Silent Mutations and RNA folding can give answer, Why COVID became Unstoppable?

Silent Mutations and RNA folding can give answer, Why COVID-19 became Unstoppable?

Till now, it’s very evident that almost every person must be knowing about the lethal impact of COVID-19 across the globe. But hardly, anyone knows the reason that how COVID-19, which was once living harmlessly in wildlife crossed the species barrier, giving it an evolutionary edge.

Recently, scientists at Duke University have found out that there have been numerous silent mutations in the genetic code of the coronavirus which helped it get the evolutionary edge and made it thrive beyond wildlife, leading to a global pandemic. These silent mutations guided the folding of RNA molecules in a unique way when present in human cells, setting the stage for the global crisis. The study has been published in the journal Peer. J.

The study involved various statistical methods that help in identifying various adaptations that the virus underwent. Researchers analyzed the genome sequence of the SARS-CoV-2 virus and other related coronaviruses often found in bats and pangolins to find out the adaptive changes in SARS-CoV2. “We’re trying to figure out what made this virus so unique,” said Alejandro Berrio, lead author of the paper and researcher at Duke University.

The earlier research highlighted the presence of positive selection within a gene that is responsible for encoding “Spike protein” on the surface of SARS-CoV2 surface. This increases the ability of the virus to infect the new cells in humans more outrageously. The study also indicated the presence of certain mutations in the viral genome that must have altered the spike protein, which made it thrive more easily among humans leading to a global pandemic. But this is not enough, the researchers also found out various other aspects which were not studies in previous researches, highlighting the reason that COVID has become so lethal and infectious. One of the critical reasons was a silent mutation in the two very important regions of the SARS-CoV2 genome, also referred to as Nsp4 and Nsp16. These mutations have been considered to give COVID-19 an evolutionary edge when compared with other similar strains, without impacting the proteins they naturally encode.

The study helped in understanding that the silent mutation instead of affecting the resultant protein affected how the RNA folds up in 3D shape, which eventually affects its functions in human cells. The deeper insights about how exactly these mutations govern the changes I RNA structure is yet to be elucidated in more detail. But never the less, the present study has very well contributed to understanding the viral leap from wildlife to humans.

“Nsp4 and Nsp16 are among the first RNA molecules that are produced when the virus infects a new person,” Berrio said. “The spike protein doesn’t get expressed until later. So they could make a better therapeutic target because they appear earlier in the viral life cycle.”

“Viruses are constantly mutating and evolving,” Berrio said. “So it’s possible that a new strain of coronavirus capable of infecting other animals may come along that also has the potential to spread to people as SARS-CoV-2 did. We’ll need to be able to recognize it and make efforts to contain it early.”

Artificial Intelligence on its way to help to predict drug resistant bacteria

Artificial Intelligence on its way to help to predict drug resistant bacteria

Researchers of Washington state university have developed a feasible software in their lab which helps to identify drug-resistant contributing genes in bacteria.

The software developed makes it feasible to use and easily identify the fatal anti-microbial resistant bacteria existing with us in nature. Figures show that anti-microbial resistance bacteria alone cause more than 2.8 million cases of deadly pneumonia, blood infection, and 35000 deaths annually. Researcher Abu Sayed- Doctoral graduate in computer science, Shira Broschat from School of Electrical Engineering and computer science, and Douglas Call from Paul G. Allen School for Global Animal Health have shared the insight of their work with the Scientific Reports journal.

Antimicrobial resistance is a process that is observed when a microbe acquires or evolves with a drug resistance gene thus further causing AMR. Bacteria responsible for staphylococcus or streptococcus infection or in that manner tuberculosis and pneumonia, all these infectious diseases have developed due to the occurrence of drug resistance strains thus causing hindrance in the treatment regime. The AMR issue is estimated to worsen more in the coming decades in terms of AMR-related infection, deaths, and an increase in health costs as the bacteria is evolving in a way where there is a limited option of antibiotic treatment against it.

