COVID-19 Archives - SciWriteGlobal

Feb, 2021

Learning how SARS-CoV2 hijacks and damages lung cells

The emergence of the SARS-CoV2 virus has caused turmoil across the globe, forcing the researchers to study it in more detail. However, the behavior of the virus has been quite notorious. The frequent mutations and very less prior knowledge has caused some obstacles. However, scientists were acquainted that if they understand the underlying pathways in lung cells and host protein being impacted during the viral infection then there can be chances of identifying potential solutions. Considering this, scientists have recently found out how SARS-CoV2 hijacks and damages the lung cells.

The study was a multi-group collaboration between the Center for Network Systems Biology (CNSB), Center for Regenerative Medicine (CReM), and National Emerging Infectious Disease Laboratory (NEIDL). The researchers have mapped the molecular responses emerging from lung cells infected with the SAR-CoV2 virus. The finding of the study has been published in the Journal of Molecular Cell.

To understand the disease pathology and gain new insights to discover potential therapeutic targets, the researchers bioengineered the human alveolar cells. The cells when combined with high-end mass spectroscopy technology, it helped the researchers to identify potential host proteins and pathways changing during SARS-CoV2 infection. The researchers found out that lung cells infected with SAR-CoV2 have abnormal phosphorylation.

Phosphorylation is a very crucial protein modification process contributing to protein functionality in the cells. The proper phosphorylation process is important for healthy cells. However, it was noticed that the infection alters this process leading to cascading abnormal changes. These changes increase the chances of the virus to thrive within the cells and eventually destroy it.

The study also showed that as soon as the virus encounters the lung cells, it initiates exploiting the resources required for the normal functioning and growth of the cell. The invasion of the virus further disrupts the functioning of the cell and damaging it extensively. The resources used, powers the virus eventually leading to rapid proliferation and expansion in nearby regions. As a result, the exhausted and damaged cells undergo self-destruction and the virus starts infecting the cells in the vicinity while evading the body’s immune system. This cycle repeats continuously leading to the hijacking of lung cells and widespread damage.

The researchers examined lung alveolar cells from one to 24 hours after infection with SARS-CoV-2 to understand what changes occur in lung cells immediately (at one, three, and six hours after infection by SARS-CoV-2) and what changes occur later (at 24 hours after infection). These changes were then compared to uninfected cells. All proteins from infected and uninfected alveolar cells, corresponding to the different time-points were extracted and labeled with unique barcoding tags called “tandem mass tag.” These tags, which can be accurately detected only by a mass spectrometer, permit robust quantification of protein and phosphorylation abundance in cells.

“Our results showed that in comparison to normal/uninfected lung cells, SARS-CoV-2 infected lung cells showed dramatic changes in the abundance of thousands of proteins and phosphorylation events,” said Darrell Kotton, MD, BUSM, CReM.

“Moreover, our data also showed that the SARS-CoV-2 virus induces a significant number of these changes as early as one-hour post-infection and lays the foundation for a complete hijack of the host lung cells,” adds Elke Mehlberger, PhD, NEIDL.

Scientists also tried to examine the data obtained from the study to identify any potential opportunities for COVID-19 treatment. They found that about more than 18 existing drugs that have been already clinically approved can be re-purposed for the treatment. The research team believes that the current findings are very crucial and can contribute a lot to the field, specifically in terms of devising a cost-effective, robust and life-saving treatment to overcome COVID-19.

Nov, 2020

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.”

Sep, 2020

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.

Jun, 2020

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.

Source

May, 2020

A brief insight on ACE receptors role in COVID-19

With the novel coronavirus, COVID-19 is spreading across the world and the fact that no drug or treatment has been found against it is creating fear among people. Coronavirus is a large family of enveloped, single-stranded RNA that infects mainly mammals including humans. In humans, coronavirus causes mild to severe respiratory illness. These viruses exhibit strong virulence and are highly contagious. While a person infected, produces mild symptoms, certain individuals respond severely, sometimes leading to death.

The SARS pandemic, back in 2002 is known to belong to the same family of viruses as COVID-19. According to WHO, SARS rapidly spread through 29 countries, with 8096 confirmed cases, but the current pandemic has surpassed all numbers by infecting over millions of people across the world. Today, it is due to SARS that has resulted in a coordinated effort to develop treatments targeting the virus or host cell components responsible for viral replication.

