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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.

Clinician-scientists have found that Irish patients admitted to hospital with severe coronavirus (COVID-19) infection are experiencing abnormal blood clotting that contributes to death in some patients.

The research team from the Royal College of Surgeons in Ireland found that abnormal blood clotting occurs in Irish patients with severe COVID-19 infection, causing micro-clots within the lungs.

According to the study, they also found that Irish patients with higher levels of blood clotting activity had a significantly worse prognosis and were more likely to require ICU admission.

"Our novel findings demonstrate that COVID-19 is associated with a unique type of blood clotting disorder that is primarily focussed within the lungs and which undoubtedly contributes to the high levels of mortality being seen in patients with COVID-19," said Professor James O'Donnell from St James's Hospital in Ireland.

In addition to pneumonia affecting the small air sacs within the lungs, the research team has also hundreds of small blood clots throughout the lungs.

This scenario is not seen with other types of lung infection and explains why blood oxygen levels fall dramatically in severe COVID-19 infection, the study, published in the British Journal of Haematology said.

"Understanding how these micro-clots are being formed within the lung is critical so that we can develop more effective treatments for our patients, particularly those in high-risk groups," O'Donnell said.

"Further studies will be required to investigate whether different blood-thinning treatments may have a role in selected high-risk patients in order to reduce the risk of clot formation," Professor O'Donnell added.

According to the study, emerging evidence also shows that the abnormal blood-clotting problem in COVID-19 results in a significantly increased risk of heart attacks and strokes.

As of Friday morning, the cases increased to 20,612 cases in Ireland, with 1,232 deaths so far, according to the Johns Hopkins University.

Washington, Feb 21: The fat around arteries may play an important role in keeping the blood vessels healthy, according to a study in rats that may affect how researchers test for treatments related to plaque buildup, as seen in conditions leading to heart attack.

The study, published in the journal Scientific Reports, noted that the fat, known as perivascular adipose tissue, or PVAT, helps arteries let go of muscular tension while under constant strain.

According to the researchers, including Stephanie W. Watts from the Michigan State University in the US, this feature is similar to how the bladder expands to accommodate more liquid, while at the same time keeping it from spilling out.

"In our study, PVAT reduced the tension that blood vessels experience when stretched," Watts said.

"And that's a good thing, because the vessel then expends less energy. It's not under as much stress," she added.

According to Watts and her team, PVAT has largely been ignored by researchers believing its main job was to store lipids and do little more.

Until now, she said, scientists only divided blood vessels into three parts, the innermost layer called the tunica intima, the middle layer called the tunica media, and the outermost layer called the tunica adventitia.

Watts believes PVAT is the fourth layer, which others have called tunica adiposa.

Tunica, she said, meant a membranous sheath enveloping or lining an organ, and adiposa is a synonym for fat.

"For years, we ignored this layer -- in the lab it was thrown out. In the clinic it wasn't imaged. But now we're discovering it may be integral to our blood vessels," Watts said.

"Our finding redefines what the functional blood vessels are, and is part of what can be dysfunctional in diseases that afflict us, including hypertension. We need to pay attention to this layer of a blood vessel because it does far more than we originally thought," she added.

Earlier studies, Watts said, had shown that PVAT plays a role in the functioning of blood vessels, finding that it secretes substances that can cause blood vessels to relax as well as substances that can cause it to contract.

In the current study, the researchers decided to test whether PVAT provides a structural benefit to arteries by assisting the function of stress relaxation.

They tested the thoracic aorta in rats, and found those with intact PVAT had more stress relaxation than those without.

The study revealed that the pieces of artery with surrounding fat had measurably relaxed more than those without.

Watts and her colleagues then tested other arteries, and were able to duplicate the same response.

"It's not something you see only in this particular vessel or this particular species or this particular strain. But that maybe it's a general phenomenon," she said.