BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Immune System (Page 1 of 2)

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 

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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.

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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

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. 

Are Plant-Based Diets The Cure to COVID?

We all know that unhealthy diets can cause medical issues, and thus sticking to healthy foods is better, but this conversation has not been so prevalent regarding COVID. Everyone is told to “mask up,” to “get vaccinated,” and to “wash your hands, yet I cannot recall the last time someone told me to “eat healthy” to stay safe from the pandemic.

In a recent study by Massachusetts General Hospital, over half a million people in the USA and the UK participated in a smart phone symptom study that analyzed each participant’s diet and gathered data for the results. Each participant added data about their diet, which was ranked by healthiness through a “Plant-BasedDiet Score that emphasizes healthy plant foods such as fruits and vegetables.” From March to December 2020, 31,831 participants were infected by COVID, and those with better diets had a “41% lower risk of developing severe COVID-19” symptoms. They also had a 9% lower chance of getting infected.

The researchers connected these sample statistics with the socioeconomic inequality caused and reinforced by COVID. They found a relationship between “poor diet and increased socioeconomic deprivation with COVID-19 risk that was higher than the sum of the risk associated with each factor alone.” Often poorer communities have less access to healthy food, specifically plant-based ingredients that led to less severe COVID results in this study. This means that they may have a higher chance at infection, and likely will have more dangerous outcomes to COVID. This means while plant-based diets can very much help prevent the dangerous nature of COVID-19, but is not a strategy many can employ.

Why does healthy eating help fighting COVID? Well, we know that the humoral and cell mediated immune responses are crucial in building immunity and fighting against COVID. Cytotoxic T-Cells destroy infected cells, and Plasma B-Cells  create antibodies.  Macrophages also destroy antigens to help out. With all these important parts of the immune system being so important, and being attacked by COVID, the body needs food to create more.

Fcell-08-00677-g001

Vitamins and Minerals are crucial for this, and plants are the prime method of acquiring such nutrients. “Vitamin C, vitamin D, zinc, selenium, iron, and protein” all crutial in building and strengthening the immune system, as per Harvard T.H. Chan. Proteins in particular can be used by the body to create more white blood cells, which are made much of protein. Consuming too much fat and sugars will not go into the immune systems, which depresses it.

Healthy diets, including plant-based diets, are not a cure for COVID, but the data has shown it may help people. Unfortunately, it will not help everyone due to socioeconomic inequality, and is another reason why governments should focus on getting better access to healthy food in poorer communities that don’t currently have much. For those who are able to eat healthy, please do so. Not only does it help the fight against COVID, but in any sickness. These statistics are not specific to COVID, but it is important for this conversation to be had about eating healthy because the focus is often only about vaccines, masks and politics with COVID. It is not a cure, though. Getting vaccinated and wearing a mask is the best way to stop the spread, and I highly suggest everyone get vaccinated.

This study also supports the new plant-based diet trend. Many skeptics do not want anything to do with this diet, but from athletes like Serena Williams using it, to this study supporting it, plant-based diets are getting results.

How Mice and Mental Health Led to This COVID-19 Treatment Breakthrough

Ever since the initial outbreak of COVID-19, scientists have worked tirelessly to innovate and find the antidote to the virus which has infected millions and tragically killed hundreds of thousands. Such unprecedented times have led researchers to reconsider everything they already know and take intellectual risks.

One innovator whose experimental hypothesis may save many is Angela Reiersen, a child psychiatrist from Washington University School of Medicine in St. Louis. When she fell ill with COVID-19 in March 2020, Reiersen thought back to a study she had read about the effects of the lack of the sigma-1 receptor in mice and how the lack of this receptor protein led to massive inflammation and overproduction of cytokines. Cytokines are a part of the inflammatory response that occurs when pathogens sneak past the barrier defenses of the innate immune system and permeate cells. Upon entry of a pathogen, mast cells secrete histamines and macrophages secrete these cytokines. These cytokines attract neutrophils which then digest and kill the pathogens and other cell debris. Although cytokines are crucial to a functioning immune system, overproduction of cytokines can be extremely dangerous as it can lead to septic shock, in which the immune system becomes extremely overactive. This has become the cause of death for many COVID-19 patients.

As a psychiatrist, Reiersen worked regularly with SSRIS, or selective serotonin uptake inhibitors, in the treatment of conditions like depression and obsessive compulsive disorder. SSRIs help the human brain by increasing the level of serotonin available between nerve cells, but they also activate the S1R in the Endoplasmic Reticulum. Reiersen wondered, if the lack of the S1R causes fatal levels of inflammation, can we prevent extreme inflammation from COVID-19 through the use of SSRIs?

