BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Virus (Page 1 of 3)

From Individual to Environmental: COVID-19 Antigen Testing Expands

Until recently, testing for COVID-19 has focused on the individual rather than on the environment. However, newly introduced technology promises to expand the scope of COVID-19 detection. Researchers at Washington University in St. Louis have developed an apparatus to detect the presence of the covert virus in SARS-CoV-2 without backgroundenvironmental settings. Previous attempts at this technology have been limited by the volume of air tested. Without adequate air quantity, the sensitivity of the technology is negatively impacted. The current system, however, is capable of concentrating up to 1000 m³ of air per minute, compared to the two to eight cubic meters assessed in previous attempts. The result is a system that increases viral detection sensitivity while maintaining specificity.

The newly introduced apparatus functions by using centrifugal force to approximate viral particles to a liquid matrix adherent to the wall of the test chamber. Within the matrix are found nanobodies, bioengineered antibody fragments derived from llama antibodies. As we discussed in class, the human immune system is composed of humoral and self-mediated factors. Antibodies fall into the humoral category. While human antibodies consist of a light chain and a heavy chain, llama antibodies are composed of two heavy chains. By isolating heavy chain llama antibody fragments sensitized to the COVID-19 spike protein and then splicing multiple sensitized heavy chains together, researchers were able to amplify the viral signal, in a manner similar to PCR.

While the device has yet to be approved, cleared, or authorized by the FDA, it holds promise for meaningful real-world application. For example, prior to a large public event, indoor spaces could be screened for the presence of COVID-19. If the virus were detected, remediation could be performed and the environment retested prior to the public event. In doing so, countless potential COVID-19 infections could be avoided.

This novel technology diverges from current efforts at viral detection in that it does not rely on the existence of an infected individual but rather focuses on environmental detection thereby constituting primary prevention. In the future, the technology could be applied to prevention of other infectious diseases, both viral and bacterial. Further work is needed to explore the potential application of this method.

I urge readers to respond to the above and offer opinions.

The “Slow but Steady” Increase of yet Another COVID-19 Variant: What are the Implications?

Globally, there has been a slow but steady increase in the proportion of BA.2.86 reported, with its global prevalence at 8.9% in epidemiological week 44” (WHO)

Another variant? Since the beginning of the epidemic, we have seen a few strains of COVID-19 arise, notably the Omicron, Delta, and Alpha variants. You may ask, how do these mutations keep on materializing?

Like all viruses, SARS-CoV-2 — the virus responsible for COVID-19 — goes under, and will continue to go under, several mutations.

File:SARS-CoV-2 without background.pngAs a coronavirus, SARS-CoV-2 uses protein spikes (visualization on right) that fit into cellular receptors, in order to infiltrate our cells. Upon entry of the virus, the invaded cell begins to translate the viral RNA into viral proteins, which leads to the production of new viral genomes. According to Akiko Awasaki, PhD, this is where mutations often arise, stating that, “When viruses enter the host cells and replicate and make copies of their genomes, they inevitably introduce some errors into the code.” While these introduced errors may be inconsequential, they can also be of benefit to the virus, increasing contagiousness. These successful mutations may change how the virus behaves in the future, becoming the foundations of new evolutionary steps.

As we learned in AP Bio, the sequence of amino acids plays a heavy role in the primary structure of the spike protein. When the sequence is altered, hydrogen bonds will be corrupted or created, affecting the stability of the secondary structures like alpha helices and beta pleated sheets. This changes will in turn affect the tertiary structure, ultimately morphing the three-dimensional shape of the spike protein.

Given this knowledge of how SARS-CoV-2 invades cells, and how it may lead to evolution and mutation, what is the significance of this newest variant, and how can it be fought?

BA.2.86 was discovered over the summer with cases from Denmark, Israel, the United Kingdom, and the United States. Later on, it spread to various countries all over the globe, being discovered in wastewater in countries such as Spain and Thailand. As weeks passed, the new strain did not seem to pose a threat compared to its predecessors. However, months later, BA.2.86 on the rise. On November 11th, the CDC estimated that 3.0% of cases came from BA.2.86. November 28th’s estimate, 8.9%, is shockingly almost triple of the earlier estimate just two weeks prior. This is apparently garnering the strain some sort of reputation, now being labelled a “variant of interest” by the World Health Organization.

