BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Virus (Page 1 of 2)

Antitoxin Mechanism Saves Us From Virus Attacks!

Researchers in Lund have recently discovered an antitoxin mechanism that may be able to protect bacteria against virus attacks by neutralizing hundreds of toxins. Understanding this antitoxin mechanism, named the Panacea, could be the next step to the future success of phage therapy, a treatment for antibiotic resistant infections.

These toxin-antitoxin mechanisms are a kind of on-off switch in bacterial DNA genomes. They are found to attack bacteriophages to defend bacteria.This activation of toxins allows bacteria to “lockdown” and limit growth and spreading of a virus. In order for Phage therapy to be successful in the future, it is important to understand these mechanisms in great depth. The goal of Phage therapy is to use viruses to treat bacterial infections. A toxin dramatically inhibits bacterial growth and an adjacent gene encoding an antitoxin counteracts the toxic effect. Although toxin-antitoxin pairs have been associated with new toxins or antitoxins before, the ability of the Panacea is unprecedented.

Phage therapy

As research continues on toxin-antitoxin systems and phage therapy it is clear that what we know is just the tip of the iceberg. As bacteria increasingly become resistant to antibiotics, other approaches are needed to help eliminate infections. The next steps of this research is to continue deepening the understanding of the Panacea and finding toxin-antitoxin systems on a universal scale.

In AP biology class we learned about inhibitors. An inhibitor is something that slows down or prevents a particular reaction or process. A toxin inhibits bacteria from growing and reproducing so the antitoxin can act against the virus that has already spread.

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?

How are new COVID variants identified?

COVID variants are of high concern for scientists studying the disease. Some variants can be more infectious or cause more severe illness. Additionally, some variants can evade vaccines by having different surface proteins than the variant the vaccine was created for. This causes the antibodies produced from the vaccine to be less effective against other variants. In AP Biology class we discussed how the Delta Variant, first identified in December 2020, has a different spike protein structure than the original virus from which the vaccine was created from. This allows the variant to be more infectious, and make the vaccine less effective against it. But, what are COVID variants? And how are they discovered? Hand with surgical latex gloves holding Coronavirus and A Variant of Concern text

COVID variants are “versions” of the virus with a different genetic code than the original one discovered. However, not every mutation leads to a new variant. This is because the genetic code of the virus codes for proteins. Some mutations will not change the structure of the protein and thus not change the virus. So, COVID variants can be defined as versions of the virus with a significantly different genetic code than the original virus.

To detect new COVID variants, scientists sequence the genetic code of virus which appears in positive COVID tests. Scientists look at the similarity of the genetic sequences they find. Then, if many of the sequences they get look very similar to each other, but different to any other known virus, a variant has been discovered.

To sequence the RNA of the virus, scientists use what is called Next Generation Sequencing (NGS). To understand how NGS works, it is best to start with what is called Sanger Sequencing. Sanger Sequencing utilizes a modified PCR reaction called chain-termination PCR to generate DNA or RNA fragments of varying length. The ending nucleotide of each sequence is called a ddNTP, which contains a florescent die corresponding to the type of nucleotide. The addition of a ddNTP also terminates the copying of the particular sequence. The goal of this PCR reaction is to generate a fragment of every length from the start to the end of the sequence. The sequences can then be sorted by length using a specialized form of gel electrophoresis. The sequence is then read by using a laser to check the color of the fluorescent die at the end of each sequence. Based on the color and size, the nucleotide at that position of the genomic sequence can be found.

Sanger Sequencing Example

The difference with NGS is that many sequences can be done in parallel, allowing for very high throughput. In other words, with NGS many COVID tests can be sequenced in once.

Changing Composition of SARS-CoV-2/Understanding the Alpha Variant in England

Since its emergence in the Fall of 2020, the original SARS-CoV-2 variant of concern (VOC) rapidly became the dominant lineage across much of Europe. Although, simultaneously, several other variants of concern were identified globally. Like B.1.1.7 or the Alpha Variant (first mutation of SARS-CoV-2 found to be more transmissible), these VOCs possess mutations thought to create only partial immunity.

Researchers are understanding when and how these additional VOCs pose a threat in settings where B.1.1.7 is currently dominant. This is where scientists in the UK examined trends in the prevalence of non-B.1.1.7 lineages in London and other English regions using passive-case detection PCR data, cross-sectional community infection surveys, genomic surveillance, and wastewater monitoring. The study period spanned from January 31st of 2021 to May 15th of 2021.