There have been multiple studies performed to test this line of reasoning, both including and independent of Reiersen. The most notable study was performed as part of TOGETHER, an international organization seeking to test possible unorthodox treatments for COVID-19. The trial was a collaboration between researchers from McMaster University of Canada and Cardresearch, a research clinic located in Brazil. The team in Brazil located 1,497 unvaccinated adults who were deemed “high risk” for COVID complications in their first week of showing symptoms of COVID. Conducted at 11 different research sites in Brazil from January to August, the study provided participants with a 10 days supply of either 100 milligrams of fluvoxamine, an SSRI, or a placebo pill. The researchers monitored the participants for 28 days after, as well.

In the end, 15.7% of participants who were given a placebo pill ended up having major complications from COVID-19, compared to 10.1% of participants who were given fluvoxamine. The gap may seem slight, but this is because not all patients took their full dosage due to gastrointestinal complaints. However, out of patients who completed their course of medication, 66% were safe from any complications and the mortality rate was cut by 91%!

Thanks to the research of Reiersen and many others, fluvoxamine is now considered a solid treatment plan for COVID-19 infections, especially in high risk individuals. As COVID-19 continues to infect millions around the world, who knows what new scientific breakthroughs will be made?

Mutation in the Nation

We constantly think of SARS-CoV-2, the virus that causes COVID-19, as a single virus, one enemy that we all need to work together to fight against. However, the reality of the situation is the SARS-CoV-2, like many other viruses, is constantly mutating. Throughout the last year, over 100,000 SARS-CoV-2 genomes have been studied by scientists around the globe. And while when we hear the word mutation, we imagine a major change to how an organism functions, a mutation is just a change in the genome. The changes normally change little to nothing about how the actual virus functions. While the changes are happening all the time since the virus is always replicating, two viruses from anywhere in the world normally only differ by 10 letters in the genome. This means that the virus we called SARS-CoV-2 is not actually one species, but is a quasi-species of several different genetic variants of the original Wuhan-1 genome.

The most notable mutation that has occurred in SARS-CoV-2 swapped a single amino acid in the SARS-CoV-2 spike protein. This caused SARS-CoV-2 to become significantly more infective, but not more severe. It has caused the R0 of the virus, the number of people an infected person will spread to, to go up. This value is a key number in determining how many people will be infected during an outbreak, and what measures must be taken to mitigate the spread. This mutation is now found in 80% of SARS-CoV-2 genomes, making it the most common mutation in every infection.

Glycoproteins are proteins that have an oligosaccharide chain connect to them. They serve a number of purposes in a wide variety of organisms, one of the main ones being the ability to identify cells of the same organism.  The spike protein is a glycoprotein that is found on the phospholipid bilayer of SARS-CoV-2 and it is the main tool utilized in infecting the body. The spike protein is used to bind to host cells, so the bilayers of the virus fuse with the cell, injecting the virus’s genetic material into the cell. This is why a mutation that makes the spike protein more efficient in binding to host cells can be so detrimental to stopping the virus.

In my opinion, I find mutations to be fascinating and terrifying. The idea that the change of one letter in the sequence of 30,000 letters in the SARS-CoV-2 genome can have a drastic effect on how the virus works is awfully daunting. However, SARS-CoV-2 is mutating fairly slowly in comparison to other viruses, and with vaccines rolling out, these mutations start to seem much less scary by the day.

 

Restaurants: A COVID-19 Hotspot

After spending months locked in our homes, eager for social interaction, you may find yourself wanting to justify grabbing a quick bite with a friend despite the risk of COVID-19. However, this MIT Technology Review article proves that not only are restaurants the riskiest location when it comes to the coronavirus, but you are actually four times more likely to catch the virus in a restaurant than in the gym, which is the second most dangerous location.

Safegraph, a company that collects anonymous location data from smartphones, curated a team of epidemiologists, computer scientists, and social scientists from Stanford University and Northwestern University. Together, Safegraph and their new team used smartphone data to predict and understand where most people were catching COVID-19. To do this, researchers tracked nearly 100 million people through their phones in 10 of the biggest US cities from March 1 to May 1, collecting the movements of people going to gyms, grocery stores, restaurants, places of worship, etc. 