While the percentage may seem scary, the rise of the strain has not brought a disproportionate growth in infections or hospitalizations. Rather than posing new or threatening danger, it seems to be much better adept to escaping our bodies’ defense systems. The improved ability to slip past antibodies, compared to previous variants, likely comes from its large number of mutations, 30, on its spike protein. Antibodies, which serve to fight these invaders, may find difficulty recognizing and defeating the new strain.

Due to the strain only taking the notice of researchers recently, there are still many things to be uncovered. Some researchers have affirmed their support in newer vaccines against BA.2.86 and future variants. As always, it is best to wear masks when necessary, wash your hands, quarantine if you are experiencing symptoms, and receive the latest vaccine.

File:Janssen COVID-19 vaccine (2021) K.jpg

 

 

 

 

Cracking Down on Long COVID

In a study funded by the National Institutes of Health (NIH), nearly 10,000 Americans, including COVID-19 survivors, became the researcher’s focus, attempting to figure out the complexities of “Long COVID-19”. This condition leaves individuals fighting with lingering symptoms even after the virus has been vanquished, which presents various challenges, ranging from persistent fatigue to cognitive fog and prolonged dizziness. Nature Reviews Microbiology further examines the ongoing challenges in “long COVID” symptoms, emphasizing the necessity for consistent research efforts. This exploration acknowledges the need for continued studies to understand and address the complexities of the condition. It urges a proactive approach, encouraging the scientific community to stay observant and work together to enhance our understanding of long COVID. By prioritizing continuous research,  strategies for diagnosis and management can adapt to the evolving nature of this condition. As part of the NIH’s 1.15 billion dollar “recover initiative,” the study revealed vital insights, showing that the severity of “Long COVID” is higher in individuals infected before the emergence of the 2021 Omicron variant. SARS-CoV-2 illustration (17)

The research identified 12 key symptoms, establishing a comprehensive scoring system that not only aids in diagnosis but also classifies patients into distinct subgroups, hence refining our understanding of the condition. Health Affairs jumps into the global impact of long COVID, stressing the significance of collaborative international efforts in research and treatment. Furthermore, the study described the influence of vaccination status and the timing of infection, compared with unvaccinated individuals and those infected pre-2021, demonstrating a higher susceptibility to severe forms of long COVID-19.
In the context of our AP Biology class, this study aligns with our exploration of infectious diseases and the biological responses to pathogens. The study advances our scientific understanding of the complexities between our immune system and the evolving nature of viral threats. B and T memory cells are formed during vaccination when specific immune cells are activated in response to antigens present in the vaccine. These memory cells, produced by both B and T cells, retain a “memory” of the encountered antigens. Upon exposure to the same pathogen, these memory cells enable a quicker and more effective immune response, contributing to long-term protection through vaccines. Throughout the year, we have learned the biology behind vaccines, and this study reinforces our learning by demonstrating that vaccines play a crucial role in preventing individuals from experiencing ‘Long Covid’ symptoms. The reason behind this is the vaccine’s ability to prime the immune system, effectively fighting the virus and reducing the risk of prolonged symptoms. Decoding the mysteries of “long COVID” through collaborative initiatives like NIH’s “RECOVER” not only fuels my scientific curiosity but also emphasizes the real-world impact of scientific research on global health.

Symptoms of coronavirus disease 2019 4.0

(Post includes edits made through Grammarly)

Have you ever been caught with a viral disease and been misdiagnosed by your doctor? New CRISPR technology may eliminate this from happening.

So first, what even are viral diseases and how can they affect your health?  Well, some common viral diseases include HIV, herpesvirus, COVID-19, or even the common cold. Any disease classified under viral can enter your body through breathing air, touching something with viruses on it, intercourse, close contact, or getting bitten by a bug “such as a mosquito or tick”. Viruses typically infect one type of cell in your body and this is why the “common cold typically infects only cells in your nose, mouth, and throat”

In a study by PubMed Central (PMC) their goal was to identify the most common errors in diagnosing infectious diseases and their causes using physicians’ reports. In their concluding results, “the most common infectious diseases affected by diagnostic errors were upper respiratory tract infections (URTIs) (n = 69, 14.8%), tuberculosis (TB) (n = 66, 14.1%), pleuro-pulmonary infections (n = 54, 11.6%)”. This data was taken from a sample of 465 patient cases and the researchers concluded that, “a substantial proportion of errors in diagnosing infectious diseases moderately or seriously affect patients’ outcomes”. So when diagnosing viral infectious diseases, steps need to be taken to improve our testing process.

