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COVID-19 mostly kills through an overreaction of the immune system, whose function is precisely to fight infections, say scientists who have decoded the mechanisms, symptoms, and diagnosis of the disease caused by the SARS-Cov-2 coronavirus.

In a study published in the journal Frontiers in Public Health, the researchers explained step-by-step how the virus infects the airways, multiplies inside cells, and in severe cases causes the immune defences to overshoot with a "cytokine storm".

This storm is an over-activation of white blood cells, which release too-great amounts of cytokines -- inflammation-stimulating molecules --into the blood, they said.

"Similar to what happens after infection with SARS and MERS, data show that patients with severe COVID-19 may have a cytokine storm syndrome," said study author Daishun Liu, Professor at Zunyi Medical University in China.

"The rapidly increased cytokines attract an excess of immune cells such as lymphocytes and neutrophils, resulting in an infiltration of these cells into lung tissue and thus cause lung injury," Liu said.

The researchers explained that the cytokine storm ultimately causes high fever, excessive leakiness of blood vessels, and blood clotting inside the body.

It also causes extremely low blood pressure, lack of oxygen and excess acidity of the blood, and build-up of fluids in the lungs, they said.

The researchers noted that white blood cells are misdirected to attack and inflame even healthy tissue, leading to failure of the lungs, heart, liver, intestines, kidneys, and genitals.

This multiple organ dysfunction syndrome (MODS) may worsen and shutdown the lungs, a condition called acute respiratory distress syndrome, (ARDS), they said.

This, the researchers explained, happens due to the formation of a so-called hyaline membrane -- composed of debris of proteins and dead cells -- lining the lungs, which makes absorption of oxygen difficult.

Most deaths due to COVID-19 are therefore due to respiratory failure, they said.

The researchers explained that in the absence of a specific antiviral cure for COVID-19, the goal of treatment must be to the fight the symptoms, and lowering the mortality rate through intensive maintenance of organ function.

For example, an artificial liver blood purification system or renal replacement therapy can be used to filter the blood through mechanical means, they said.

The team noted that especially important are methods to supplement or replace lung function, for example with non-invasive mechanical ventilation through a mask, ventilation through a tube into the windpipe, the administration of heated and humidified oxygen via a tube in the nose, or a heart-lung bypass.

The researchers stressed the importance of preventing secondary infections.

They noted that SARS-Cov-2 also invades the intestines, where it causes inflammation and leakiness of the gut lining, allowing the opportunistic entry of other disease-causing microorganisms.

The researchers advocate that this should be prevented with nutritional support, for example with probiotics -- beneficial bacteria that protect against the establishment of harmful ones -- and nutrients and amino acids to improve the immune defences and function of the intestine.

"Because treatment for now relies on aggressive treatment of symptoms, preventative protection against secondary infections, such as bacteria and fungi, is particularly important to support organ function, especially in the heart, kidneys, and liver, to try and avoid further deterioration of their condition," Liu added.

The deadly coronavirus that entered India while there was still nip in the air has beaten rising mercury, humid conditions, unique Indian genome and has entered monsoon season with more potency as fresh cases are only breaking all records in the country.

India recorded a single-day spike of record 24,850 new coronavirus cases on Sunday, taking its total tally to 6.73 lakh corona-positive cases.

Top Indian microbiologists were hopeful in March that after the 21-day lockdown, as summer approaches, the rise in temperature would play an important role in preventing the drastic spread of COVID-19 virus in India.

Several virologists hinted that by June this year, the impact of COVID-19 would be less than what it appeared in March-April.

The claims have fallen flat as the virus is mutating fast, becoming more potent than ever.

According to experts, the novel coronavirus is a new virus whose seasonality and response to hot humid weather was never fully understood.

"The theory was based on the fact that high temperatures can kill the virus as in sterilisation techniques used in healthcare. But these are controlled environment conditions. There are many other factors besides temperature, humidity which influence the transmission rate among humans," Dr Anu Gupta, Head, Microbiologist and Infection Control, Fortis Escorts Heart Institute, told IANS.

There is no built-up immunity to COVID-19 in humans.

"Also, asymptomatic people might be passing it to many others unknowingly. New viruses tend not to follow the seasonal trend in their first year," Gupta emphasized.