After accumulating this smartphone data, they used it to predict the level of risk each location had based on three categories: “how big the venue was, how long people stayed inside it, and how many people were likely to be infectious in the given area.” After comparing their predictions to the official records of cases, it was proven that their new prediction model was accurate. Like one may have already guessed: the smaller the venue is, the longer people stay inside it, and the larger the number of people inside the venue are all of the factors that make a location more dangerous when it comes to catching COVID-19.

Epidemiology has proved that the three factors stated above make someone more susceptible to getting COVID-19 because the virus spreads most prominently through respiratory droplets. These droplets can be spread through breathing, talking, eating, etc. In restaurants, people don’t wear masks, allowing these respiratory droplets to infect everyone around them, as they can land on surfaces as well as drift through the air. Another danger with restaurants and not wearing a mask is being asymptomatic: unknowingly contracting the virus, having no symptoms, and then going to restaurants, where you take your mask off, allowing the virus to spread to all those around you. 

Eating, talking, breathing, and possibly even laughing are almost all guaranteed when going out to eat. However, those are all the primary methods by which respiratory droplets spread. 

If you acquire an asymptomatic or mild coronavirus case, research suggests that your immune system works the same as it normally would for other viruses. When you come in contact with COVID-19, your innate immune system immediately reacts; it is the first line of defense in your immune system and releases a rapid response. This quick response is nonspecific, meaning that it is recognized as simply a pathogen, with minimal specifics. As that rapid response begins, your adaptive immunity begins to develop and form antibodies to fight the specific virus you are infected with. Because this response is more specific to the virus you have, it is also slower acting, which is why viruses take days or weeks to recover from. 

Anyway, going back to the research: Using this new prediction model, the research team simulated different restaurant situations, such as 10% capacity, 50% capacity, and even full capacity. The model suggested that implementing a 20% maximum capacity in restaurants would cut infection rates by 80%. However, from an economic standpoint, a 20% maximum capacity would result in a likely loss of 42% of customers during “peak hours.”

So, it is crucial to think about what is more important: minimizing infection rates or keeping businesses alive? Personally, I think it is necessary to find a balance where people can stay safe, and businesses can remain open, especially small ones. Restaurants have already begun thinking of safe and innovative ways to dine. For example, a restaurant in NYC has an outdoor patio with large, private pods where groups of people can eat out without exposure to the people around them. Though even this system has its loopholes and issues, it is a step in the right direction. 

Will you be going out to eat this week? 

COVID-19 May Be Behind Dangerous Blood Clots in Patients

According to an article by Erin Garcia de Jesus, a new study shows that some of COVID-19’s lethal blood clots may originate from the immune system attacking the patient’s body instead of the virus. These clots form due to excessive inflammation from an overactive immune response in severely ill patients. Researchers are now trying to figure out how this response happens. Currently, the belief is that some of the clottings may come from auto-antibodies that go after the cell membrane-forming molecules instead of the foreign invader. This attack would prompt neutrophils to release a “web of genetic material geared at trapping virus particles outside the cells.” While this process may control infections in tissue, it causes clotting in the bloodstream. Cardiologist Yogen Kanthi and her colleagues at the National Institutes of Health in Bethesda, Md., reported that “some blood clots may form when the webs trap red blood cells and platelets, creating a sticky clump that can clog blood vessels.” Blood clots in the lungs have become a significant cause of death for COVID-19 patients.

Auto-antibodies that recognize phospholipids can cause antiphospholipid syndrome (APS). APS is an autoimmune disease in which auto-antibodies can activate clot-forming cells, putting patients at a higher risk of blood clots. Extremely ill COVID-19 patients sometimes have high levels of neutrophils as well as phospholipid-binding antibodies in their blood. The belief is that antibodies may be causing the neutrophils to release traps that create clotting.

According to the study, of 172 hospitalized COVID-19 patients, more than half had auto-antibodies that recognized one of three various types of host phospholipids. When the researchers combined auto-antibodies taken from six COVID-19 patients with lab-grown neutrophils, the neutrophils cast their nets. Furthermore, when the researchers injected the same patient auto-antibodies into mice, the mice formed blood clots.

While this research is promising, Thomas Kickler, a hematologist at Johns Hopkins School of Medicine, states that “it’s unlikely that phospholipid auto-antibodies are the whole story.” Other inflammatory immune responses can also trigger clots, so the antibodies may only be part of the mystery.

On a brighter note, a process called plasmapheresis (filtering the liquid part of blood), could assist severely ill COVID-19 patients by removing the problematic antibodies.