Researchers from the American Chemical Society are looking at using “glow in the dark” proteins to help diagnose viral diseases. Fireflies, anglerfish, and phytoplankton all create a glowing effect using bioluminescence, which is caused by a chemical reaction involving luciferase protein. This protein has been used in sensors for point-of-care testing, but lacks the high sensitivity needed for clinical diagnostic tests. Researchers wanted to combine CRISPR-related proteins with a bioluminescence technique to improve sensitivity. They developed a new technique called LUNAS, which uses recombinase polymerase amplification (RPA) to amplify RNA or DNA samples. Two CRISPR/Cas9 proteins bind to targeted nucleic acid sequences and form the complete luciferase protein, causing blue light to shine in the presence of a chemical substrate. This new technique successfully detected SARS-CoV-2 RNA in clinical samples within “20 minutes, even at low concentrations“. The researchers believe this technique could be used to detect many other viruses effectively and easily.

In relation to AP Biology, we have learned about the process of gene expression where RNA and proteins are produced due to a specific gene being activated. The regulation of gene expression conserves energy and allows organisms to turn on and off genes only when they are required. The CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) gene which are found in prokaryotes cut DNA phages and plasmids to prevent damage to the prokaryote itself. It is used as a rudimentary immune response system. The CRISPR can be associated with other proteins to create an associated complex which allows for the excision and insertion of genes along the length of the genome. Using this process, viral diseases can be identified when combined with the bioluminescence mentioned above.

Looking into the future, researchers are searching for ways to apply CRISPR proteins to detect a greater range of viral diseases so that all patients can get the proper care that they need.

Analyzing Viruses in One Step Using LUNAS

In this article from the American Chemical Society, Maarten Merkx and his colleagues research how to use and combine CRISPR-related proteins with a bioluminescence technique whose signal could be detected with a digital camera. This new technique can diagnose illnesses faster while being much more efficient and practical. Bioluminescence is a chemical reaction involving the luciferase protein that causes the luminescent, glow-in-the-dark effect. The luciferase protein has been incorporated into sensors that emit an easily observed light when they find their target, but they lack the incredibly high sensitivity required of a clinical diagnostic test.

Mareel - Bioluminescence in Norra Grundsund harbor 2

CRISPR, a gene-editing technique, has the ability to increase sensitivity, but it requires many steps and additional specialized equipment. With the new technique, called LUNAS (luminescent nucleic acid sensor), two CRISPR/Cas9 proteins specific for different neighboring parts of a viral genome each have a distinct fragment of luciferase attached to them. If a specific viral genome that the researchers were testing for was present, the two CRISPR/Cas9 proteins would bind to the targeted nucleic acid sequences and come close to each other, allowing the complete luciferase protein to form and shine blue light in the presence of a chemical substrate. RPA-LUNAS successfully detected SARS-CoV-2 RNA within 20 minutes, even at concentrations as low as 200 copies per microliter.

This is similar to the process of gene regulation that uses an inducible operon as we learned in class. An inducible operon is a type of negative regulation that turns on when it interacts with an inducer. It is usually off which means there is an active repressor that binds to the operator to block the RNA polymerase from transcribing the DNA. When there is the inducer, such as the virus, the inducer inactivates the repressor by binding to the allosteric site which allows the RNA polymerase, such as the CRISPR/Cas9 proteins, to transcribe and eventually produce the protein, such as the luciferase protein.

As we are recovering from the devastating COVID-19 Pandemic, how can new medical advancements and technology help us prepare for future outbreaks?

Is Monkeypox even around anymore?

According to the CDC, monkeypox is a virus that can cause many symptoms ranging from respiratory problems to rashes and scabs, as research studies have shown. While, according to the world health organization, the virus was first identified in 1970, and there have been multiple outbreaks since. The first outbreak to reach the US occurred in 2003, when a young girl was bitten by a prairie dog and exhibited symptoms days later. Typically, the virus has an incubation period of 3-17 days which a patient may not show symptoms. However, once the virus emerges, it may stay with a patient for up to four weeks. Often the virus enters the system through either the skin or the respiratory system. After this,  the virus binds the D8L protein to chondroitin sulfate, a cell surface receptor. Once the virus has bound to a cell, it can enter through either endocytosis or by fusing through the cell membrane. After this, the virus can infect the cell and spread to others.