“We need to develop tools to easily and efficiently predict antimicrobial resistance that increasingly threatens health and livelihoods around the world,” said Chowdhury, lead author of the paper.

With the ease of large-scale genetic sequencing, scientists are looking in the environment for the presence of AMR genes. They are interested to know the habitat of such genes and how potentially such AMR microbes can spread and affect human health. While they can identify genes that are similar to known AMR-resistant genes, they are probably missing genes for resistance that look very unique from a protein sequence perspective.

The team at WSU developed a machine learning algorithm that has a unique feature of having data of AMR proteins instead of using gene sequences to find a similarity and identify AMR genes. The above algorithm was developed with the help of a theory known as Game theory. Game theory is a tool used in various fields more precisely in economics, to model strategic interactions between game players, here, in this case, helps to identity AMR genes. Using algorithm and theory together, the researcher looked at the interaction of various aspects such as genetic material, structure and physicochemical properties, and properties of protein sequences rather than simply looking at sequence similarity.

“Our software can be employed to analyze metagenomic data in greater depth than would be achieved by simple sequence matching algorithms,” Chowdhury said. He further added, “This can be an important tool to identify novel antimicrobial resistance genes that eventually could become clinically important.”

“The virtue of this program is that we can actually detect AMR in newly sequenced genomes,” Broschat said. “It’s a way of identifying AMR genes and their prevalence that might not otherwise have been found. That’s really important.”

The pioneer research team at WSU took Clostridium, Enterococcus, Staphylococcus, Streptococcus, and Listeria species where resistance genes are found. The above-mentioned bacteria are one of the major causes of infections such as staph infection, food poising, life-threatening pneumonia, and colitis. The algorithm developed by the team was able to categories the resistance genes accurately up to 90 percent.

The algorithm is embedded as a software package that is downloadable easily and can also be used by the scientific fraternity to look into AMR in a large pool of genetic material. The software can be updated timely. As more sequences and data become available, researchers will be able to continue with the algorithm without any hassle. “You can bootstrap and improve the software as more positive data becomes available,” Broschat said.


COVID-19: Ridgeback working on anti-viral tests for patients in the hospital and at home

With efforts underway to find treatments for COVID-19 patients at the hospital, Ridgeback therapeutics are doing things differently.

By the looks of it, COVID-19 does not seem to slow down anytime soon. Thousands of fresh cases are being reported every day, and hospitals are flooded around the world. Most of the pharmaceutical companies are right now focused on finding a treatment for hospitalized patients, in a way that makes sense. After all, they are the most severely affected patients. But Miami based Ridgeback biotherapeutics are currently working differently. 

Currently, the company is kicking off its phase 2 trial for an antiviral that can serve as a treatment for both hospitalized patients and freshly diagnosed patients who are staying at home. The underway antiviral- EIDD-2801 is first being tested on hospitalized COVID-19 patients and the second with cases at home. 

What is EIDD-2801?

Although doctors and scientists around the world are testing out a variety of existing drugs to fight COVID-19, EIDD-2801, an oral antiviral drug stands apart. 

The drug can be used as both prophylactic and a therapeutic against the COVID-19 virus. It is a nucleoside analog that shows broad spectrum activity against RNA viruses, which includes the current coronavirus, COVID-19 and previous virus MERS and SARS. 

EIDD-2801 attacks RNA dependent RNA polymerase the same way as Gilead Sciences’ Remdesivir, a previously FDA-appointed drug for emergency use. But unlike remdesivir which is administered intravenously, EIDD-2801 can be taken orally. 

Why EIDD-2801?

Since the convenience of taking EIDD-2801 orally, patients could take it at home rather than  risking themselves and others by coming to the hospital. By this, the drug is taken at the earlier stages of the infection, potentially killing the virus before it causes havoc on the body. 