Through this data, the percentage of non-B.1.1.7 variants has been increasing since late March 2021. This increase was initially driven by a variety of lineages with immune escape. From mid-April, B.1.617.2 (WHO label of Delta) spread rapidly, becoming the dominant variant in England by late May, similarly to the Alpha Variant.

Shown by many mutations in the spike protein receptor (RBD), studies suggest B.1.1.7 is 50–80% more transmissible with greater severity than previously circulating Covid Variants. B.1.1.7 rose rapidly, from near 0% to over 50% in under two months, and soon made up greater than 98% of sequenced samples in England. Its rapid spread necessitated a third lockdown in England during last January. Subsequent spread in Europe and North America has highlighted the threat this variant poses to a continued alteration of the Coronavirus.

The 69–70 deletion in B.1.1.7′s Spike gene causes PCR tests to return negative results for that gene target which is a major problem when identifying and testing for Covid. One of the most important changes in lineage of B.1.1.7 seems to be a spike protein substitution of N501Y, a change from asparagine to tyrosine in amino-acid position, that enhances transmission. These alterations can change antibody recognition while also affecting ACE2’s (receptor protein) binding specificity which can then lead to the virus becoming more infectious. We are seeing a pattern of the same type of mutation in Covid consistently.

An example of a similar mutation that has been recent is the new Omicron variant out of South Africa. Omicron is similar in which their has been a specific change in the spike protein where antibody recognition is limited and it is highly transmissible between any living organism. Our class has understood and studied the importance of our body being able to identify and create an antibody for the specific antigen being displayed by a pathogen.  These mutations within the spike protein allow another immune response to happen which a different antibody has to be created to mark the different antigen being displayed. Unfortunately, this will be a continuing problem without vaccine mandates since it gives the virus more time to mutate where outbreaks like in South Africa will continue to transpire around the world.

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!

 

Mu Vs. Delta: Which is the Scarier SARS-CoV-2 Variant?

The Mu variant has been a term of interest in a lot of peoples conversations. This is due to the fact that it has been getting a lot of news coverage as one of the latest variants of the world wide virus SARS-CoV-2. It has been portrayed to be the next big virus ready to take over the world, but, does it have the legs to do so and how much more dangerous is it than other mutations such as the Delta variant?

Laboratoire de Physique de la Matière Condensée laboratoire PMC - 46940329992

The Mu variant first popped up on January 2021 in Columbia and has spread to about 39 countries since then. Mu is very similar to the original version of the SARS-CoV-2 virus. However, where it differs is at the two mutations E484K and K417N. These are what cause Mu to be seen as a variant of the original virus. The traditional anti-bodies that would normally be able to stop SARS-CoV-2 are seemingly ineffective against Mu leading the World Health Organization to classify it as a “Variant of Interest”. This classification means that it will continue to be monitored closely to derive the best possible plan on how to contain it. The mutations of Mu give it different properties such as mutation E484K, this mutation caused a drastic change in the structure of the original Covid-19 protein and thus made it so that it is able to by pass the human immune system easier. This is seen as a big problem because studies of how the anti-bodies effect SARS-CoV-2 conducted in US and UK compared to those conducted African countries have shown that African cases seem to be severely less effective against SARS-CoV-2. Researchers believe this is due to Africa being exposed to significantly more cases with the E484K mutation. As discussed in class this sequence of numbers and letters means that in the original amino acid sequence at spot 484 there was a Glutamic Acid amino acid (which is a negatively charged), and then once the mutation occurred it then became Lysine which is positively charged. This change in properties is what causes the protein to fold differently thus causing a severe changes as to how it behaves in humans. The Mu variant seems to have been able to disregard the anti-bodies and still effect the human body. However this seems to be the reach of its dangerous mutations because as of now scientist have no reason to believe that Mu is any more transmissible than the original virus which is a good sign.

The Delta variant has been an extremely worrisome mutation for some time now with the first case being noted back in October of 2020 believing to have originated in India. The Delta variant has been one that has taken over the world recently and it seems as though the former version of Covid-19 is a thing of the past and that Delta is the new pandemic. This is due to Delta’s interesting mutation P681R. The original amino acid at place 681 was Proline which has no charge, however after the mutation occurred it became Arginine which is negatively charges causing the amino acids to behalves differently with each other and the environment. This mutation is the cause of Delta’s incredibly rapid spread throughout the world. This ability to be globally spread in months is just one of the reasons why it has also taken the lives of so many as more people are getting Delta over the initial virus now.