This topic relates to our AP Biology study of the immune system. COVID-19 is a threatening virus that penetrates our immune system, and it can cause various problems in our body once it makes its way past our defenses. One of our main defenses is antibodies. Antibodies are specialized, Y-shaped proteins that bind to a foreign invader inside the body. The immune system uses the antibodies to search and mark the invader. Antibodies are a humoral response in part of the adaptive immune system which learns to recognize and eliminate specific invaders. People recovering from COVID-19 may have antibodies that are effective against the virus. Another bodily defense system is inflammation. Inflammation is an internal defense that is part of innate immunity. During inflammation, cells release histamine, and macrophages secrete cytokines. The histamines dilate local blood vessels and increase capillary permeability and cause the area to swell with fluid. Cytokines attract neutrophils and dendritic cells, and natural killer cells kill damaged or infected cells. A fever (a common symptom of COVID-19),  is a systematic inflammatory response triggered by pyrogens released by macrophages.

Is Air Pollution Exposure In Childhood Linked To Schizophrenia?

Research has shown that pollution affects physical health, but does air pollution also affect our psychological health? A study, which combines genetic data from iPSYCH with air pollution data from the Department of Environmental Science, reveals that children who are exposed to a high level of air pollution while growing up have an increased risk of developing schizophrenia.

“The study shows that the higher the level of air pollution, the higher the risk of schizophrenia. For each 10 ?g/m3 (concentration of air pollution per cubic metre) increase in the daily average, the risk of schizophrenia increases by approximately twenty per cent. Children who are exposed to an average daily level above 25 ?g/m3 have an approx. sixty per cent greater risk of developing schizophrenia compared to those who are exposed to less than 10 ?g/m3,” explains Senior Researcher Henriette Thisted Horsdal, who is behind the study.

To put this research into perspective, the lifetime risk of developing schizophrenia is approximately two percent, which is equal to two out of a hundred people developing schizophrenia in one’s life. For people exposed to the lowest level of air pollution, the lifetime risk is just under two percent. The lifetime risk for people exposed to the highest level of air pollution is approximately three percent.

“The risk of developing schizophrenia is also higher if you have a higher genetic liability for the disease. Our data shows that these associations are independent of each other. The association between air pollution and schizophrenia cannot be explained by a higher genetic liability in people who grow up in areas with high levels of air pollution,” says Henriette Thisted Horsdal about the study, which is the first of its kind to combine air pollution and genetics in relation to the risk of developing schizophrenia.

The study included 23,355 people in total. Out of those people, 3,531 developed schizophrenia. Through the results of this research one can see that there is an increased risk of schizophrenia when the level of air pollution during childhood increases; however, the researches cannot comment on the cause. Instead, the researched emphasize that further studies are needed before they can identify the cause of this association.

Schizophrenia is thought to mainly be a result of genetics, brain chemistry, substance use, and exposure to viruses or malnutrition before birth. So, I think it is very interesting that exposure to air pollution during childhood may be a cause as well. Additionally, I hope that these findings and further studies become very useful to schizophrenia research and prevention, as schizophrenia is a very serious mental illness and there is no cure.

 

Health and Disease in a New Light

Microbiota are groups of organisms that live on and in some mammals. Animals, such as humans, who live in a state of mutualism with these organisms have them mostly on parts of their body with large surface areas. This includes skin and the intestinal tract. The human gut microbiome is a complex community of organisms that have been studied over the past decades and most intensely within the past fifteen years. So far the information on the human gut microbiome is limited and the research on it is somewhat inconclusive, raising more questions than it answers questions; however, that is a side effect of most research that is just beginning to be analyzed more in depth. The idea that we are just now starting to study and understand these organisms that have lived on and in us for centuries is a topic that is cutting edge and very interesting.

Microbiota

A short coverage of information about microbiota in the intestinal tract includes the following. In mammalian animals, these organisms play an important role in the formation of intestinal mucosa as well as a healthy systematic immune system. Animals that lack microbial cells contain abnormal numbers of several immune cell types and immune cell products, as well as have deficits in local and systemic lymphoid structures. Therefore, their spleens and lymph nodes in them are poorly formed and their intestinal mucosa, deficient. Mice with a lack of microbiota were known to have a lower amount of plasma producing cells – which make antibodies of a certain type. This is due to the fact that the microbiota is regulated by the plasma cells in mammals and it is found unnecessary to have a large amount of them in animals lacking the organisms. These mice also exhibited an impaired ability to regulate cytokine levels – any of a number of substances, such as interferon, interleukin, and growth factors, which are secreted by certain cells of the immune system.

