search for antibody treatments against the SARS-CoV-2 virus. The universal goal is to find a longer-term solution and stop the rising mortality count.

I originally chose the topic of prevention, because I thought it was only going to include mask-wearing and social distancing. It’s incredibly interesting that this article is another scientific take on preventative measures. The article shows how hard scientists and companies are working on developing a treatment. My main intention for this topic was to show how important it is for everyone to partake in the effort to stunt the spread of the pandemic. With recommended safety procedures as well as current trials, I’m optimistic that there will be great progress in our near future. I was able to link this to our AP Biology class, because we recently covered the immune system! The article refers to antibodies, and I know that they are the humoral defenses that go for pathogens. These antibodies are originally secreted from B-Plasma cells in order to bind to and neutralize the pathogens. By using plasma from recovered patients, I assume they are relying on the B-Memory cells to prevent infection/re-infection in other patients.

Please let me know what your thoughts are in the comments! How much longer do you think we’ll have to wait? Do these new updates give you hope about returning to a state of normalcy? I’d love to know.

UPDATE

Since the summer of 2020 (when this article was released), a lot has changed. Regeneron’s antibody cocktail was granted an Emergency Use Authorization in November. While this seemed to be heading the trials towards an optimistic future, that was not the case. Presently, only the Moderna and Pfizer mRNA vaccines are FDA-approved for public use. What happened to REGN-COV2? According to this Washington Post article, 80% of the allocated dosage supply is remaining unused in overcrowded hospitals. There is a common sentiment that resources should not be going towards an “unproven treatment”. The only FDA-approved antibody in the Regeneron cocktail is bamlanivimab. Although we are all eager to return to normalcy, we must be conscious of what is the best for our health.

Testing!

When you hear the word “COVID -19 testing” what comes to mind? I have this vivid image of a cotton swab being pushed up my nose. But what exactly is testing? Why is it so important? And what are the types of testing available for our use?

We’ve all heard that testing is important but why? To summarize a supplementary article, COVID testing “leads to quick identification of cases, quick treatment for those people and immediate isolation to prevent spread” (Dr. Eduardo Sanchez). When discovered at an early stage, COVID will be less a threat to a person because doctors can plan accordingly while COVID is still less severe. Even when a person discovers they have COVID not as early as hoped, testing helps to identify anyone who came into contact with infected people so they too can be quickly treated. Contact tracing would not be possible without testing because a person would never know if they are spreading the virus. The only way to be better safe than sorry is to get tested. Someone may show symptoms that are COVID-like but there is still a chance that it could be a common cold, or allergies. It is important to confirm COVID suspicion.

Now that we know why testing is important, what kind of testing is out there? What I found in this FDA article is what I like to call a family of tests; there are numerous different tests to take.

To start things off, let’s talk about Diagnostic testing. Diagnostic testing shows if you have an active coronavirus infection. As of right now, there are two types of diagnostic tests: molecular and antigen tests. Molecular tests detect the virus’ genetic material in a sample from the patient’s nose or throat. This is where test results will take longer because they are sent to labs. From there, the lab essentially converts the virus’s RNA into DNA, and then make millions of copies of the DNA to be processed in a machine. The test is “positive” for infection with SARS-CoV-2, the virus that causes COVID-19. Examples of molecular diagnostic tests include nucleic acid amplification test (NAAT), RT-PCR test, and the LAMP test. Next, there is Antigen diagnostic testing. Antigen tests provide results from an active coronavirus infection faster than molecular tests. The downside to these tests are that they have a higher chance of missing an active infection. Sometimes an antigen test may come back negative, but a doctor might still order a molecular test to confirm.

Different from Diagnostic Tests, there are Antibody (different from Antigen) tests. These tests looks for antibodies that are made by your immune system in response to a threat, such as a specific virus. As we learned in biology class, antibodies can help fight infections. These tests are taken by finger stick or blood draw, and the results are quick. The antibody test only shows if you’ve been infected by coronavirus in the past. But do antibodies help diagnose COVID-19? As we learned in class about the Immune System, our body can fight pathogens, bacteria, and viruses that we have been previously exposed to. While this was a popular belief earlier on in the year, sadly, researchers do not know if the presence of antibodies means that you are immune to COVID-19 in the future. It is possible to contract COVID-19 for a second time, therefore adaptive immunity does not apply.