EIDD-2801 is completely safe and effective and has a rather intriguing feature of being highly resistant. Usually drugs alert the viruses to quickly mutate that aren’t affected by the drug, making it incompetent. But EID-2801 when tested hasn’t prompted any such resistance.

“We always worry about resistance,” says Andy Mehle, a virologist at the University of Wisconsin–Madison. Though drug resistance is inevitable, sometimes the viruses work on changing so much to overcome a drug’s effects that they cripple. Alternatively, resistance may seem as a simple change, the changes occur with a difficulty of the virus’s ability to multiply. Experts speculate this might be the case with EIDD-2801.

What’s next for Ridgeback?

Though the first set of clinical studies are just beginning, Ridgeback is confident about the drug and is currently gearing up to manufacture hundreds of thousands of doses of the drug. In the near future the company is planning to ramp up the production to millions. 

“While we still need to wait and see the intended efficacy of the drug as ridgeback believes it to be, it is imperative to have a backup of immediate and ample supply to the world, once the clinical trials are successful” stated Wendy Holman, CEO and co-founder of Ridgeback.

Good news as researchers find a key to cystic fibrosis detection and treatment

Good news as researchers find a key to cystic fibrosis detection and treatment

Groundbreaking research by Monash University paves the way to a possibility of better monitoring and treatment of the cystic fibrosis lung disease

For years, cystic fibrosis (CF) has known to be a serious hereditary condition that causes severe damage to the respiratory and digestive systems. The damage starts with a build-up of thick mucosal kind of fluid in the organs especially lungs. 

In particular cystic fibrosis affects the cells that produce digestive enzymes, sweat, and mucus. Usually, these secretions are thin and watery, which function as lubrication for various organs and tissues. However, when affected with CF, due to faulty genes the person experiences thick fluid build-up, clogging up the passages and ducts.  

Early diagnosis and treatment are important for improving the quality and the length of the affected life. Currently available lung assessment tools have many drawbacks, especially the inability to accurately identify the origin of the changes seen in lung health. 

Monash University research team announced the results of the World’s first research promising a possibility of better diagnosis and treatment of cystic fibrosis using X-ray velocimetry. 

What is X-ray velocimetry?

A phase-contrast X-ray imaging makes use of the refractive properties of materials to produce high definition soft tissue images. Recently X-ray velocimetry (XV) has caught the eye of researchers. In particular, XV is used to study the airflow through the lungs and the technique is based on particle image velocimetry. Particle image velocimetry (PIV) is a well-established technique known for years. 

XV is known to provide high quality, non-invasive, real-time images of the airflow through the lungs. The X-ray was first designed and developed by 4DMedical, in hope for clinical use. The technology has also recently been approved by the FDA for its all respiratory indications in adults. 

All about the study:

An effective assessment of the lung cystic fibrosis should be capable of capturing its patchy nature and fluid buildup. This is in particular important for detecting the disease at early stages. 

With the help of XV, a multidisciplinary collaboration of engineers, physicists, and clinicians were able to measure real-time airflow through the lungs. 

The research was led by one of the University’s leading scientists Dr. Freda Werdiger. The study revealed that by using XV, it was possible to pinpoint the precise locations where there was an obstruction of airflow in the lung of a cystic fibrosis patient.  

“In this study, we present two developments in XV analysis. Firstly, we show the ability of laboratory-based XV to detect the patchy nature of CF-like disease in affected mice. Secondly, we present a technique for numerical quantification of that disease, which can delineate between two major modes of disease symptoms,” Dr. Werdiger said.

This particular model provides a very simple, easy top interpret approach, which in the future can be readily applied to large quantities of data generated in XV imaging. 

What does the future hold?

The success of XV lies in its capability of drawing reliable and quantitative measures, and the above study shows how that can be accomplished. 

The researchers of the study recommend that this promising technique should be applied to the numerical characterization of CF lung disease. The analysis can be applied in a straight forward fashion with minimal manual labour required. 