When the virus had a recent outbreak this past May the CDC and WHO were quick to react. As the virus emerged soon after the COVID-19 pandemic, it could be said that both WHO and the CDC were “warmed up” for this monkeypox outbreak and the virus was quickly dispelled in the continental US. However, before it could be dealt with, 30 thousand people in the US were infected and across the world, just over 85 thousand cases were reported. Similarly, a study was done across the US, surveying hundreds of cases between April and June of 2022, and the study revealed that while monkeypox is very infectious, it doesn’t necessarily target those with immune system problems nor the elderly. However, 95% of people who contracted the virus did develop some sort of rash, meaning that was the most common symptom. While the mortality rate of monkeypox is relatively low, at around 3%, it is still a debilitating disease, affecting nearly a hundred thousand people across the world. As such, it is impressive how countries have come together to deal with this virus so quickly. But how?

While the first US outbreak was from animal to human, the 2022-23 outbreak has been somewhat trickier for eradication as the recent outbreak has spread from human to human. However, the monkeypox virus is quite similar to the smallpox virus, for which a vaccine exists. Luckily, this vaccine is up to 85% effective for those experiencing symptoms.Smallpox vaccine (cropped)

However, more measures had to be taken than simply a vaccine that is only 85% effective. The CDC and WHO implemented measures such as mask-wearing, vigorous hand washing, and awareness campaigns in areas heavily affected by monkeypox. With these protocols implemented across the world, monkeypox was tamped down quite quickly in relation to how quickly it spread. As such, monkeypox left the media just as soon as it emerged, and generally, people can sleep soundly at night without worry of waking up feverish, with large painful rashes and scabs.

 

Can Your Lungs Work Against COVID-19?

Within the last two to three years there has been an immense focus in the field of science, COVID-19. This pandemic has sparked a myriad of research opportunities as well as brought up questions we didn’t even know we needed answered.

With this, recent research at the University of Sydney shows that our lungs contain a protein that blocks the COVID-19 infection and works to create a protective barrier within our body. The way it works is that a protein receptor found in our lungs sticks to the virus, and then pulls it away from the targeted cells. The protein is known as the Leucine-Rich Repeat-Containing Protein 15 or in short, LRRC15. For context, leucine is an essential amino acid for protein synthesis as well as many other biological functions. The protein is a built-in receptor inside of our bodies that binds to the COVID-19 virus and doesn’t pass on the infection.

Lungs diagram detailed

Initially, the research was published on February 9, 2023, in the PLOS Biology Journal. Led by Professor Greg Neely and his team members, the findings serve to open a new sect of immunology and COVID research, specifically around the protein, LRRC15. Moreover, it creates a path to develop new drugs and treatments to prevent infections such as COVID-19. Greely states that ” This new receptor acts by binding to the virus and sequestering it which reduces infection,” essentially the receptor is able to attach to the virus and “squish” it before it moves to infection. He also pushes the idea that the new receptor can be used to “design broad-acting drugs that can block viral infection or even suppress lung fibrosis.” Continually Dr. Lipin Loo, one of Greely’s team members, mentions, “We think it acts a bit like Velcro, molecular Velcro, in that it sticks to the spike of the virus and then pulls it away from the target cell types,” here he outlines the stickiness of both the receptor and the virus as well as the receptor’s nature to latch onto the virus and “hold” it. In addition, Loo states, “When we stain the lungs of healthy tissue, we don’t see much of LRRC15, but then in COVID-19 lungs, we see much more of the protein,” here he fronts the idea that COVID-19 lungs are far richer in the LRRC15 protein than normal lungs, this may be due to a result of the protein’s ability to immobilize the virus.

