Type of ultraviolet light kills airborne coronavirus; effect on platelets helps explain blood clot issues

By Nancy Lapid
(Reuters) - The following is a brief summary of some of the latest scientific studies on the novel coronavirus and efforts to find treatments and vaccines for COVID-19, the disease caused by the virus.

Safe form of ultraviolet light kills coronavirus in the air
Ceiling lights that emit a safe form of ultraviolet light, known as long-range UVC, would very effectively kill coronaviruses in the air, according to a study by Columbia University researchers. "Very little exposure to distant UVC light killed well over 99.9% of the exposed virus," said lead researcher Dr. David Brenner told Reuters. The researchers put coronavirus particles in small droplets and hovered them in the air in front of distant UVC light. Then they collected the viruses and tested them to see how many were still active. The study, published in Scientific Reports on Wednesday, used coronaviruses that cause colds. "However, in our subsequent ongoing studies, we found that the coronavirus that causes COVID-19 is killed in the same way by distant UVC light," said Brenner. The idea would be to install overhead, long-range UVC lights in public places where they "continuously kill microbes, including the COVID-19 virus, thereby limiting the spread of the virus," Brenner said, adding that manufacturers by Fern-UVC Production is already ramping up. "We don't see distant UVC light as an alternative to masks and social distance," said Brenner. "We see it as a new additional weapon that we can use in the fight against COVID-19." (https://go.nature.com/3hYdWYA)

Cells that help the coronavirus overactivate blood
The effect of the new corona virus on platelets in the blood can 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 from clot formation. They also recruit immune cells and create inflammation. On Tuesday, researchers in Blood magazine reported that the new coronavirus is dramatically changing the expression and function of platelet genes. The inflammatory proteins produced by the virus cause platelets to become "hyper-reactive" and form clots more easily and frequently, University of Utah co-author Robert Campbell told Reuters. The effect correlated with the severity of the patient's illness, his team found. In a separate study, not yet reviewed by experts, the researchers found that platelets in 20% of COVID-19 patients contain molecules with the genetic code of the coronavirus. It is not yet clear whether the virus actually targets the platelets or whether the platelets contain the complete virus, said study co-author Eric Boilard from the Universitaire de Québec. "What was very obvious was the impressive level of platelet activation in COVID-19," said Boilard. The results could open new avenues for the treatment of coagulation complications in COVID-19. (https://bit.ly/2Z3pj8Z; https://bit.ly/2B6Zmx9)

Antibodies may not be the only evidence of previous coronavirus infection
Antibodies against the novel coronavirus should not be seen as the only evidence that someone has recovered from COVID-19, researchers say. They examined nine confirmed coronavirus patients from seven families and eight of their household members who later developed COVID-19 symptoms. The original patients all developed antibodies to the virus, as shown by blood tests after their recovery. However, the sick relatives had negative antibody tests, but six of the eight had other immune cells in their blood that indicated they were infected. Up to 80 days after their symptoms started, they had T cells - a key component of the immune system - that could recognize and fight the coronavirus. "T-cell responses may be more sensitive indicators of SARS-Co-V-2 exposure than antibodies," the researchers said Monday in an article that has not yet been reviewed by experts. "Our results suggest that epidemiological data based only on the detection of SARS-CoV-2 antibodies can lead to a significant underestimation of the previous exposure to the virus." (https://bit.ly/2Yt2Frl)

Details of the dexamethasone study show that a reduced risk of death is released
Last week's announcement that the cheap and widely used steroid dexamethasone significantly reduced deaths in critically ill COVID-19 patients caused both excitement and skepticism as British researchers announced the result without disclosing any details. On Monday they published their data online before the full assessment. They compared 2,104 coronavirus patients who received dexamethasone with 4,321 patients who did not. Overall, 21.6% of the patients receiving dexamethasone and 24.6% of the patients receiving standard care died within 28 days. However, the effects on mortality rates varied depending on how sick the patients were at the start of the study. Dexamethasone reduced the mortality rate by a third (from 40.7% to 29.0%) in patients who needed a ventilator and by a fifth (in 25.0% of those who received assisted oxygen without an invasive ventilator) to 21.5%). The steroid did not reduce deaths in patients without respiratory support. The World Health Organization has stated that dexamethasone should be reserved for serious COVID-19 cases that have been shown to be beneficial. (https://bit.ly/2Yuc7L9; https://reut.rs/2BFVm6H)

Open https://graphics.reuters.com/HEALTH-CORONAVIRUS/yxmvjqywprz/index.html in an external browser to get a Reuters graphic of vaccines and treatments in development.

(This story was rewritten to specify the name of the first article in the publication.)

(Reporting by Nancy Lapid; editing by Bill Berkrot)

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