A quadruple helix DNA discovered in a healthy human cell for the first time

Yes, you heard it right for the first time ever, scientists find quadruple DNA in healthy human cells. 

It’s been 67 years since Watson and Crick first established that DNA forms a double-stranded helix. Every now and then it is identified that the double-stranded DNA can double up, to form a special quadruple stranded helix form. 

Previously, quadruple DNA has been developed synthetically but was only seen in a curious point of view. Around 2013, scientists for the first time noticed quadruple DNA in human cancer cells. Today another milestone was set, when scientists for the first time have identified the peculiar DNA in healthy human cells. 

“We’ve undoubtedly demonstrated that the quadruple-strand DNA forms in living cells,” says Marco Di Antonio at Imperial College London. “This forces us to rethink the biology of DNA.”

How does quadruple DNA form?

The DNA molecule is made up of 4 nucleobases- guanine, adenine, cytosine, guanine, and thymine, which can configure themselves in multiple ways. 

At times, it happens so that the DNA can double up to form quadruple helix DNA, formed by sequences rich in guanine. Guanine is the only known nucleobase that is capable of forming bonds with each other. The quadruple DNA usually occurs helically in nature and contains the guanine bases stacked on top of each other.

The unimolecular regions are usually seen at the ends of the chromosome/ telomeric regions. This is usually seen in microbes, oncogenes and now in healthy human cells.

Time to rethink the biology of DNA:

The DNA was viewed by Di Antonio and team from the University of Cambridge. The team viewed the DNA within the human cell by attaching a novel fluorescent marker.

Quadruplexes, in the primary region of the DNA, act as an “on” and “off” switch particularly for the genes associated with cancer. Previous research suggests that the quadruple DNAs can be used as molecular targets to diagnose cancer at early stages. 

Although Di Antonio and the team are aware of the DNA function, it is still a mystery on how a cell knows where to express the gene or decrease its activity. The researchers hypothesize that the quadruple structure may hold the door open to facilitate the reading of the genetic code. 

“There is a sort of crosstalk between the formation of quadruplex DNA and epigenetic markers,” says Di Antonio. “The quadruplex form is an epigenetic mark in its own right.”

Concluding remarks:

This recent discovery adds to the evidence that the quadruple portions are a normal part of DNA regulation and function. It has also made us realize that we need to rethink our whole biology and that our view of double-stranded DNA may be out of date. 

Though the new discovery can be assumed to be a native state of DNA, it is another example proving that DNA is not a fixed shape or structure. 

Discovery of ‘on-off’ switch in plant immune defense

Living systems are known to be equipped with self defense mechanisms, and plants are no exception. For the first time, experts find a novel “on-off switch” in plant defense. 

The main purpose of an immune system is to protect the host from any harm. All living organisms are equipped with an immune system, and plants are no exception. Plants are home to rich sources of nutrients attracting many organisms including fungi, bacteria and vertebrates. Although plants lack an immune system as complex as humans, they do have stunning forms of chemical, structural and protein defense that experts are trying to understand. 

Plant immune defense:

Plants immune defenses are designed to detect any living organism and stop them from causing any extensive damage. Plants are equipped with multi layers of surveillance mechanisms that are capable of recognising potentially dangerous pathogens. 

The defense mechanisms are specifically programmed and operate through a complex network. They are timed for effective and rapid response against the predators, yet at the same time are controlled to avoid any damage to the host. 

The novel discovery:

Keini Dressano, Alisa Huffaker and team from the University of California San Diego, have recently discovered a novel ‘on-off’ switch in the plant defense system. 

The new switch mechanism is an RNA binding protein that can help turning on immune responses a few minutes after being attacked. They also observed that it was capable of switching off the immune response hours later, to prevent self inflicting damage.