Globally, as several countries are now experiencing hot weather, the World Health Organization (WHO) reported a record hike in the number of coronavirus cases, with the total rising by 2,12,326 in 24 hours in the highest single-day increase since COVID-19 broke out.

So far over 11 million people worldwide have tested positive for the disease which has led to over 5,25,000 deaths, according to data from Johns Hopkins University. The US remained the worst-hit country with over 28 lakh cases, followed by Brazil with 15.8 lakh.

According to Sandeep Nayar, Senior Consultant and HOD, Respiratory Medicine, Allergy & Sleep Disorders, BLK Super Speciality Hospital in New Delhi, whether temperature plays a role in COVID-19 infection is highly debated.

One school of thought said in the tropical regions of South Asia, the virus might not thrive longer.

"On the other hand, another school of thought has found that novel Coronavirus can survive in a hot and humid environment and tropical climate does not make a difference to the virus. According to them, this is what distinguishes the novel coronavirus from other common viruses, which usually wane in hot weather," stressed Nayar.

Not much has been studied in the past and no definite treatment or vaccine is available to date.

"Every day, new properties and manifestation of the disease come up. As of now, the only way to prevent this monster is by taking appropriate precautions. Hand hygiene, social distancing, cough etiquette and face masks definitely reduce spread of COVID-19 infection," Nayar told IANS.

Not just top Indian health experts, even Indian-American scientists had this theory in mind that sunshine and summer may ebb the spread of the coronavirus.

Ravi Godse, Director of Discharge Planning, UPMC Shadyside Pennsylvania in the US told IANS in April: "In the summer, the humidity can go up as well, meaning more water drops in the air. If the air is saturated with water and somebody sneezes virus droplets into such air, it is likely that the droplets will fall to the ground quicker, making them less infectious. So the short answer is yes, summer/sunshine could be bettera.

According to Dr Puneet Khanna, Head of Respiratory Medicine and Pulmonology, Manipal Hospital, Delhi, COVID-19 death rates are not too different in tropical countries but since the disease affected them late it was yet to show its peak in these areas.

"The virus can survive well in hot and humid countries and this is proven now," he stressed.

New York, May 19: Cigarette smoke spurs the lungs to make more of the receptor protein which the novel coronavirus uses to enter human cells, according to a study which suggests that quitting smoking might reduce the risk of a severe coronavirus infection.

The findings, published in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to severe COVID-19 disease.

"Our results provide a clue as to why smokers who develop COVID-19 tend to have poor clinical outcomes," said study senior author Jason Sheltzer, a cancer geneticist at Cold Spring Harbor Laboratory in the US.

"We found that smoking caused a significant increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells," Sheltzer said.

According to the scientists, quitting smoking might reduce the risk of a severe coronavirus infection.

They said most individuals infected with the virus suffer only mild illness, if they experience any at all.

However, some require intensive care when the sometimes-fatal virus attacks, the researchers said.

In particular, they said three groups have been significantly more likely than others to develop severe illness -- men, the elderly, and smokers.

Turning to previously published data for possible explanations for these disparities, the scientists assessed if vulnerable groups share some key features related to the human proteins that the coronavirus relies on for infection.

First, they said, they focused on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers.

The scientists said both mice that had been exposed to smoke in a laboratory, and humans who were current smokers had significant upregulation of ACE2.

According to Sheltzer, smokers produced 30-55 per cent more ACE2 than their non-smoking counterparts.

While the researchers found no evidence that age or sex impacts ACE2 levels in the lungs, they said the influence of smoke exposure was surprisingly strong.

However, they said, the change seemed to be temporary.

According to the data, the level of the receptors ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.

The study noted that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells.

Smoking is known to increase the prevalence of such cells, the scientists said.

"Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers' lungs could be a byproduct of smoking-induced secretory cell hyperplasia," Sheltzer explained.

However, Sheltzer said other studies on the effects of cigarette smoke have shown mixed results.

"Cigarette smoke contains hundreds of different chemicals. It's possible that certain ingredients like nicotine have a different effect than whole smoke does," he said.

The researchers cautioned that the actual ACE2 protein may be regulated in ways not addressed in the current study.

"One could imagine that having more cells that express ACE2 could make it easier for SARS-CoV-2 to spread in someone's lungs, but there is still a lot more we need to explore," Sheltzer said.