In 2010 there was a study done that was comprised of making cultures of these organisms and bacteria in the human intestinal tract outside of the human body because we do not have the necessary technology to study the microbiota in their hosts. This study yielded the publication of a paper titled “Gut Microbiota in Health and Disease” which gives a detailed overview of the findings of this study. Briefly, a colonization of mice lacking microbiota with altered Schaedler flora (ASF) was insufficient to promote differentiation of Th17 cells (which play an important role in defense against infection), despite the fact that ASF includes a number of bacteria from the Bacteroidetes phylum (microbiota). Researchers concluded the there is no way to be sure of the affects of microbiota. Meaning although there was no lack of microbiota, the mice still had an immune system deficiency in the same way that mice lacking any microbiota did. Since the health and abundance of microbiota in the gut microbiome is so closely related with the ability of the immune system of the host, it is concluded that changes in the microbiome can lead to onset of diseases/illnesses in the host. These factors can also change with environmental changes such a dietary choices of the host. Understanding the dynamics of the gut microbiome under different conditions will help us diagnose and treat many diseases that are now known to be associated with microbial communities.

Analyzing the affects of microbiota in the human gut can reveal topics about human pathology that we did not know before. Therefore, scientists look forward to the development of studies on this topic.

Don’t Kill Me Immune System! I’m a Friend.

Believe it or not, but not all bacteria is out to get you, especially some of your gut bacteria. These helpful bacteria can aid in digestion and overall healthy, but the question is, why doesn’t your immune system kill them just like harmful bacteria? In other words, how does the immune system differentiate between good and bad bacteria? For now, we are not really sure, but a study from March of this year by Immunologist Ivaylo Ivanov and his team at Columbia University could bring us closer to understanding this form of cell signaling.

The study focuses particularly on the interaction between T cells and segmented filamentous bacteria in the gut. Normally, the immune system would produce antibodies that would bind to antigens on the foreign cell’s surface. As a result, the cell would be marked for destruction by the immune system. However, through an experiment on mice, the researchers found that although the T cells were activated by the segmented filamentous bacteria, the T cells did not destroy the bacteria.

These gut bacteria located in human, mouse, and fish intestines cling themselves to the gut wall and have antigens. So why aren’t they killed? Well, the antigens are packaged in tiny vesicles located near the tip of the hook-like appendage that the bacteria uses to cling to the gut wall: the holdfast. Sorry, that’s about all I can give you. The rest is speculation at this point.

Nonetheless, Ivanov and his team discovered something previously unnoticed by finding these vesicles that hold antigens in segmented filamentous bacteria. They speculate that the T cells read antigens in different ways based on whether or not it’s exposed on the outside of the cell or packaged in a vesicle. In the end, this a big discovery that peaks my interest, especially for its implications on the study of cell signaling. What’s your hypothesis as to why the T cells don’t attack the gut bacteria?

Does Exposure to Toxins In the Environment Affect One’s Offspring’s Immune System?

A study has recently surfaced stating that maternal exposure to industrial pollution may harm the immune system of one’s offspring and that this impairment is then passed from generation to generation, resulting in weak body defenses against viruses.

Paige Lawrence, Ph.D., with the University of Rochester Medical Center’s Department of Environmental Medicine, led the study and conducted research in mice, which have similar immune system functions as humans. Previously, studies have shown that exposure to toxins in the environment can have effects on the respiratory, reproductive, and nervous system function among generations; however, Lawrence’s research is the first study to declare that the immune system is also impacted.

“The old adage ‘you are what you eat’ is a touchstone for many aspects of human health,” said Lawrence. “But in terms of the body’s ability to fights off infections, this study suggests that, to a certain extent, you may also be what your great-grandmother ate.”

“When you are infected or receive a flu vaccine, the immune system ramps up production of specific kinds of white blood cells in response,” said Lawrence. “The larger the response, the larger the army of white blood cells, enhancing the ability of the body to successfully fight off an infection. Having a smaller size army — which we see across multiple generations of mice in this study — means that you’re at risk for not fighting the infection as effectively.”

In the study, researchers exposed pregnant mice to environmentally relevant levels of a chemical called dioxin, which is a common by-product of industrial production and wast incineration, and is also found in some consumer products. These chemicals eventually are consumed by humans as a result of them getting into the food system, mainly found in animal-based food products.