The most common testing that I knew of before researching was rapid testing. Rapid testing can be both a molecular or antigen diagnostic; a doctor uses a mucus sample from the nose or throat. The test can also be taken at home only by prescription of a doctor. The results are available in minutes. There is also saliva testing where a person can spit into a tube; this also keeps the doctor or worker safer from the potentially infected person.

Testing is the best way to keep yourself and those around you safe. While testing is still not 100% accurate, there is currently no better way to confirm if someone has COVID-19 unless he/she get tested. With this pandemic, we can never be too safe!

 

 

 

 

 

The Reoccurring Virus?

The spread of the SARS-CoV-2 virus, the virus that causes Covid-19, which is more notoriously known as the coronavirus, has been deemed by some to be one of the worst pandemics ever seen. With over 13.5 million cases and over 200 thousand deaths, the pandemic has taken the world by storm. In an article, Jop de Vrieze speaks on a topic that is of concern in regards to the subsiding of this virus, the topic of reinfection.

In our body, antibodies are our natural defenders. These antibodies are part of the body’s adaptive response to pathogens. Generally, B Lymphocytes(B cells) binds to an antigen and recognize it. T-Helper cells then cause the selected B cells to divide into B-Plasma cells and B-Memory cells. The B-Plasma cells then secrete antibodies which bind to the pathogen and then neutralize it, allowing Macrophages to engulf and destroy the antibody-covered pathogen. B-Memory cells help the cell be able to remember the pathogen, ultimately preventing reinfections. Antibodies are defined by Mayo Clinic as “proteins produced by your immune system in response to an infection. Your immune system — which involves a complex network of cells, organs and tissues — identifies foreign substances in your body and helps fight infections and diseases.” When you contract the virus, your body develops these antibodies that can help provide protection. But there’s a catch. The CDC says that ” we do not know how much protection the antibodies may provide or how long this protection may last,” which opens up the possibility for reinfection.

Specific to de Vrieze’s article, a man in Hong Kong tested positive for the coronavirus in March and tested positive again in August, becoming the first official reinfection case. Neurologists have, reasonably, expected much milder symptoms from reinfection cases, but that hasn’t been the case for some. As the CDC stated, the amount of protection and the protection’s longevity is still a big question. The leading case in de Vrieze’s article was that of Sanne de Jong. After having the virus and mild symptoms in Mid-April, she tested negative in May and then tested positive again in June. What is so special about her “reinfection” case is that when her virus samples were taken, they were very similar. This is of significance because it correlates to another, yet more unlikely, theory mentioned in the article. When the article was written, “no proof exists of mutations that would make the virus more pathogenic or that might help the virus evade immunity. But a recent preprint by a team at the Swedish Medical Center in Seattle suggests one may exist. The team describes a person who was infected in March and reinfected four months later. The second virus had a mutation common in Europe that causes a slight change in the virus’ spike protein, which helps it break into human cells. Although symptoms were milder the second time, neutralization experiments showed antibodies elicited by the first virus did not work well against the second, the authors note, ‘which could have important implications for the success of vaccine programs.'”
The possibility of reinfection is rare but is still very possible. And other mysteries of the coronavirus are still present. Here is my advice: Play it safe. With the uncertainty and danger surrounding the virus, the best thing we can do is prevent the spread and protect ourselves and others. The need for concern can pass if we are simply patient.

The Superhero Powers of COVID-19 Antibodies!

Antibodies are superheros that could save many people from the devastating effects of COVID-19. Defined broadly, antibodies are proteins in the blood that are formed in order to fight against antigens and foreign substances. An article put out by the CDC on November 3, 2020, states that there is not enough information to make a formal conclusion regarding the ability of COVID-19 antibodies to protect someone from being infected again by the virus. Nonetheless, a more recent article released by Nature on December 7, 2020, counteracted that statement by analyzing a study in which Dan Barouch and his colleagues tested which elements defend against COVID-19 using rhesus macaques (monkeys). According to the study, only a very low level of antibodies is required to defend a host against COVID-19. Furthermore, when antibodies are low, T cells are found to contribute to immunity.

In the study, the team took antibodies from masques recovering from SARS-CoV-2 and distributed the antibodies to healthy masques. The antibodies successfully protected the masques from the virus and even activated antibody-dependent natural killer cells, boosting immunity. These results suggest that the injection of antibodies could be very successful in defending individuals from COVID-19.

