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Geneva, May 17: Spraying disinfectant on the streets, as practised in some countries, does not eliminate the new coronavirus and even poses a health risk, the World Health Organization (WHO) warned on Saturday.

In a document on cleaning and disinfecting surfaces as part of the response to the virus, the WHO says spraying can be ineffective. "Spraying or fumigation of outdoor spaces, such as streets or marketplaces, is... not recommended to kill the Covid-19 virus or other pathogens because disinfectant is inactivated by dirt and debris," explains the WHO.

"Even in the absence of organic matter, chemical spraying is unlikely to adequately cover all surfaces for the duration of the required contact time needed to inactivate pathogens." The WHO said that streets and pavements are not considered as "reservoirs of infection" of Covid-19, adding that spraying disinfectants, even outside, can be "dangerous for human health".

The document also stresses that spraying individuals with disinfectants is "not recommended under any circumstances".

"This could be physically and psychologically harmful and would not reduce an infected person's ability to spread the virus through droplets or contact," said the document.

Spraying chlorine or other toxic chemicals on people can cause eye and skin irritation, bronchospasm and gastrointestinal effects, it adds.

The organisation is also warning against the systematic spraying and fumigating of disinfectants on to surfaces in indoor spaces, citing a study that has shown it to be ineffective outside direct spraying areas.

"If disinfectants are to be applied, this should be done with a cloth or wipe that has been soaked in disinfectant," it says.

The SARS-CoV-2 virus, the cause of the pandemic that has killed more than 300,000 people worldwide since its appearance in late December in China, can attach itself to surfaces and objects.

However, no precise information is currently available for the period during which the viruses remain infectious on the various surfaces.

Studies have shown that the virus can stay on several types of surfaces for several days. However, these maximum durations are only theoretical because they are recorded under laboratory conditions and should be "interpreted with caution" in the real-world environment.

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.