To outline COVID-19 infects us by using a spike protein to attach to a specific receptor in our cells. It mainly uses the ACE2 receptor to enter human cells. Moreover, our lung cells have high levels of ACE2 receptors, which is why being infected can often cause severe problems in our lungs. Similar to ACE2, LRRC15 is a receptor for COVID. But, LRRC15 does not support infection, instead, it sticks to the virus and immobilizes it. This prevents other cells from becoming infected. LRRC15 attaches to the spike of the virus and pulls it away from certain target cell types. The LRRC15 protein is widely present throughout our body, it is in the: lungs, skin, tongue, fibroblasts, placenta, and lymph nodes. However, the researchers observe that the lungs “light up” with LRRC15 after infection. They think the new protein is a part of our body’s natural response to combatting the COVID-19 infection. It creates a barrier that separates the virus from our lung cells most susceptible to COVID-19 infection

SARS-COV-2

To connect to our AP Bio Class, we learned about adaptive immunity where we develop an acquired immunity after being exposed to pathogens, a specific response. I see some similarity here in that the LRRC15 protein is specific to immobilizing the COVID-19 infection. Additionally, in our Cell Signalling Chapter, we focused on signal transduction and its stages, reception, transduction, and response. Specifically in the reception stage, we focused on intracellular and transmembrane receptors. I think that LRRC15 would be transmembrane in order for it to efficiently bind to the COVID-19 Spike. With this, however, I would like to see more about the transduction component of the LRRC15 receptor. Lastly in our Enzyme Unit, we learned about how different factors can affect enzymatic activity; heat, pH, and even general surroundings. I wonder which factors work to hinder and work to stimulate the purpose of the LRRC15. I invite any and all comments with additional info relevant to the topics discussed.

Researchers Find Ways To Combat COVID-19

Ever since COVID-19 was discovered scientists had no idea how to stop this virus. After lots of research we were able to know that there were many different variants of  COVID-19. We understood that some variants were stronger than others according to research. There is an article that talks about how they can be able to stop all kinds of COVID-19 viruses and the different variants. In the article, Professor Seung Soo Oh had an idea on how to stop all kinds of variants in one go. He says that the virus can change its structure whenever. It will then bind to the angiotensin-converting enzyme receptor which is a receptor protein. His team developed a hybrid neutralizer that is able to bind to the virus which then cause the virus to not interact with the protein receptor. This neutralizer was able to be about 5 times more effective then what they first had when COVID-19 was discovered.

According to this article, Omicron which was found in November of 2021 in South Africa, is the most dangerous variant of COVID-19. It is a variant of COVID-19 and is one of the strongest variants. In December of 2019, sub-variants of Omicron began to appear. Some of the sub-variants include BA.5, BQ.1, and BQ.1.1. According to the article, the Omicron sub-variants were very effective and was more transmissible then the Delta variant. The neutralizer should be able to stop Omicron and the sub-variants.

According to another article, variants aren’t weakened by covid vaccines that were had a while ago. In order to help stop COVID-19, the article says that getting boosters will be more effective for any new variants that are discovered. This doesn’t mean they will 100% work. With this knowledge, the new neutralizer that was developed should be able to stop all these viruses from mutating and from entering the cell.

This relates to what we have learned in class this year because we have learned cell structure. When COVID enters the cell, it must bind to a receptor. Once it enters the cell the RNA or DNA would then reproduce. This is similar to what we have learned about how other things enter the cell such as glucose and amino acids. In receptor mediated endocytosis, the ligands must bind to the receptor and then enter the cell. This relates to what we have learned in class because we have learned how molecules are able to enter the cell and how receptors work.

 

SARS-CoV-2 without background

 

There Are More Viruses On Earth Than Stars In The Universe. Why do only some infect us?

Scientists have estimated that there are 10 nonillion (10 to the 31st power) viruses currently on our planet. They are everywhere. Many viruses are beneficial for their host, many inflict no harm, but why do so few viruses affect us and even fewer severely affect us? The short answer: “These pathogens are extraordinarily picky about the cells they infect, and only an infinitesimally small fraction of the viruses that surround us actually pose any threat to humans” says virologist Sara Sawyer.

Understanding how certain viruses affect humans is crucial for protecting and preventing future outbreaks. COVID-19, the most recent outbreak that experienced a “spillover event,” was initially spread through interactions with an animal that is a “non-human primate”. This is called zoonosis. Multiple outbreaks have been introduced this way, but not can be started this way. Pathogens can also enter through cuts, scrapes, mosquitoes, ticks, etc. Once a virus has entered, it needs to find a way to get inside the cells and replicate. To do this, it must first attach to the surface of a host cell and then inject its genetic material (RNA) into the cell. The virus’s genetic material then takes over the machinery of the host cell, using it to replicate itself and produce new viruses. Viruses with a lot of genetic flexibility, and particularly those that encode their genomes as RNA rather than DNA, are well-suited to crossing the species divide. The majority of pathogens that have infected the human population in recent decades have been RNA viruses, including Ebola, SARS, MERS, Zika, several influenza viruses, and SARS-CoV-2. The more lethal viruses were found to have been hiding in their hosts for longer periods of time before showing any symptoms. This would allow it to replicate and spread to new species.