This information regarding antibodies connects to topics covered in AP Biology. Our immune system protects our body against pathogens such as SARS-CoV-2 through adaptive immunity. Two types of lymphocytes are necessary for an adaptive response: B Lymphocytes and T Lymphocytes. B cells are responsible for a humoral response (or antibody-meditated response) and secrete antibodies. Thus, when someone contracts COVID-19, the activated B cells in their body secrete antibodies that will bind to and neutralize SARS-CoV-2.

The fact that only a low level of antibodies is required to defend a host against COVID-19 is vital information for scientists. Extracting the antibody-producing B cells of an infected patient, medical experts could use the genetic information to create a massive amount of antibodies to be turned into a drug for distribution. This injection would help patients infected with SARS-CoV-2 fight off COVID-19. Thus, antibodies could save many lives and are, therefore, real life superheros!

ARE WE DOOMED? Maybe not

     Well, this year has been a ride. Starting off with a potential WWIII, continuing with the tragic loss of hall of fame athlete Kobe Bryant, 2020 has been one roller coaster of a year. But the most bizarre of it all was the COVID-19 pandemic. The pandemic swept the nation way back in March and it still has its grasp on us today. At the time it started, there was very little information on this virus. But now, due to our vast intricate technologies, we were able to find out lots of information on this virus. But, specifically, I want to talk about life after contracting the virus. See, normally when you have a virus and successfully heal from it, you develop antibodies so you will not get this type of virus again. The case is a bit different for COVID-19, or it might be the same. Read to find out!

     This topic is very interesting because there have been more than 10 million people who have acquired the virus. The people that have successfully recovered from the virus want to know the main question: Will I be able to get this virus again? The answer isn’t so simple. Early on the data provided to us gave us hope that the immunity to this virus was possible, but numerous cases also suggest that this immunity to the virus is brief (on a larger scale). Nothing is definite as of now, there is more research to be done, but for now we remain hopeful. 

 

So why do we say the immunity to the virus is brief?

     We know there is hope because there is proof that people who have contracted COVID-19 produce antibodies that protect our immune system, but this production of antibodies lasts maybe 3 to 4 months based on the data provided. The length of time still remains unclear. 

 

So how does this actually work?

     Researchers from Massachusetts General Hospital tested three types of antibodies in blood samples: immunoglobulin G (IgG), immunoglobulin A (IgA), and immunoglobulin B (IgB). Immunoglobulin is a large Y-shaped protein used in the immune system to detect foreign invaders in the blood such as viruses. These proteins bind to these foreign invaders in order to fight them off. We learned from our unit with proteins that antibodies are a form of proteins that can influence the life of a molecule/virus. The most important of all the immunoglobulins stated above is IgG. The reason is because IgG has the potential to sustain immunity in the body. This is because when all three of these antibodies were found in the blood after being infected by COVID-19, IgA and IgB were obliterated by the spike protein found in COVID-19. But, IgG lasted in the stream for up to four months! Now, the researchers could not test IgG for that long, but the four months that they could observe showed that these IgG antibodies do persist to beat the virus! A more long term study is definitely needed. This study is also confirmed by another research group from the University of Toronto. This group also showed how IgA and IgB levels dropped rapidly about 12 days after infection while IgG levels remained steady. 

 

So can you get COVID more than once?

     Although it is very rare, there have been some cases where people contracted the virus more than once. But, there is no evidence that suggests that immunity is or is not possible. All in all, evidence shows that immunity after acquiring the virus is generally protective and the persistence of the IgG antibody provides hope for immunity to the virus. – Ghohesion

How Reliable Are Covid-19 Tests and What Are The Different Types of Tests?

For my study of research, I’ve decided to learn more about Covid-19 testing and its effectiveness. In this article, How Accurate Are COVID-19 Tests? Many Factors Can Affect Sensitivity, Specificity of Test Results, it discusses several methods of testing, along with how accurate the results are. The article also goes into detail about what factors can affect the tests accuracy. 

Sensitive tests, which are positive results, are less likely to produce a false-positive outcome, and a specific test, negative results, are less likely to produce a false-negative outcome. Labs can provide the analytics of sensitivity and specificity for a test, which is concluded from confirmed specimens of positive and negative results. These results, however, come from when someone either had a great exposure, or none, so they are true under ideal conditions. Since there is so much variability between patients, the numbers are often lower when they are under real life conditions. 