Ultimately, it is clear which variant has been seen as the more dangerous by the media: Delta. However, while the Delta variant is scary in it’s own right, it just seems to be a faster spreading SARS-CoV-2. Meanwhile Mu has a way to almost be a completely different virus as it spreads just as fast as the original virus (it only took 4-5 months to completely shut down the world). It is also able to completely bypass the anti-bodies if you already had Covid-19 or have the vaccine. If this virus reaches levels of spread to the likes of Delta then scientist are going to have to create a new vaccine for Mu as it is simply to dangerous to ignore. Feel free to share how you feel about all of this and let me hear your take on the more menacing variant!

It’s in the Air – The transmission of COVID-19

Since the start of this global pandemic in March, a major issue has been the lack of knowledge on the virus. It has been the job of scientists to research and informs the general public of the virus. As more research has been conducted, we have a better understanding of the virus and its effects. The most important part of stopping the virus though is understanding how the virus is transmitted.

What is Covid-19? 

Covid-19 is an infectious disease caused by a newly discovered coronavirus, called SARS-CoV-2. This virus took America by storm, killing almost 350 thousand Americans. This disease cause mild to moderate respiratory illness in healthy patients with no medical problems. In older people with health issues, this becomes an extremely serious illness. Health problems that put people at a risk include cardiovascular disease, diabetes, chronic respiratory disease, and cancer. The virus is transmitted three main ways.

Contact Transmission

The first way the virus is spread is by contact transmission. Contact transmission is an infection spread through direct contact with an infectious person. For example, shaking someone’s hand, high-fiving someone, or touching a surface that someone infected has touched.

Droplet transmission

Another way the virus spreads is by droplet transmission. Droplet transmission is the spread through respiratory droplets that contain the virus. This type of transmission usually occurs when someone is within six feet of an infected person. For example, if you are sitting in the car with someone who is infected without your mask for too long, you will probably end up with the virus due to droplet transmission. This is the reason masks are so essential to stopping the spread of this virus.

Airborne Transmission

The last way this virus spreads is through airborne transmission. Airborne transmissions similar to droplet transmission, but airborne transmission contains smaller droplets and particles that travel distances longer than six feet. This is dangerous because the guideline that everyone follows is six feet apart but the virus can actually travel further than that and still be dangerous.

How to stop the spread?

Wearing your mask and social distancing is the most important thing to do when trying to stop the spread of Covid-19. SARS-CoV-2 enters the body preferably through the mouth and nose. After that, it enters your cells by binding to the receptor on the cell membrane and begins to reproduce. Masks are a physical barrier between our noses and mouths, preventing the droplets that cause the virus to be released or inhaled. Masks are essential in this fight against the virus so we all need to do our part so we can return to some sort of normalcy in 2021.

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.

 

LION: The King Of The COVID Vaccines

As the SARS-CoV-2 virus (also known as COVID-19) continues to rage across the world killing millions, more time, effort, and money is being put into researching the best vaccines to help bring the world back to a state of normalcy.  One such vaccine is being developed at the University of Washington using replicating RNA is called LION (Lipid InOrganic Nanoparticle). In its animal trials in July, the vaccine already found some success inducing “coronavirus-neutralizing antibodies” in mice young and old which has given researchers a lot of hope for the future of the vaccine.

 

One might wonder, why do we need a vaccine at all? Vaccines are used to expose your body to small doses of a virus or in this case by mRNA, which teaches your body to produce the antibodies needed to fight the virus and makes memory cells. The next time you are exposed to the virus, your body will be able to produce the necessary antibodies to a much larger degree, much quicker, for longer so you will be protected from becoming sick.