The deadly virus, COVID-19 enters the human body and binds to the target cells through angiotensin-converting enzyme 2 (ACE2) which is mainly expressed in endothelial cells and Leydig cells. ACE-2, a transmembrane metallo carboxypeptidase, is an enzyme which for years has been important for the treatment of hypertension. With further Polymerase Chain Reaction (PCR) analysis it was determined that the ACE-2 receptor is also present in the lung and gastrointestinal tract, tissues harboring COVID-19.

Inhibiting ACE2 receptor blocks COVID-19 entry:

ACE-2 belonging to the family of ACE receptors, plays a key role in the Renin-Angiotensin System (RAS) and in the treatment of hypertension. ACE2 is known to degrade angiotensin II and thereby, negatively regulating RAS. Recently experts have revealed that the COVID-19 virus uses ACE-2 receptors as their entry in HeLa cells. Additionally, it was found that by using anti- ACE-2 antibodies in other mammals like monkeys, it was seen that there was an entry blockage of pseudotypes expressing the COVID-19 virus.

For the virus to enter the host cell, its spike glycoprotein (S) needs to be cleaved at 2 sites, termed S protein primming so the viral and host cells membrane can fuse. A serine protease TMPRSS2 is essential for cleaving the S protein. It was found by treating Calu-3 human lung cell line with a serine inhibitor- camostat mesylate the entry of the COVID-19 virus was partially blocked. Angiotensin-converting enzyme (ACE) inhibitors is also found to play a role in preventing the formation of angiotensin II. ACE multifaceted functions include treating heart failure, controlling high blood pressure, and preventing kidney failure in diabetic patients.

Existing concerns about ACE inhibitors:

Though ACE inhibitors might seem like a promising solution for COVID-19, there are certain concerns regarding the increased susceptibility to COVID-19. These are considered based on the fact that ACE inhibitors are also used in treating millions of people with hypertension, heart, and kidney disease. When administered with inhibitors, diabetes and hypertension patients were observed to have an increase in ACE2, which in turn would facilitate infection with COVID-19. It is hence hypothesized that treating diabetic and hypertension patients with ACE inhibitors might make them more susceptible to COVID-19.

Furthermore, several studies have reported that long term usage of ACE inhibitors can modify the adaptive immune response, which is a key and much-needed defense against any infection. These particular effects must be taken into noticed and investigated further in context to COVID-19.

Road to COVID-19 therapies:

These findings could greatly impact the efforts being taken in developing treatments for the current pandemic. For instance, TMPRSS2 inhibitors can be potentially used to prevent virus entry into the host cells. Though there are certain drawbacks in using ACE inhibitors, there is a lack of scientific evidence and clinical data to support the discontinuing of ACE inhibitors in COVID-19 patients with existing hypertension and diabetes. The proof that reduction in mortality due to ACE inhibitors and the beneficial effects outweigh the theoretical risks.

Our interpretation of this hypothesis should not lead to changing drugs for patients with diabetes or hypertension, without consulting an expert physician. Though it’s of utmost urgency for the scientific community to come up with some solution for this deadly virus, further research and clinical trials need to be performed before any of the said theory can become a reality.

Source

May, 2020

Mutant Poliovirus from vaccine more infectious than the wild type

How it all began?

Back in the 20th century, there were many more diseases that worried parents then Polio did. Polio struck during summer, making its way through towns, every few years. Most people were reported to recover quickly, though some suffered temporary or permanent damage leading to paralyzation and even worse, death. With many polio survivors disabled for life, it was a constant reminder to the society the toll it took on young lives. Polio reached the level of epidemic proportions back in the 1900s affecting the infant and young kids, where the infant’s immune system is still aided by maternal antibodies could not fight the virus.

Polio is caused by a family of viruses belonging to the Enterovirus genus. These viruses are highly contagious usually spreading through contact with people either by oral or nasal secretions, or by contacting a contaminated area. The virus enters the mouth and is found to multiply by the time it reaches the digestive tract, where it continues to multiply. In cases of paralytic polio, the virus makes its way from the digestive tract to the bloodstream attacking nerve cells.