There are two main types of testing for the novel Coronavirus. The first type of test detects RNA from the virus by using methods such as, polymerase chain reaction (PCR). I have never heard of this process before, so I decided to find a source explaining what it is. PCR is used to amplify, which is making many copies of a gene or DNA. Using this process, many copies can be created, just from a small part of the DNA taken for the sample. This process can help to identify a pathogen when trying to detect a virus, such as the novel Coronavirus. This past week in class, we learned about the immune system and about the characteristics of viruses. We learned that a virus has spike proteins on the outside, and it has RNA strands in the inside of the cell. This connects to what we learned about RNA and viruses, because this test actually tests for RNA to see if a patient has the virus. they are more accurate because they are from the genetic sequence from the virus itself, which is unique to it. If a test comes back positive, it is most likely accurate. The second type of test is molecular testing. The nasopharynx is said to have the largest concentration of a virus. Since using NP swab samples, nasopharyngeal swabs, are hard to get, the sensitivity of a test can be altered or tampered. This can create a false-negative result in a patient, who really could have it. Testing with saliva and blood has more of a likeliness to reduce the sensitivity. The article also mentions that swabbing the patient in the oropharynx or nose can also have a lower sensitivity. 

Antibody testing is through drawing blood from a vein, and it can detect whether or not someone was infected by Covid-19. The test uses enzyme immunoassays and rapid lateral flow immunoassays. By day 14 following symptoms appearing, most patients did have the IgG antibodies. I wasn’t exactly sure what an IgG antibody was, so I found a source to explain that in some more detail. It is an immunoglobulin and is found in all fluids within the body. They are the most common and small antibodies that are in the body. These antibodies help to fight bacterial infections and viruses. These antibodies are actually the only ones that can help protect a woman’s fetus, which is very interesting. As time goes on, it is less likely that the antibodies will be detected. There is some evidence, not confirmed yet, that suggests that children and asymptomatic or mild-symptom patients could be less likely to have detected antibodies. 

I found this article to be very fascinating because it went into detail about each test and its effectiveness. I didn’t know that children and asymptomatic or mild-symptom patients were less likely to have detectable antibodies. I am excited to research more as I continue to further my studies in Covid-19 testing. 

 

Can your common cold help you beat vicious COVID-19?

Season colds are quite common, and while they are inconvenient and make us feel icky, they may be our advantage for our battle with COVID-19. 

To start off, when reading this article, I noticed that the author used the term “coronavirus” more casually. He referred to a “coronavirus” as a common cold, which of course left me confused. So I dug a little deeper…

Here’s a fun fact that I learned from this:

Many of us having been thinking that COVID-19 is the same as what we call the “coronavirus.” After reading an article differentiating the difference between the terms, I found that the term coronavirus is actually the broad term to describe a whole range of viruses. SARS-CoV-2 is the specific virus that causes only COVID-19 and is causes what doctors call a respiratory tract infection.

Basic biology tells us that while there are many cells that make up our body, they are all interconnected. A pathogen, like the SARS-CoV-2 virus, is an enemy to the cell. We learned about how things enter the cell in biology: the pathogen enters the cell, travels through the cytoplasm, and enters the nucleus. Because the virus has genes, it is able to rapidly produce copies of itself to infect the other cells. And of course, we know how scary these infected cells are when they start spreading to the lives around us given our situation with a global pandemic.

What we now know is that the SARS-CoV-2 virus, our “bad guy,” can actually induce memory B cells. These memory B cells survive for quite a long time; they are important in identifying pathogens, and creating antibodies to destroy such pathogens. So when we got sick during the winter last year, chances are these memory B cells fought them off. The key part of the memory B cell in our fight against COVID-19 is the cell’s ability to remember the antibodies it created from past illness for the future.

What does this mean?

The belief is that anyone infected by COVID-19 already has the memory B cells from past common colds to fight the virus off.  Taking a further step, it is believed that since everyone already has the memory B cells, anyone who has had COVID-19 in the past is unlikely to get it a second time. If the SARS-CoV-2 virus were to enter your body a second time (which is likely considering the virus has not gone away and is literally all around us), our bodies would be prepared with former knowledge of the antibodies used to fight and win this time.

A study performed at the University of Rochester Medical Center is the first to demonstrate how this may be so.