One of the lead researchers on LION, Professor Deborah Fuller of the University of Washington School of Medicine qualified the goals of a successful COVID-19 vaccine saying it, “will ideally induce protective immunity after only a single immunization, avoid immune responses that could exacerbate virus-induced pathology, be amenable to rapid and cost-effective scale-up and manufacturing, and be capable of inducing immunity in all populations including the elderly who typically respond poorly to vaccines.” This is quite a lot to accomplish but LION lends itself very well to these goals, conquering most of the problems a typical DNA vaccine would have. DNA vaccines work by coding for the antigens which are then exposed to the immune system to create memory cells so the body can treat the virus later. The downsides of a DNA vaccine is sometimes those antigens fail to create an immune response or can even cause the cell to become cancerous when the DNA joins the host cells DNA, disrupting it. There is far less risk with RNA vaccines which occupy the cytoplasm and only interact with ribosomes.

Shown above us a basic drawing of what SARS-CoV-2 virus looks like.

LION is a replicating RNA vaccine, but how does replicating RNA work? RNA codes for spike proteins and ribosomes in the body make the necessary proteins. Replicating RNA allows for more spike proteins and ribosomes to be coded at a greater rate, which produces a greater number of proteins continuously while triggering “a virus-sensing stress response that encourages other immune activation.” For the vaccine the RNA replicates proteins that tell the body to reject the SARS-CoV-2 and attack them “with antibodies and T cells”  which stop the protein spikes on the virus from interfering with the cell. The development of B cells, which remember how to make the antibodies to fight the virus when infected again, as well as T cells is especially critical for the vaccine as they can develop immunity to the SARS-CoV-2 antigens. What makes the LION vaccine special is the nanoparticle it is named after which “enhances the vaccine’s ability to provoke the desired immune reaction, and also its stability.” This makes it more valuable than other vaccines of the same kind as it can achieve effective results with a longer shelf life. It can also be mixed simply using a two vial method as the mRNA component is made separately from the main vaccine formulation. For all these reasons, the scientists are optimistic as the vaccine goes into the next stages of testing that this vaccine could help provide a long term solution to the COVID-19 pandemic.

As COVID-19 vaccines start becoming available to essential workers in the coming weeks and my father prepares to take one, it can be quite unnerving to think about all the potential negative side effects of the vaccine. These vaccines have been developed without the typical ten years of testing, so knowing more about the research behind the vaccines serves as a comfort me and many others. Our future is in these vaccines and research so knowing which we should invest our time and money in is always a good idea.

“Covid Winter” is Coming: The Power of Humidity in our Return to Normal

As “Covid Winter” approaches, especially in states with seasonal changes such as New York, it calls into question what this will mean for the virus in the coming months. When thinking about when the pandemic will end, temperature, humidity, and seasonal shifts are large factors which work against stopping the spread of the virus. Externally, as the air outside becomes colder, it is able to hold less water vapor, which decreases humidity. HVAC (heating, ventilation, and air conditioning) units inside office buildings work by taking in outside air and heating it to channel through the indoor space, which similarly dries the air out. 

Why is humidity important in preventing the spread of the virus on a biological level? In an aerosol study conducted at Virginia Tech, the researches demonstrated that as humidity levels decrease, the particles of moisture released from actions such as talking, coughing, sneezing become smaller. This becomes a problem because the dry air causes the water in the molecules to evaporate faster, therefore becoming even smaller and staying in the surrounding air for a longer period of time. Any droplets can then travel around the closed, indoor space further. Their minuscule size allows them to be inhaled and move deeper into the lungs, where, as we learned in the video we watched in class, a spike on the virus will insert into a receptor molecule on a healthy cell membrane, allowing it to infect the healthy lung cell, leading to a susceptible person contracting COVID-19 and being able the virus further.

Other coronaviruses, like the common cold, influenza, and rhinoviruses, have exhibited similar spreading patterns dictated by the seasons, demonstrated by flu season occurring in the winter, calming down in summer, and coming back again in fall. Scientists believe COVID-19 could do the same, and are currently conducting research and gathering data to see the correlation between the virus and humidity levels. Stephanie Taylor, a physician and fellow at Har-

An example of how the virus remains in the air after released through talking, singing, etc

vard Medical School, is part of a joint study with the Massachusetts Institute of Technology that “found that the most powerful correlation between national numbers of daily new coronavirus cases and daily Covid-19 deaths was indoor relative humidity.” In reflecting upon their findings, she says that humidity “is so powerful, it’s crazy.” 

The only way to know exactly how the coming winter months will affect the spread of the virus is through time and observation, but it is interesting to look at the biological processes and movement of particles in relation to humidity to understand how the virus may have an increased spread as it becomes colder. I also feel this background helps us be able to make intelligent, informed decisions about the risk of social gatherings as it becomes harder to stay outdoors and the weather changes. What do you think is lying ahead in “Covid Winter?” Do you think we will inevitably have to wait until the humidity changes in spring to declare an official end to the pandemic? 

