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The World Health Organisation on Wednesday said that anti-malarial drug hydroxychloroquine (HCQ) will return to the solidarity trial for the potential treatment of coronavirus disease.

At a press conference in the WHO headquarters in Geneva, Director General Tedros Adhanom Ghebreyesus said: "On the basis of the available mortality data, the members of the committee recommended that there are no reasons to modify the trial protocol. The Executive Group received this recommendation and endorsed continuation of all arms of the solidarity trial, including hydroxychloroquine."

The world health body had temporarily suspended the usage of HCQ from the solidarity trial for coronavirus treatment on May 25 soon after a study published in one of the most reliable medical journals, which had suggested that the drug could cause more fatalities among COVID-19 patients.

However, the WHO chief said that the decision was taken as a precaution while the safety data was reviewed.

Ghebreyesus also said that the Data Safety and Monitoring Committee will continue to closely monitor the safety of all therapeutics being tested in the solidarity trial.

"So far, more than 3,500 patients have been recruited in 35 countries. WHO is committed to accelerating the development of effective therapeutics, vaccines and diagnostics as part of our commitment to serving the world with science, solutions and solidarity," he said.

Soon after HCQ was suspended from the trial, the Indian government had said that the antimalarial drug has been known for its benefits for a long time and its usage will be continued on the frontline workers, including police and healthcare professionals, as prophylaxis. The government had also said that studies were being conducted and the drug would be included in the clinical trial also for the treatment of coronavirus disease.

US President Donald Trump also had strongly advocated the use of HCQ and called it a "game-changer". He went to the extent of saying that he had taken the medicine.

Launched by WHO and partners, solidarity trial is an international clinical trial to find an effective treatment for COVID-19, including drugs to slow the progression of the disease or improve survival. The trial, which enrols patients from different countries, "will compare four treatment options against standard of care to assess their relative effectiveness against COVID-19", said WHO. 

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.