 

Coronavirus. SARS-CoV-2

So the answer is; that a virus has to be incredibly sophisticated for it to cause harm to a human, pandemics are so rare because of precautionary measures such as vaccines, healthcare, and proper sanitation. The continuous study of viruses and their behavior is an important task for the human population and its future as current viruses are continuously mutating and developing with each given day.

 

Got a weird COVID-19 symptom? You’re not alone

COVID-19 is one of the most commonly known diseases of the decade, for most people today are familiar with its many symptoms, including chills, cough, difficulty breathing, etc. Rarely, SARS-CoV-2 will affect people in ways not expected by a respiratory virus; however, people are starting to see it cause odd symptoms. Peter Chin-Hong, an infectious diseases physician at the University of California, San Francisco said that people have developed patchy tongues, puffy digits, and hair loss as a result of SARS-CoV-2.  Chin-Hong still notes that these symptoms may be less dangerous because they are capable of going away on their own.

It is not always confirmed that COVID tongue, COVID toe, COVID eye, or other strange symptoms are due to COVID-19, but the large scale of coronavirus infections means that SARS-CoV-2 has many chances to show the public how it affects people differently. The U.S. announced they already have had 98 million cases confirmed, and Chin-Hong informed Science New that “statistically speaking, you’re going to find people with more and more weird things.” 

In October, the  Journal of Medical Case Reports released a study done by Saira Chaughtai, an Internal medicine doctor, after a patient obtained unbelievable symptoms after ten days of testing positive for COVID-19. Their tongues swell up and eventually erupted in white-ringed lesions. Chaughtai told Science News “I was like, ‘Oh my god, COVID can do anything.'”

Chin-Hong has also seen patients with unusual tongues; however, they had that looked “as if they’d chewed a mouthful of tortilla chips.”  

Changhai was perplexed about how she was going to treat her patients with COVID tongue. She began by researching scientific literature while giving her patients various types of mouthwash to help in the meantime. She even went to such great lengths in teaming up with a sports medicine doctor who shined a low-level laser light on patients’ tongues, a photobiomodulation therapy normally used to treat muscle injury. Chaughtai thought laser light therapy could heal swollen tongues because it increases blood flow. It showed good results as her patient’s tongue lesions healed even though she still feels some sensitivity. 

Another abnormal effect of COVID-19 is COVID finger or toe which causes swelling in peoples’ fingers or toes. The symptoms also included toes or fingers turning a pink, red, or purplish color. It is know to be very painful. Michael Nirenberg of Friendly Foot Care has seen at least 40 people with this symptom who have been exposed to the coronavirus. He found that fingers or toes will normally heal within a couple of months. Nirenberg told his patient to apply nitroglycerin ointment which he thinks increases blood flow to their fingers or toes. 

“We can’t predict who’s going to get what,” Chin-Hong states, for he feels people should be aware that COVID-19 is capable of causing a wide variety of symptoms. He noted that strange symptoms occur mainly with unvaccinated people. “If this is a reason why some people might get vaccinated,” Chin-Hong says, “I think that would be great,” for these symptoms may seem less severe and harmful as symptoms involving the heart or lungs, but they still can be alarming to see. 

In AP Biology this year, we discussed how there are specific receptor proteins integrated into the plasma membrane. The binding between the receptor protein and a ligand, or signaling molecule, is highly specific. Recent studies found that SARS-CoV-2 enters the cell through a specific receptor protein called ACE2. SARS-CoV-2 spike binds to its receptor human ACE2 (hACE2) and an enzyme called proteases activates it. We also talked about enzymes in AP Biology; they are proteins that function and set off reactions or processes. It is important to understand how the unfamiliar virus enters into cells to learn more about its influence on the human body; this can help scientists discover more information on how and why these strange symptoms occur.

Is the recently discovered hidden cavity on the SARS-CoV-2 protein a target for drugs?