 

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!

 

 

A Super Self-Assembling Vaccine Booster to the Rescue!

Vaccines: a topic on the forefront of the minds of scientists, researchers, and the general public. With the novel coronavirus and fiery online debates led by coined “anti-vaxers” about the effectiveness and dangers of vaccination, biologists are racing to discover more methods to improve these life-saving injections. An essential component of many vaccines, including ones used to prevent cervical cancer, influenza, and hepatitis is the adjuvant: a “booster” ingredient that helps the vaccine create a longer-lasting, stronger immune response in the patient. Recently, a team of scientists in Japan discovered a new adjuvant—a molecule called cholicamade—that was equally as effective in treating influenza in mice as its predecessor, Alum. The emergence of this new ingredient is exciting, but the real novelty lies in the process these biologists used in discovering chloicamade: looking at molecules that could self-assemble.

What is the self-assembly of a molecule, or multiple molecules? Multiple molecules are said to self-assemble if they are able to organize into a defined pattern without the intervention of an external source, such as heat. These molecules will form ionic or hydrogen bonds with each other, similar to the joining of water molecules, since they don’t share electrons equally, as we learned in AP Biology. Identifying molecular structures that self-assemble is a common practice in materials science, but not often used in researching adjuvants. This team of biologists and chemists hypothesized that utilizing molecules that form in this fashion for disease treatments may be effective because pathogens in viruses also form through self-assembly. They wondered if a similar method in structural formation between a treatment and its virus would trigger a similar immune response.  

And it did! Cholicamide self-assembles through ionic bonds to create a structure which looks almost identical to a virus, triggering the same immune system cells to react. The structure of the molecule

An image of the influenza virus, which the treatment would attempt to replicate.

lends itself to the formation of ionic bonds because of its inherent polarity and electronegative elements. The molecule can be injected directly into vacuoles that will connect it with the specialized receptors which will trigger the appropriate immune response. A vacuole’s ability to store water and other nutrients (as we learned in AP Biology) as well as transport these nutrients throughout an animal cell is vital in ensuring the treatment binds to the correct receptors. Uesugi, a leading scientist in the study, hopes “the new approach paves the way for discovering and designing self-assembling small molecule adjuvants against pathogens, including emerging viruses.” What do you think about this new method in discovering vaccine treatments? How do you see the future of vaccines changing as more adjuvants are researched? I believe there is nothing more exciting than not only confirming the effectiveness of a new treatment, but also conducting the research with a new approach or perspective.

 

 

 

New anti-CRISPR Proteins Serving as Impediments to this Miraculous System.

CRISPR-Cas9 systems are bacterial immune systems that specifically target genomic sequences that in turn can enable the bacterium to fight off infecting phages. CRISPR stands for “clusters of regularly interspaced short palindromic repeats” and was  first demonstrated experimentally by Rodolphe Barrangou and a team of researchers at Danisco. Cas9 is a protein enzyme that is capable of cutting strands of DNA, associated with the specialized stretches of CRISPR DNA.

Diagram of the CRISPR prokaryotic antiviral defense mechanism.

Recently, a blockage to the systems was found by researchers which are essentially anti-CRISPR proteins. Before, research on these proteins had only showed that they can be used to reduce errors in certain genome editing. But now, according to Ruben Vazquez Uribe, Postdoc at the Novo Nordisk Foundation Center for Biosustainability (DTU), “We used a different approach that focused on anti-CRISPR functional activity rather than DNA sequence similarity. This approach enabled us to find anti-CRISPRs in bacteria that can’t necessarily be cultured or infected with phages. And the results are really exciting.” These genes were able to be discovered by DNA from four human faecal samples, two soil samples, one cow faecal sample and one pig faecal sample into a bacterial sample. In doing so, cells with anti-CRISPR genes would become resistant to an antibiotic while those without it would simply die. Further studies found 11 DNA fragments that stood against Cas9 and through this, researchers were ultimately able to identify 4 new anti-CRIPRS that “are present in bacteria found in multiple environments, for instance in bacteria living in insects’ gut, seawater and food,”  with each having different traits and properties.  “Today, most researchers using CRISPR-Cas9 have difficulties controlling the system and off-target activity. Therefore, anti-CRISPR systems are very important, because you want to be able to turn your system on and off to test the activity. Therefore, these new proteins could become very useful,” says Morten Sommer, Scientific Director and Professor at the Novo Nordisk Foundation Center for Biosustainability (DTU). Only time will tell what new, cool, and exciting discoveries will be made concerning this groundbreaking system! What else have you guys heard? Comment below!