Mark Sangters, Ph.D., is a research professor of Microbiology and Immunology at URMC; he has backed up his findings by comparing different blood samples. When looking at 26 blood samples of recovering moderate COVID- 19 patients (people who have had it for their first time now), it seems that many of them had a pre-existing pool of memory B cells that could recognize the SARS-CoV-2 virus and rapidly produce antibodies to destroy it. He also studied 21 blood samples of healthy donors, collected years before COVID-10 existed. What he found was that these B cells and antibodies were also already present.

When we are sick with a common cold, our antibodies are created by memory B cells to attack the Spike protein. This protein is what helps viruses infect our cells. What Sangters noticed, is that although each Spike protein is different for each illness, the S2 portion of the Spike protein is the same throughout all sickness. Our antigens can not differentiate the parts of the S2 subunit, so they attack the Spike protein regardless. This was his final piece in his conclusion that our common colds that caused our memory B cells to make antibodies, could be used to fight against COVID-19.

The Long Road Ahead:

My concern with this article is that this is the biggest issue we face with COVID-19 is patient outcome. As of right now, there is no way to fully prevent everyone from COVID-19 because it is still all around us. The issue the world is facing, is how to treat those who have already contracted the virus. This information just simply is not enough to help. How will these memory B cells help those who are currently sick? The answer: Scientists are unsure. There is still the uncertainty of the future vaccine and study of these memory B cells for a possibility of milder symptoms or shorter length of illness from COVID-19.

 

Despite all of this concern, this is still a step in the right direction. Any information about this terrorizing virus is still helpful given how little we know about COVID-19. If we were to expand more on this information, we could save the lives of those around the world!

 

 

Milking Scorpions yields $10,300/ml Antibiotic Venom

Why is it important?

Who would have thought that Scorpions could be providing useful antibiotics through their venom, something most would think of as a harmful substance. It was found that while testing the venom of a Mexican Diplocentrus melici scorpion, a previously studied venom, the venom could be split into two parts. The two types are called Escherichia coli and Mycobacterium tuberculosis bacteria” and when separated they both have specific uses. One of the parts was red and the other blue, it was found that one part was good at killing Staphylococcus, and the other was good at combatting Tuberculosis. Due to these findings, the scientists saw parts of the venom as potential antibodies.

(Scorpion Diagram) 

The Testing:

The two parts of the venom where both tested on rats. It was found that both parts respectively combatted the staph bacteria and the TB. The researchers, however, are skeptical as to whether the antibodies would work as well in humans, and how they would measure the correct amount to be administered to a human given that the substance is so difficult and/or expensive to obtain.

The High Pricetag:

“When electrical stimulation is used to “milk” the venom glands of scorpions, an average yield of anywhere from 0.006 mg to about 2.0 mg of venom can be obtained from a single scorpion.” Not a lot, right? But according to Scientific American, the “milk” from a single scorpion sells for about $10,300 per Milliliter, thats nearly $39 Million per gallon. The reason for its high price tag is its low quantity per scorpion and how inconvenient it is to extract the venom. Each scorpion also takes about two weeks to replenish its venom.

Conclusion:

While the thought of administering scorpion venom as a medical treatment, in my opinion, sounds awesome, it may not be the most realistic method. The testing proves that it does work for combating TB and Staph microorganisms, however, the tests were done on rats. Until the venom can be said for certain to be effective for humans, and there is a MUCH cheaper cost, I’m not sure how feasible it is to treat people with scorpion venom.

 

Strong Genes Equal Strong Immune System

Although scientists have long agreed that antibodies are in integral part of building up the body’s immune system, there is new evidence that strongly suggests genetic factors play a large role in determining how well the immune system builds and uses these antibodies when fighting disease.

https://commons.wikimedia.org/wiki/File:Redhead_twins.jpg

In a recent study, “researchers from James Cook University’s Australian Institute of Tropical Health and Medicine (AITHM) and the University of Queensland’s (UQ) Diamantina Institute have analyzed blood samples from 1835 twins and thousands of their siblings.” The team looked at the body’s immune response to “six common human viruses, including the Human Herpes virus, Parvovirus, Epstein Barr virus and the Coxsackie virus.” The team determined that genes passed down by parents are the major factor in how powerfully an immune system responds to diseases. “These genes determine whether you mount an intense or weak immune response when confronted with a viral infection,” says Associate Professor Miles.

“Demonstrating that antibody response is heritable is the first step in the eventual identification of individual genes that affect antibody response.” The researchers’ next goal is to identify the superior genes in order to, “imitate ‘super defenders’,” and “design next generation vaccines.”