Development of vaccines to eradicate polio:

A vaccine is made from a very small amount of wither weak or dead germs that cause the disease, for example-poliovirus. When administered, the vaccine introduces the said virus into the body to trigger an immune response, causing it to recognize and combat the actual disease if encountered in the future.

The antibodies specific to the poliovirus was first discovered in 1910. Using immunologic techniques, it was in 1931 different serotypes of the poliovirus were identified. By identifying that the virus can be grown in large amounts using tissue culture, it was just a short time before the first inactivated polio vaccine (IPV) was developed. With human trials being deemed a success, the number of polio cases drastically dropped over the years. Later an improved version of the vaccine using live attenuated virus was developed, which could be administered orally, known as oral poliovirus vaccine (OPV). Soon it became the predominant go-to vaccine for developing countries all over the world, declining the number of cases drastically till a new problem raised recently.

Vaccine-derived poliovirus:

Over the past few years, more than 10 billion doses of OPV have been administered to millions of children worldwide, preventing more than 10 million cases during that period, bringing down the number of cases drastically.

So far in the year 2017, only as many as 6 “wild” polio cases were detected worldwide. By wild it means that the number of cases affected by polio “wild type” strain found naturally in the environment. Recently, new cases have been reported of children paralyzed by a vaccine-derived poliovirus. Around nine new cases were identified in countries- Nigeria, the Democratic Republic of the Congo, Central African Republic, and Angola last November, along with Afghanistan and Pakistan. The WHO reported that as long as a single child is infected, all the other children are at risk.

In developing countries, the oral vaccine is used profusely among all children due to its low cost and accessibility. The vaccine-associated paralytic polio is caused by a strain of poliovirus which was previously termed wild type. The onset was found to be caused by a type 2 virus contained in the oral vaccine. Type 2 virus was a wild type virus eradicated years ago, but in rare cases can mutate into a form that can breach the vaccine protection.

Erradication possible:

With the COVID-19 outbreak, the WHO has also additionally undertaken the goal of eradicating the new mutant poliovirus before its too late. The role model here is smallpox, which was completely wiped out thanks to a consistent vaccination strategy. The same applies to polio. Similar to smallpox, the polio vaccine also offers impeccable protection, though not applicable to virus mutants. Reports state that the latest mutant outbreak is due to the low vaccination rates. The rise in vaccine-derived polio cases is due to the mutant form of the disease affecting the non-vaccinated children through contaminated matter.

The coverage of vaccination and hygiene measures must be extended so that the new mutant can no longer continue to survive, the same way the previous polio epidemic in Congo was eradicated. Though the current vaccines appear to be good enough to be effective, the new pathogen is nonetheless a warning. The need for new protectant vaccines is more important now than ever. It is only this way there is a chance of permanently wiping out polio.

Source

May, 2020

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.

Source

May, 2020

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.

Source

May, 2020

Coronavirus can spread through sewage systems, say experts

While the phrase may start to sound cliche, it still rings true! These are truly unparalleled times. The past few weeks have been nothing short of an immense change for all of us, leading us to adapt and change our lives and businesses to deal with the COVID-19 outbreak.

With the lockdown being lifted in several countries, health officials all over the world are broadening the search for the people infected and focusing on slowing the spread. This includes finding all possible sources through which the virus can spread. When the response to the pandemic has been focused mostly on preventing community spread, Professor Quilliam and colleagues at the University of Stirling, recently released a paper warning that sewage system can play as a potential COVID-19 transmission risk and that it must not be neglected in this battle to protect human health.

Can COVID-19 really survive in human feces or sewer systems? POSSIBLY.

With years of studying the transport of bacteria in various marine environments, Professor Quilliam stated that “We know that COVID-19 is spread through droplets from coughs and sneezes, or via objects or materials that carry infection. However, it has recently been confirmed that the virus can also be found in human feces – up to 33 days after the patient has tested negative for the respiratory symptoms of COVID-19″.

The authors explained that given the structure of COVID-19, specifically its lipid envelope covering, makes its behavior unpredictable in different aqueous situations. Though the information on COVID-19 environmental persistence is limited, from previous research it should be noted that other coronaviruses have known to survive in viable sewage for around 14 days.