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?

Learn From the Greeks: The “Trojan Horse” Method to Cure Ebola

The study to find a cure for the dangerous virus Ebola has resulted in a promising new find: a new strategy has shown positive results.  This new technique involves the placement of antibodies into the cell with the Ebola virus and then it binds to the NPC1 protein before the virus can, essentially rendering it useless.

To understand exactly how these special rainbow unicorn antibodies work, it is essential if we know how the Ebola virus spreads.  The different strains of the Ebola virus (Sudan, Zaire, Tai Forest, Bundibugyo, and Reston) are genetically a little different but they do the same thing.  The virus enters the cell through glycoproteins and gets engulfed into a lysosome. Once inside a lysosome, the virus transforms into a new state where it can bind to a human protein called NPC1.  Once bound to this protein the virus can eject its information into the cytoplasm of the cell and spread.

The solution lies in the binding of the special antibody.  The antibody ZMapp can effectively destroy the Ebola virus, but it is only effective on the Zaire strain. The other strains of Ebola are a little genetically different that the ZMapp antibody does not detect the other strains. Thus, a different approach is required to fight the virus.  The virus can be stopped if an antibody is able to enter the cell with the virus and either bind to the NPC1 protein before the virus does or bind to the virus to disable its ability to bind to anything else.

When the Ebola virus is in a cell’s lysosome it structurally alters itself to enable it to bind with the NPC1, and an advantage that scientists have discovered is that between the different strains of Ebola virus, the transformed versions are very similar, thus an antibody can be made that can bind to all of the different strains.  The problem with this, however, is that antibodies cannot enter the cell the same way that viruses can.

Ebola Virus

The solution that the researchers came up with stems back to the Trojan Horse story from Ancient Greece. The researchers added an extra arm to the antibody, enabling it to latch onto the virus and hitch a ride with it into the lysosome.  Once in the lysosome with the virus, the virus alters and the antibody can then bind again and disable the virus.  This method can potentially be a cure for all of the strains of the Ebola virus, causing an end to a very dangerous virus.

A Cure for Zika? Scientists successfully test a DNA-based Zika Vaccine

The Zika virus, widely known for its 2015 Latin and North America outbreak, is a mosquito-borne and transmitted virus that develops neurological complications and birth-defects in those infected. The Zika virus is able to be transmitted from a pregnant woman to her fetus, causing microcephaly– abnormal development of the brain. Currently, there exists no vaccine that would fully treat the virus, however, a solution may be in the works.

(Photo from Wikipedia Commons)

David B. Weiner, Ph.D., an executive vice president of The Wistar Institute and a developer of the Zika vaccine notes that, “Synthetic DNA vaccines are an ideal approach for emerging infectious diseases like Zika”. Synthetic DNA vaccines are vaccines with genetically engineered DNA. They work in the same way as regular vaccines, inciting cells to produce specific antigens for immunological responses. Synthetic DNA vaccines can also have potential benefits over traditional vaccines, including a higher predictability, stability, and ability to be manufactured and distributed safely and rapidly.

The current Zika vaccine in development, GLS-5700, houses multiple strains of genes with DNA instructions that tell a hosts’ cells how to react and fight off a Zika virus antigen. In late 2016, researchers tested the vaccine on 40 participants. Two groups of 20 received different does of the vaccine at zero, four, and twelve week intervals. At the end of the experiment, researchers found that all participants had developed Zika-specific antibodies and 80 percent of the participants developed neutralizing antibodies against the Zika virus.

Zika 2015-2016 Outbreak (Photo from Wikipedia Commons)

Although rare in the United States, Zika continues to threaten millions living in South and Central America. Despite being in its last stages of development, GLS-5700 and other Synthetic DNA vaccines are still prohibited from being used in the United States- although this may change with the introduction of the Zika vaccine. The future of Synthetic DNA vaccines and viral disease prevention lies in the success of the GLS-5700.