“These findings have provided new insights into how the complex intricacies of plant immune responses are orchestrated to successfully fight off pathogens, and lay a path forward for improving plant disease resistance to ensure future food stability,” said Huffaker, an assistant professor in the Section of Cell and Developmental Biology.

Science behind the discovery:

The novel discovery was found in arabidopsis plants, and it was found to control splicing of the mRNA transcripts that encode signalling protein regulators if the plants defense system.

According to the researchers, a simple chemical modification of the RNA binding protein was seen to reverse mRNA splicing that usually keeps the immune response deactivated. To turn on the immune response, a second chemical modification returns the mRNA splicing to normal resuming the inactivation process. 

“This work went beyond simply identifying a new regulator of plant immunity,” said Huffaker, of the detailed mechanisms uncovered. “We discovered specific chemical modifications that control regulatory function, transcriptional targets of the regulator, differential splicing of the targets and precise effects of splicing on both target function and overall plant immune responses and disease resistance.”


COVID 19: A battle between heat and humidity Vs Sunshine

COVID 19: A battle between heat and humidity Vs Sunshine

Though some experts suggest that heat and humidity can help in slowing down COVID-19, others argue that long hours of sunshine can risk a higher incidence of the disease. Let’s investigate further. 

With the deadly COVID-19 affecting the economy all over the world, lockdowns are slowly being lifted to compensate for the damage. People are slowly crawling back to public places like the beaches and soaking in the much-needed vitamin D from sunshine. But there is a price to pay. 

A sign of a sunny day attracts many people to go out, in turn increasing the risk of infection due to a lack of social distancing. Experts speculate long exposure to sunlight also poses a high risk of contracting the virus. While on the other hand, reports state that heat and humidity can potentially slow down the spread of COVID-19. 

A recent report published in the journal Geographical Analysis gives insights on how seasonal changes influence the spread of the novel virus. 

Temperature a crucial factor:

For several weeks now, research has been conducted revolving around the effect of temperature and humidity on COVID-19. Several experimental studies explain that it is possible for the COVID-19 virus to be sensitive to heat and humidity, and with further study, experts are convinced that the rate at which the virus spreads can vary in places with different temperatures and humidity. 

Studies reveal that humidity and temperature may make the COVID-19 virus less viable by disrupting their surface proteins and outer membranes. On the other hand, the change in infection rate might differ due to the ways people change their behavior from being enclosed in spaces to spending more time outdoors. But currently, there is no solid proof to confirm that summertime can bring improvement in this current pandemic. 

Not all Pandemics or diseases follow the same seasonal patterns seen more commonly in seasonal flu outbreaks. Spanish flu, for example back in 1918, peaked during the summer months, while most of the common flu outbreaks erupt during winter. 


At high levels of humidity and heat, the authors of this study noticed a steady decline of 3% in the confirmed COVID-19 cases, possibly due to the virus dying under warmer temperatures. The opposite was observed at long exposure to the sun. More the sunshine more the rate at which the virus spread, raising concerns if it’s due to the human behavior post lockdown measures. 

The authors of the study stated that We will likely see a decrease in the incidence of COVID-19 as the weather warms up, which is an argument for relaxing social distancing to take advantage of the lower incidence associated with higher temperatures” he says. “But a more conservative approach would be to use the months of summer to continue to follow strict orders to remain in place and to crush this pandemic.”


COVID-19: Loss of smell, a new symptom added to the list

COVID-19: Loss of smell, a new symptom added to the list

New evidence finds that anosmia- loss of smell as a new symptom caused by the COVID-19 virus. Experts believe that it can be added as a potential screening tool for the novel viral infection, and here’s why!

Cases of post-viral anosmia are one of the leading causes of loss of smell among adults suffering from viral infection. This has been associated with previous coronaviruses which are usually known to cause upper respiratory tract infections and have accounted for 10-15% of the cases. Therefore it comes off as no surprise that the current novel COV ID-19 virus also causes anosmia in the infected. 