Many of us have been vaccinated against COVID-19 and have had the virus, leading us to become used to the virus being prevalent in our lives during the past few years. Even though a successful vaccine has been rolling out for a while now, new therapies have not yet been discovered for future strains. Finding new therapies for the virus remains a major priority in the field of science, even if many of us have been protected already. This issue remains a priority because new variants and strains have been continuing to emerge, and some resist present therapy mechanisms.

SARS-CoV-2

The most effective approach to attempting to combat the virus is addressing the proteins on the surface of therapeutic targets, known as spike proteins. The spike protein (S proteins) located on the surface of the virus leads to its spiky protrusions, and its mechanism to enter human cells. Like we learned in AP Biology class, the spike proteins of the virus latch to cells by matching with a specific receptor on a cell’s surface. The spike proteins of the virus have to latch on to the new cell to infect. Successful messenger RNA vaccines properly target this spike protein, which is the main goal when creating new therapies for viruses. 

                                             Spiky appearance of SARS CoV-2 virus

Luigi Gervasio, a chemistry and structural/molecular biology professor at University College London, and his team have been working towards addressing this issue. By partnering with the University of Barcelona’s research team, the two teams took the first steps to discover a possible mechanism for future drugs to detect and protect against the SARS CoV-2 Virus. Through thorough research and investigation, they uncovered a “hidden” cavity on the surface of a prominent infectious agent of the virus known as Nsp1. The team was able to make this discovery by testing small molecules that had the potential to bind to the Nsp1 cavity. The team identified one, 5 acetylaminoindane, which is essential for the development of new drugs against viruses. They concluded that this cavity permitted the calculation of the cavity’s atomically spatial arrangement, which will allow the development of these drugs.

The results of their breakthrough findings set the stage for developing new therapies that will be able to target the NSp1 protein against SARS-CoV-2 and present Nsp1 proteins in future coronavirus strains. Not only will this finding be impactful for targeting SARS-CoV-2 and future variants, but also new cavities on the surface of other proteins that have yet to be found by scientists. Finally, this research is monumental for both SARS-CoV-2 and virus treatment in years to come!  

 

Shhhhhhh! Some Viruses Can Sneak into Cells and Cause Cancer

Viruses! We all hate the colds we get in the fall that come with a cough, a runny nose, and a sore throat.  These bugs have gone around since nursery school, so we were taught that viruses were transmitted through touching door knobs, getting coughed on, and touching someone who is sick.  While these are how viruses are spread from person to person, the infection that occurs on a cellular level is much more complex.  

For starters, only a handful of viruses are known to actually cause illness in humans, but the ones that do have adapted to do it very efficiently, and some are even known to cause cancer.  Viruses that cause cancer include human papillomavirus, Kaposi Sarcoma-associated Herpesvirus, and Epstein-Barr virus.  The way that these viruses get into the cells is very unique compared to the common cold virus, and a team at the University of Michigan Medical School decided to take a closer look at just how they invade to try and get a better grasp on how to prevent cancers caused by viruses in humans.

The virus they researched is called SV40 and it causes tumors in monkeys.  The way that SV40 infects monkey cells is by burrowing itself through the cell membrane and then into its nucleus in order to duplicate itself.  SV40 is used as a tool to understand how the cancer causing viruses work because of the biological similarities that monkeys and humans have.  An earlier team studied how SV40 travels through the cell.  It goes from the surface, through the endosome, the ER, and then enters the cytosol.  

The most recent study illuminates the rest of the virus’ passage through the cell. The way SV40 gets into the nucleus is through the nuclear pore complex.  This is how many viruses enter the nucleus, but the SV40 is too large to enter through this pore.   The virus must disassemble in order to gain access to the nucleus. This process partially disassembles the virus into a smaller package made of two proteins and genetic material (DNA).  As we have learned in class, the DNA is the macromolecule that codes for how to build the proteins that build the virus.  When the DNA for the virus is connected with the two proteins, it uses both the nuclear pore complex and another complex called LINC.  LINC connects the two membranes of the nucleus together.  Many other viruses grab onto the little fingers sticking out of the nuclear pore complex (seen below), while SV40 seeks out LINC in order to get into the nucleus.  

202012 Nuclear pore complex

The difference in entrances between more common viruses and SV40 could be what makes SV40 cancer-causing.  The next step is to research how SV40 exploits LINC in order to expand upon how other diseases could enter the nucleus, and hopefully find a way to trigger the immune system in order to expel or digest the viruses before it is too late.  

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.

 

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