 

 

 

 

XRN1: The Virus Hitman

When I think of the words killer and assassin, my mind drifts to shady men in all black equipped with sniper rifles. However, recent research conducted by the University of Idaho and the University of Colorado Boulder has indicated that I should expand that mental list to include XRN1, a gene in saccharomyces cerevisiae which, according to a recent study, kills viruses within the yeast. Upon stumbling onto this subject, I was intrigued because it was a fairly simple procedure that led to a huge discovery. To grasp the significance of such a discovery, one must understand it on a molecular level. XRN1’s duty in yeasts is to create a protein which breaks down old RNA. The image below shows the generic process of the creation of a new protein through gene regulation.

Wikipedia- Regulation of Gene Expression

Wikipedia- Regulation of Gene Expression

Yeasts also contain viral RNA since practically all yeasts are infected by viruses. When scientists removed XRN1 from the yeasts, the viruses within yeasts replicated much faster, and when they expressed high amounts of XRN1, the virus was completely eradicated. This is because the XRN1 gene was inadvertently breaking down the viral RNA, mistakenly taking it for the yeast’s RNA. Scientists continued the research by using XRN1 from other saccharomyces yeast species. The virus continued replicating rapidly but the XRN1 did continue its job of breaking down the yeast’s RNA. This shows that the XRN1 from each yeast species evolves to attack the specific viruses that occur in its host while still maintaining their basic role as the RNA eaters. Scientists are hopeful about this study’s human health implications. Viruses such as Polio and Hepatitis C work by degrading XRN1 and not allowing it to break down RNA, respectively. Dengue Fever also occurs when XRN1 is unable to perform its function of RNA breakdown. These studies on Dengue Fever and Hepatitis C elaborate on the implications of XRN1 not breaking down RNA. Scientists hope that this discovery could lead to the triumph of XRN1 over these viruses. Could this really be the discovery that leads to the first ever Hepatitis C vaccine? Do you think that XRN1’s success against virus in yeasts guarantees eventual success against viruses in humans?

 

Original Article: http://phys.org/news/2016-10-yeast-gene-rapidly-evolves-viruses.html

 

HIV Resistance to CRISPR/Cas9

A recent study, described in the Science Daily, shows that researches who used the CRISPR/Cas9 to mutate HIV-1 within cellular DNA found that the mutation led to unexpected resistance.

When HIV enters a cell, its RNA genome is converted into DNA and becomes intertwined with the cellular DNA. So the goal for the CRISPR/Cas9 is to target a DNA sequence and cleave viral DNA. The problem is HIV is too good at surviving and thriving despite new mutations, making it more difficult for the CRISPR/CAS9 to target.

PDB_1wj9_EBI

Photo Source

Chen Liang, Senior Investigator at the Lady Davis Institute at the Jewish General Hospital, noted that when they sequenced the viral RNA of escaped HIV, they were surprised to see that majority of the mutations the virus had, instead of resulting from the errors of viral reverse transcriptase, were rather introduced by the cellular non-homologous end joining machinery when repairing the broken DNA.

The mutations to the sequences caused by the HIV were unrecognizable to the Cas9. Thus the resistant viruses just continued to replicate.

This study serves as a cautionary tale for scientists hoping to apply CRISPR/Cas9 as an antiviral. Liang does not believe these efforts are useless, however, as he is hopeful about strategies that could overcome this roadblock. One such strategy would be to target multiple sites with CRISPR/Cas9 or use other enzymes besides Cas9. After the solution is identified, the next step will be figuring out ways to deliver the treatment to patients. Liang is confident that CRISPR/Cas9 will open doors for finding a cure for HIV-1 and many other viruses.

More Info:

http://www.genengnews.com/gen-news-highlights/hitting-hiv-with-crispr-cas9-can-arouse-resistance/81252590/

http://www.techtimes.com/articles/148378/20160409/crispr-cas9-gene-editing-is-not-good-enough-to-beat-hiv-whats-next-in-humanitys-fight-against-the-deadly-disease.htm

 

 

This new tropical virus is not as fun as it’s name sounds!!!

Although it may be fun to say, the Zika Virus is no laughing matter.