A significant number of cases from South Korea, Italy, and China prove as good evidence for COVID-19 patients developing anosmia. More than 2 out of 3 confirmed cases in Europe have been diagnosed with anosmia. It is also noticed that several COVID-19 cases also present anosmia as the only symptom. Given the above evidence, experts contemplate using anosmia of a screening tool to diagnose people with COVID-19 at the early stages. 

Cases of anosmia reflect how COVID-19 affects the brain:

“There’s something unusual about the relationship between COVID-19 and smell,” states Sandeep Robert Datta a neuroscientist from Harvard Medical School and one of the leading scientists in the study. It is well known that common cold, is associated with stuffy noses leading to a temporary loss of smell, but it found that the COVID-19 virus leaves the nose free. “But recently lots of people are complaining about losing their sense of smell when they don’t feel stuffed up at all,” Datta says. 

The team further experimented on nose cells, including the support cells and nerve cells sending messages to the brain using both mice and human models. This was especially performed to see if there were any signs of a link between the cells and the ACE2 receptor. A small recap: ACE2 receptor is the primary receptor in humans which the COVID-19 viruses used to attach to the host and cause infection. 

The researchers from the study found that the results demonstrated a molecular signal showing that ACE2 receptors were present in nose cells and the subsidiary cells. These cells generally maintain a chemical balance in the nose, which allows the nerve cells to send smell signals to the brain. 

A Contradicting study published by a team from Nicolaus Copernicus University, Poland resulted that the olfactory neurons did not pose any ACE2 receptors, implying that the novel virus cant infect the cells themselves. 

It was also noticed that the timing of the onset of anosmia symptoms was varied, with some patients developing the symptoms at early stages, while another group of patients reported the loss of smell in the later stages of their illness. 

How will this help in the fight against COIVD-19?

More studies need to be conducted regarding the frequency of the symptoms and the exact science behind how the COVID-19 virus affects the olfactory senses. To collect more data on the cases posing these symptoms, the AOS-HNS Infectious Disease and Patient Safety Quality Improvement Committees have developed a COVID-19 anosmia detecting tool for health care workers. Using this tool the clinicians of all specialties will be able to confidently confirm cases portraying the loss of smell. 

The idea of adding the symptoms of unexplained anosmia as an official symptom of COVID-19 can help with earlier detection and isolation of potential carriers of the virus and improve safety by containing the spread of the virus. 


Breakthrough: 2003 SARS survivor antibody, a potential cure for COVID-19

Breakthrough: 2003 SARS survivor antibody, a potential cure for COVID-19.

With the number of COVID-19 cases surpassing 4.3 million worldwide and counting, scientists are working around the clock in efforts to develop vaccines and treatments to slow the pandemic. Currently, scientists are looking into whether existing drugs might work or whether new treatments need to be developed to try and tackle the virus. 

In this article, we discuss the latest scientific finding, how an antibody identified in a survivor of the 2003 Severe Acute Respiratory Syndrome (SARS) outbreak has the potential to neutralize COVID-19, providing a glimmer of hope in this current battle.

How do these antibodies work against COVID-19?

Development of immunity to a pathogen through natural infection is usually a multi-step process taking around 1-2 weeks. The body immediately reacts to fight the infection with a nonspecific innate response which will slow the progress of the virus and may even prevent it from causing symptoms. This is then followed by an adaptive response where the body produces antibodies specifically binding to the virus and eliminate it along with the cells infected. 

Recently a research team came forward and publisher a paper stating that they have identified an antibody from a patient recovered from SARS 2003, which can potentially inhibit the cause of COVID-19. The antibody S309 is now on a fast track development and testing at Vir Biotechnology. 

The scientists first identified monoclonal antibodies from the memory B cells of the SARS survivor. The memory B cells reproduce cells and have a long lineage, sometimes for life. The cells have the tendency to remember a pathogen or one similar to it and have the potential to fight against it in the future if re-infected.  