Should wastewater treatment plant operators take extra precautions? YES, BE SAFE!

The authors further added that there is a good possibility for the virus to aerosolize, particularly during the pumping and transfer of wastewater through different sewer systems. This could lead to atmospheric loading of the virus in the form of water droplets, giving it direct access to the respiratory tract of the people exposed. It must be acknowledged that people working at the sewage pumping stations or wastewater treatments are more at risk and need to be provided protective equipment. They must also be educated to seek medical care when showing any signs or symptoms.

Areas with open sewage systems, especially in developing countries and places where safely managed sanitation systems are limited are high at risk. The authors further added that “Such settings are commonly accompanied by poorly resourced and fragile healthcare systems, thus amplifying both exposure risk and potential mortality,”

Is this finding a possible breakthrough? MAYBE, MAYBE NOT.

The authors stated that “It is not yet known whether the virus can be transmitted via the fecal-oral route, however, we know that viral shedding from the digestive system can last longer than shedding from the respiratory tract. Therefore, this could be important – but as yet unquantified – a pathway for increased exposure.”

As the limited number of adequate testing in many places has made it difficult to keep pace with the quick-spreading virus, scientists believe that monitoring sewage for the virus will provide a cheap and reliable alternative. The experts further added that this removes the guesswork about when to impose local lockdowns — or when to lift them.

Though an interesting way to keep track of the virus, monitoring wastewater for the said virus is hardly an easy task. The approach poses many challenges, including deploying it on a large scale and winning the government’s approval.

The authors concluded the paper by stating that In the immediate future, there needs to be an investment of resources to improve our understanding of the risks associated with the fecal transmission of SARS-CoV-2 and whether this respiratory virus can be disseminated by enteric transmission.

Source

Apr, 2020

Genetic variation in immune system may impact the severity of COVID-19

Can your genes be the reason for increased susceptibility to COVID-19 infection? For years, scientists know that genes play a very important role in underlying biological mechanisms. And therefore, over these years many pieces of research have been carried to understand the link between genetic variability and diseases. Recently, new research published in the Journal of Virology (Well-known publication of American Society for Microbiology) highlights that variation in the genes involved in the human immune system can impact the susceptibility and severity of COVID-19 infection.

Human Leukocytes Antigen Genes

You must have seen people of a certain group be more susceptible to disease than others, why? Well, the answer to this lies in your genes. Individual gene variation is known to be one of the major reasons behind the differences in the immune responses. Our immune system works with the help of multiple biomolecules. One such important component of the immune system that plays a very crucial role in determining the strength of the response is the human leukocyte antigen. The genes coding for this antigen is involved in detecting the pathogen upon invasion. The gene variation among different individuals can influence how well the immune system detects the pathogen in an individual. If a person has a weak response than a pathogen such as the Sar-CoV2 virus could easily invade making a person vulnerable to the infection.

Understanding the variation

As we all know that the number of COVID-19 cases is rising across the globe, researchers and scientist are working towards finding better solutions to curb the menace. In the present study, the author of the paper indicated the importance of understanding the variation of human leukocytes antigen (HLA), which forms a very important component of the immune system. Knowing the gene variants of HLA and their respective responses towards the condition can help identify people posing a higher risk towards the COVID-19 infection.

The researchers showed that the HLA, haplotype, and also the full genotype variation may impact the ability of an individual’s immune system to respond against Sars-CoV infection. Moreover, certain alleles can be responsible for more severe infections than others.

“This is the first study to report global distributions of HLA types and haplotypes with potential epidemiological ramifications in the setting of the current pandemic,” write the authors, from Oregon Health & Science University, Portland, and the Portland VA Research Foundation.

One of the important benefits of HLA based study is that HLA typing is quite fast and less expensive. If there is a pairing of HLA typing with that of COVID-19 tests than there can be a significant improvement in the identification of high-risk individuals. Moreover, once the vaccine against COVID-19 is available, high-risk HLA type individuals can be prioritized for the vaccination. This will help in creating herd immunity and help prevent the future spread of the disease.

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Should wastewater treatment plant operators take extra precautions? YES, BE SAFE!

Apr, 2020