(Reuters) - The following is a brief roundup of some of the latest scientific studies on the novel coronavirus and efforts to find treatments and vaccines for COVID-19, the illness caused by the virus.
Safe form of ultraviolet light kills airborne coronavirus
Ceiling fixtures emitting a safe form of ultraviolet light called far-UVC would be very efficient at killing airborne coronaviruses, according to a study by researchers at Columbia University. "A very low exposure to far-UVC light killed well over 99.9% of the exposed virus," lead researcher Dr. David Brenner told Reuters. The researchers put coronavirus particles into little droplets and floated them in the air in front of far-UVC lights, then collected the viruses and tested them to see how many were still active. The study, published on Wednesday in Scientific Reports, used coronaviruses that cause common colds. "But in our subsequent ongoing studies we have found that the coronavirus that causes COVID-19 is killed in just the same way by far-UVC light," Brenner said. The idea would be to install overhead far-UVC lights in public locations, where they would be "continuously killing microbes, including the COVID-19 virus - and so limiting the spread of the virus," Brenner said, adding that far-UVC manufacturers are already ramping up production. "We don't see far-UVC light as an alternative to masks and social distancing," Brenner said. "We see it as a new extra weapon that we can use in the battle against COVID-19." (go.nature.com/3hYdWYA)
Cells that help blood to clot over-activated by the coronavirus
The effect of the new coronavirus on platelets in the blood may help explain the excessive blood clotting that has led to serious complications and strokes in some COVID-19 patients. It is the job of platelets to recognize wounds and prevent bleeding by forming clots. They also recruit immune cells and generate inflammation. On Tuesday, researchers reported in the journal Blood that the new coronavirus drastically changes platelet gene expression and function. The inflammatory proteins generated by the virus cause platelets to become "hyperreactive" and form clots more easily and more often, coauthor Robert Campbell of the University of Utah told Reuters. The effect was correlated with patient illness severity, his team found. In a separate not-yet-peer-reviewed study, researchers found that platelets in 20% of COVID-19 patients contain molecules with the genetic code of the coronavirus. It is not clear yet whether the virus actually targets the platelets, or if the platelets contain the full virus, said study coauthor Eric Boilard of Universitaire de Québec. "What was very obvious was the impressive level of platelet activation in COVID-19," Boilard said. The findings may open up new avenues to treat clot related complications in COVID-19. (bit.ly/2Z3pj8Z; bit.ly/2B6Zmx9)
Antibodies might not be sole proof of prior coronavirus infection
Antibodies to the novel coronavirus should not be considered the only evidence that someone has recovered from COVID-19, researchers say. They studied nine confirmed coronavirus patients from seven families, along with eight of their household members who later became ill with COVID-19 symptoms. The original patients all developed antibodies to the virus, as shown by blood tests after they recovered. The relatives who got sick, however, had negative antibody tests, but six of the eight had other immune cells in their blood that suggested they had been infected. For up to 80 days after their symptoms began, they had T cells - a key component of the immune system - that could recognize and target the coronavirus. "T cell responses may be more sensitive indicators of SARS-Co-V-2 exposure than antibodies," the researchers said on Monday in a not-yet-peer-reviewed paper. "Our results indicate that epidemiological data relying only on the detection of SARS-CoV-2 antibodies may lead to a substantial underestimation of prior exposure to the virus." (bit.ly/2Yt2Frl)
Details of dexamethasone study showing reduced death risk released
Last week's announcement that the cheap and widely used steroid dexamethasone significantly reduced deaths in severely ill COVID-19 patients generated both excitement and skepticism, because the British researchers announced the result without publishing full details. On Monday, they posted their data online, in advance of full peer-review. They compared 2,104 coronavirus patients who received dexamethasone with 4,321 patients who did not. Overall, 21.6% of patients who got dexamethasone and 24.6% of those who got standard care died within 28 days. But the effect on mortality rates varied depending on how sick patients were when they entered the study. Dexamethasone reduced the death rate by one-third in patients who needed a ventilator to help them breath (from 40.7% to 29.0%) and by one-fifth in patients receiving supportive oxygen without an invasive ventilator (from 25.0% to 21.5%). The steroid did not reduce deaths in patients not receiving respiratory support. The World Health Organization has said dexamethasone should be reserved for serious COVID-19 cases in which it has been shown to provide benefits. (bit.ly/2Yuc7L9; reut.rs/2BFVm6H)
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(This story has been refiled to fix name of publication first item)
Reporting by Nancy Lapid; Editing by Bill Berkrot
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