16735-close-up-of-a-mosquito-feeding-on-blood-pv

According to the U.S. Centers for Disease Control and Prevention the number of Zika Virus infections has increased to 147 in recent months (only 107 of which are from international travelers from Zika-infected areas). Moreover 117 more cases of Zika were reported from Puerto Rico after the CDC released those aforementioned numbers. The CDC urges that people refrain from traveling to highly infected areas like Puerto Rico and especially Brazil for the 2016 Summer Olympics.

The 2016 Olympics in Rio de Janero, Brazil is a hotspot for Zika infection through mosquito bites

The 2016 Olympics in Rio de Janero, Brazil is a hotspot for Zika infection through mosquito bites

 

Zika is spread through the bite of an infected female mosquito (typically of the Aedis Aegipty type) and 80% of the infected showed a variety of the following symptoms: mild fever, skin rash around area of bite and other, conjunctivitis (pink eye), muscle and joint pain that last for approximately 1 week, and fatigue.

 

Now you may be asking yourself, “What’s so dangerous about a virus that sounds like it should be a Pokémon? People get over viruses every day?” Well the answer is not with Zika itself, but rather with what Zika causes.

 

Several studies have emerged that claim Zika is directly connected to Guillain-Barre Syndrome and Microcephaly. Additionally, the PAHO (Pan American Health Organization) claims there is no evidence that Zika can cause death, but there have been several reports of it worsening pre-existing medical conditions.

CDC_map_of_Zika_virus_distribution_as_of_15_January_2016

Areas of Zika Virus infection and density of cases (the darker the purple the more amounts of cases in that area)

Guillain-Barre Syndrome – an extremely rare disorder in which your body’s immune system attacks the nervous system, systematically destroying it over a long period of time. Although weakness and tingling to extremities are first symptoms, they can quickly spread eventually leading to full-body paralysis. Most people with the rare disease must be immediately hospitalized for rigorous treatment.

 

Microcephaly – a rare neurological condition in which an infant’s head is significantly smaller than average. Most often it can be detected at birth and sometimes avoided with late-stage abortions but recent U.S. laws have prevented such actions. Microcephaly results in abnormally low brain function and development (not growing enough in the womb and not developing at a normal pace after birth.) Children with Microcephaly have severe developmental issues and there is no treatment or cure.

 

Microcephaly can be caused by Zika if a woman contracts the virus in the first and second trimester of the pregnancy. 9 cases of pregnant women contracting Zika have been recorded and of those 9 cases, two women had miscarriages, two women terminated their pregnancies, one woman had a baby with very severe Microcephaly, and most other women contracted the virus in the late stages of the pregnancy and had generally healthy babies

 

In conclusion, if you are a pregnant woman try not to travel to exotic and/or tropical areas where Zika-infected mosquitos usually live.

 

Original Article: http://news.yahoo.com/factbox-why-zika-virus-causing-alarm-202231278.html;_ylt=AwrC1jHwztFW5m0AGIHQtDMD;_ylu=X3oDMTBydWNmY2MwBGNvbG8DYmYxBHBvcwM0BHZ0aWQDBHNlYwNzcg–

Do Viruses Make Us Smarter?

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Sanofi Pasteur

A study conducted at the Lund University shows that “inherited viruses” that are millions of years old play an important role in building up the complex networks that characterize the human brain.” It is well known that retroviruses are make up about five percent of our DNA. Research under Johan Jakobsson indicate that retroviruses may play a critical role in the basic functions of the brain, “in the regulation of which genes are to be expressed, and when.”

Studies of neural stem cells show that these cells use a particular molecular mechanism to control the activation processes of the retroviruses. Findings have shown to have increasingly gained control in our cellular machinery. Because tumors are unable to form in nerve cells, different from other teachers, viruses are activated specifically in the brain. The results open up potential for new research paths concerning brain diseases linked to genetic factors.

“I believe that this can lead to new, exciting studies on the diseases of the brain. Currently, when we look for genetic factors linked to various diseases, we usually look for the genes we are familiar with, which make up a mere two per cent of the genome. Now we are opening up the possibility of looking at a much larger part of the genetic material which was previously considered unimportant. The image of the brain becomes more complex, but the area in which to search for errors linked to diseases with a genetic component, such as neurodegenerative diseases, psychiatric illness and brain tumors, also increases”.

Original Article: http://www.biologynews.net/archives/2015/01/12/do_viruses_make_us_smarter.html

For More Info:

http://www.sciencedaily.com/releases/2015/01/150112093129.htm

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