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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.

UN, Jul 14: There will be no return to the "old normal" for the foreseeable future as a result of the ongoing COVID-19 pandemic, and too many countries were still headed in the wrong direction, the chief of the World Health Organization (WHO) warned.

"The virus remains public enemy number one, but the actions of many governments and people do not reflect this," Xinhua news agency quoted WHO Director-General Tedros Adhanom Ghebreyesus at as saying a regular briefing on Monday.

He noted that mixed messages from leaders are undermining trust, which is the most critical ingredient of any response, while the only aim of the virus is to find people to infect.

Things are going to "get worse and worse and worse", he warned, unless governments communicate clearly with their citizens and roll out a comprehensive strategy focused on suppressing transmission and saving lives, while populations follow the basic public health principles of physical distancing, hand washing, wearing masks, coughing etiquette and staying home when sick.

COVID-19 has been gaining its momentum lately.

According to Tedros, Sunday saw a record of 230,000 cases reported to WHO, of which almost 80% were from just 10 countries and about half from just two countries.

"But it does not have to be this way," he said, asking every single leader, government and individual "to do their bit to break the chains of COVID-19 transmission and end the collective suffering".

To control the disease and get on with people's lives, Tedros said, three things are required. The first is to focus on reducing mortality and suppressing transmission; the second is to focus on an empowered, engaged community that takes individual behaviour measures in the interest of each other.

And the third is a strong government leadership and coordination of comprehensive strategies that are communicated clearly and consistently.

"We weren't prepared collectively, but we must use all the tools we have to bring this pandemic under control. And we need to do it right now," he added.

At the WHO briefing on Monday, health experts also said there was evidence to suggest that children under the age of 10 were only very mildly affected by Covid-19, while those over 10 seemed to suffer similar mild symptoms to young adults.

To what extent children can transmit the virus, while it appears to be low, remains unknown.

On Tuesday, the number of global coronavirus cases cross the 13 million mark, according to the Johns Hopkins University.

The total number of cases currently stood at 13,070,097, while the fatalities rose to 572,411, the University's Center for Systems Science and Engineering (CSSE) revealed in its latest update.

The US accounted for the world's highest number of infections and fatalities at 3,363,056 and 135,605, respectively, according to the CSSE.

Brazil came in the second place with 1,884,967 infections and 72,833 deaths.