 

IS THAT POISON IVY???

Scientists have discovered a possible new treatment to prevent itching from poison ivy, a painful nuisance that affects up to 50 million Americans annually. Using an antibody for the protein interleukin-33, scientists were able to drastically reduce itching in test mice. As treatment now generally doesn’t do much to combat the discomfort of itching, this is a major breakthrough in poison ivy treatment.

What is Poison Ivy?

 Poison Ivy is a plant that produces resinous oil called urushiol that covers the entire plant: stems, leaves, and roots. When this oil comes into contact with human skin, either directly or through a secondary source like an animal or tool, it triggers an allergic reaction in 85% of people, causing your immune system to attack and create an itchy rash. This rash can escalate into hives and blisters.

What is this discovery?

So far there is treatment such as antihistamines and corticosteroids that help swelling, pain and accelerate recovery, but there is no real cure for the itchiness and discomfort this rash can cause. However, by blocking a certain protein in the immune system with an antibody, one can block the signals to the brain communicating an itch on the skin. This protein is interleukin 33 (IL-33), a common protein that acts directly on the nerve fibers in the skin, exciting them and telling the brain that the skin is severely itchy. When blocking this protein, scientists conducting an experiment on lab mice were able to reduce not only inflammation, but the amount of scratching.

What does this mean?

If this treatment could be used on humans, it would provide a far more affordable and effective treatment for victims of this pesky condition, and eliminate the doctors visits, lost time at work or school, and costs of only partly helpful drugs that are now necessary for people suffering from this rash. Hopefully, the pain and annoyance that comes with Poison Ivy will soon be a thing of the past.

Image: https://commons.wikimedia.org/wiki/File:Poison_ivy-20141524-038.jpg

A Breath of Fresh Air: Epigenetic Studies Help Asthmatics

Asthma and allergies affect many people worldwide. Up until recently, treatments for both asthma and allergies were administered without an appropriate prediction of responses; However, this is about to change. In a recent study conducted by scientists at Imperial College London, “30 new genes that predispose people to allergies and asthma” were found. The discovery of these genes means that new treatments for allergies are possible and more accurate predictions for current treatment responses will be available.

Photo by Author

Photo by Author

By observing the epigenetic changes, ones that influence gene activity- not genetic code, the scientists were able to identify genes which are linked to triggering allergic responses. Such genes regulate specific antibodies. Genes become inactive through methylation: the attachment of methyl molecules to DNA. The scientists studied white blood cells of families with asthma to see if methylation levels in specific genomic locations were associated with levels of an antibody in the blood. Immunoglobin E (IgE) is the antibody studied in the case. The antibody IgE was known prior to this study, but the genes which activities it regulates were not. After monitoring the IgE levels in the blood, researchers saw a strong correlation between IgE and low methylation at 36 places in 34 genes. These genes are overstimulated in asthmatics, thus the production of IgE is increased, contributing to asthma symptoms. In expanding the investigation, researchers came to believe that IgE-involved genes may activate eosinophils, a type of white blood cell which in asthmatics promotes airway inflammation by gathering and releasing chemicals in airways/lungs. Researchers believed that these genes, and their ability to activate eosinophils, then cause the most damage. In order to test this, researchers isolated eosinophils from the blood of subjects and demonstrated that all 34 genes have high activity levels in asthmatics with high IgE levels. Thanks to the findings of new activation signals, patients can avoid high costs and ineffective “treatment-trials” because we’ll be able to predict responses to treatments with more accuracy. Professors Cookson and Moffatt, the leaders of the investigation, give credit to epigenetics for allowing them to make a breakthrough in discovering new potential drug targets for allergies and asthma and sharpening the accuracy of treatment-response predictions. Professor Cookson explained that, “the genetic code that can influence disease and DNA sequencing can only take you so far. Our study shows that modifications on top of the DNA that control how genes are read may be even more important.”

As someone who suffers from allergic asthma, I find it intriguing how the disease-triggering genes aren’t inactive, thus leading to poor lung function, but rather they are overstimulated. Our genes’ ability to regulate disease-triggering antibody activity is amazing. With new studies like this one, we can see that the solution to proper activity regulation is in epigenetic changes, rather than the broad expectations of “our genes”.  This just goes to show that epigenetics is helping us make strides in the ever-changing world of medicine. It should be interesting to see how epigenetic medical-solutions, the current gold mine of Biological research, evolve in the near future.

 

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