The scientists found the production and function of the mice’s white blood cells was impaired after being infected with the influenza A virus. Researchers observed the immune response in the offspring of the mice whose mothers were exposed to dioxin. Additionally, the immune response was also found in the following generations, as fas as the great-grandchildren (or great- grandmice). It was also found that this immune response was greater in female mice.  This discovery now allows researchers to have more information and evidence to be able to more accurately create a claim about this theory.

As a result of the study, researchers were able to state that the exposure to dioxin alters the transcription of genetic instructions. According to the researchers, the environmental exposure to pollutants does not trigger a genetic mutation. Instead, ones cellular machinery is changed and the immune response is passed down generation to generation. This discovery explains information that was originally unexplainable. It is obviously difficult to just avoid how much toxins you are exposed to in the environment, but it is definitely interesting to see the extent of the immune responses in subsequent generations. We can only hope that this new information, and further discoveries, help people adjust what they release into this world that results in these harmful toxins humans are exposed to, and their offsprings.

 

 

 

Stem Cells and CRISPR

Many cells can reproduce but there are a few types of cells that are not able to reproduce. One of these types are nerve cells, the cells that cary messages from your brain to your body.  There are many ways nerve cells can be destroyed or damaged, by trauma or drug use.  Millions of people are effected by losing nerve cells and for so long no one could think of a way to recreate them; until the discovery of stem cells.

After fertilization, and when the newly formed zygote is growing, it is made up of a sack of cells.  Some of these cells are stem cells which develop according to their environment. Because of the behavior of stem cells, scientists theorized that if they placed stem cells in the brain or spinal chord, two areas that have an abundance of neurons, the stem cells would turn into a neuron because of the environment it was in.  But, when they tried introducing stem cells into the body, the immune system treated them as an foreign body, as it should. Our immune system has to treat anything that does not come from our body as an enemy or we could get extremely sick.  However, the downside is organ transplants, blood transfusions, etc. are dangerous because they could cause a serious immune rejection.

Someone experiencing a spleen transplant rejection

Cells have a surface protein that displays molecular signals to identify if it is self or foreign.  Removing the protein causes NK (natural killer) cells to target the cell as foreign. Scientist haven’t been able to figure out how to make a foreign cell not seem foreign until Lewis Lanier, chair of UCSF’s Department of Microbiology and Immunology, and his team found a surface protein that, when added to the cell, did not cause any immune response.  The idea would be to use CRISPR/cas9 to edit the DNA of the stem cells, and in doing so would remove the code for the current surface protein and add the code for the new surface protein.

After the scientists had edited the stem cells, to have the correct signal protein, they released them into a mouse and observed that there was no immune rejection. Truly amazing. Maybe brain damage could be helped by this science one day. Tell me your thoughts on Stem Cells in the comments!

For more information, please go check out the primary source of this article.

 

 

Message Intercepted – Commence attack on bacteria!

Tevenphage – Photo credit to Wikimedia Commons

While experimenting, a group of scientists noticed that a A virus, VP882, was able to intercept and read the chemical messages between the bacteria to determine when was the best time to strike. Cholera bacteria communicate through molecular signals, a phenomenon known as quorum sensing, to check their population number.  The signal in question is called DPO.  VP 882, a subcategory of bacteria’s natural predator, the bacteriophage, waits for the bacteria to multiply and is able to check for the DPO.  Once there is enough bacteria, in the experiment’s case they observed cholera, the virus multiples and consumes the bacteria like an all-you-can-eat buffet. The scientists tested this by introducing DPO to a mixture of the virus and bacteria not producing DPO and found that that the bacteria was in fact being killed.

The great part about VP 882 is it’s shared characteristic with a plasmid, a ring of DNA that floats around the cell. This makes it easier to possibly genetically engineer the virus so that it will consume other types of bacteria. This entails it can be genetically altered to defeat other harmful bacterial infections, such as salmonella.

Ti plasmid – Photo credit to Wikimedia Commons

Current phage therapy is flawed because phages can only target a single type of bacteria, but infections can contain several types of different bacteria.  Patients then need a “cocktail” with a variety of phages, which is a difficult due to the amount of needed testing in order to get approved for usage.  With the engineering capability of using a single type of bacteria killer and the ability to turn it to kill bacteria, phage therapy might be able to advance leaps and bounds.

As humans’ storage of effective antibiotics depletes, time is ticking to find new ways to fight bacterial infections.  Are bacteriophages and bacteria-killing viruses like VP 882, the answers?

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