The S309 antibody, in particular, is directed at a protein structure of the coronaviruses. The structure is essential for the virus, to recognize a host cell receptor and infect it. This particular infectivity capability is present in the spikes that crown the virus. S309, in particular, attacks the spike- disabling it, hence hindering the coronavirus to enter the cells. It should also be noted that the antibody showed the capability to target binding sites of several sarbocoviruses, not just COVID-19 and SARS. 

What next- Will this be the breakthrough we all are hoping for COVID-19?

In this paper titled “Cross-neutralization of SARS-CoV and SARS-CoV2 by a human monoclonal antibody”, scientists have reported that by combining the S309 antibody with other similar antibodies identified in the recovered SARS survivor, there is a chance of neutralizing the COVID-19 virus. This cocktail of antibodies could be the answer to limit the coronavirus from forming mutants capable of escaping the single ingredient antibody. 

“We still need to show that this antibody is protective in living systems, which has not yet been done,” said David Veesler senior author. “Right now there are no approved tools or licensed therapeutics proven to fight against the coronavirus that causes COVID-19”, he added. 

At this point in the pandemic, there is not enough evidence to prove the effect of antibody-mediated immunity against the virus. It cannot guarantee an immunity passport or a risk-free certificate. Further research and studies need to be performed before we can reach a conclusion. 



T-cells can play a crucial role in combating COVID-19

The only thing that is keeping researchers across the globe on their toes is the present pandemic situation. The scientists are working hard to find out a potential solution that can help fight the menace. Looking at this, they are exploring the known immune warriors in the human system, one of them is T- cell. Though known for fighting various viruses, the understanding of how T cells interact and fight against Sars-CoV2 is yet not clear. Recently, two studies suggest that patients infected with COVID harbor T-cells to target viruses that might have helped them in recovery. The study reveals that some of the people already have these cellular defense mechanisms mostly because they have a history of infection with any of the coronaviruses.

“This is encouraging data,” says virologist Angela Rasmussen of Columbia University. Although the studies don’t clarify whether people who clear a SARS-CoV-2 infection can ward off the virus in the future, both identified strong T cell responses to it, which “bodes well for the development of long-term protective immunity,” Rasmussen says. The findings of the research study can help scientists come up with a potential vaccine candidate.

“One reason that a large chunk of the population may be able to deal with the virus is that we may have some small residual immunity from our exposure to common cold viruses,” says viral immunologist Steven Varga of the University of Iowa.

Presently, most of the vaccine candidates are developed by targeting the other component of the immune system. For example, many biotech companies are coming up with antibodies based vaccines which are mainly made by B-cells when they interact with the virus. Whereas the T-cell based mechanism differs a little. There are two different mechanisms that define the working of T-cells. One way is where helper T-cells interact with other biological components like B-cells, interleukins, and more to put them into action against the virus. The second way is where killer T-cells directly recognize and target the virus to destroy them from the site. This is the reason that the severity of disease among different patients varies depending upon how strong their Tcell response is.

The scientist team used some bioinformatics tools to assess the interaction between the viral protein and Tcell. For this, they exposed immune cells of few patients to the viral spikes, who have recovered fro the COVID infection. The results showed that all patients harbored helper T cells that helped in the recognition of viral spike protein. This spike protein plays a crucial role while invading a cell. The team also identified killer T0cells in almost 70% of patients, as reported in the ‘Cell’. “The immune system sees this virus and mounts an effective immune response,” says the researcher.

“It is encouraging that we are seeing good helper T cell responses against SARS-CoV-2 in COVID-19 cases,” says a researcher involved in the study.

The present study highlights the importance of looking at other potential immune mechanisms to target COVID-19. Moreover, understanding the detailed role of T-cell in the fight against the virus can have significant implications in the development of potential vaccine candidates. The study has come on time to help researchers find ways to implement it and develop a therapy that can help in turning down the pandemic.