The type of ultraviolet light kills the coronavirus in the air; effect on platelets helps explain blood clotting problems

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

Safe form of UV light kills coronavirus in air

According to a study by researchers at Columbia University, ceiling devices that emit a safe form of ultraviolet light called far UVC would be very efficient at killing coronaviruses in the air. “Very low exposure to far UVC light killed more than 99.9% of the exposed virus,” lead researcher Dr. David Brenner told Reuters. The researchers placed coronavirus particles in tiny droplets and floated them in the air in front of the far UVC lights, then collected the viruses and tested them to see how many were still active. The study, published 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 removed in the same way by far UVC light,” said Brenner. The idea would be to install distant UVC overhead lights in public places where they would be “continually killing microbes, including the COVID-19 virus, and thus limit the spread of the virus,” Brenner said, adding that manufacturers of far UVC already they are increasing production. “We don’t see far UVC light as an alternative to masks and social distancing,” said Brenner. “We see it as a new additional 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 caused serious complications and strokes in some patients with COVID-19. The job of platelets is 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 dramatically changes the function and expression of the platelet gene. Inflammatory proteins generated by the virus make platelets “hyperreactive” and clot more easily and more frequently, co-author Robert Campbell of the University of Utah told Reuters. His team found that the effect was correlated with the severity of the patient’s illness. In a separate study not yet peer-reviewed, the researchers found that platelets in 20% of COVID-19 patients contain molecules with the genetic code for the coronavirus. It is still unclear whether the virus actually targets platelets, or whether platelets contain the entire virus, said study co-author Eric Boilard of the University of Quebec. “What was very obvious was the impressive level of platelet activation in COVID-19,” said Boilard. The findings may open new avenues to treat clot-related complications in COVID-19. (bit.ly/2Z3pj8Z; bit.ly/2B6Zmx9)

Antibodies may not be the only proof of previous coronavirus infection

According to the researchers, antibodies against the new coronavirus should not be considered the only evidence that someone has recovered from COVID-19. They studied nine confirmed coronavirus patients from seven families, along with eight of their household members who later became ill with the symptoms of COVID-19. All of the original patients developed antibodies to the virus, as evidenced by blood tests after recovery. However, family members who became ill had negative antibody tests, but six of the eight had other immune cells in their blood that suggested they had been infected. Up to 80 days after their symptoms began, they had T cells, a key component of the immune system, that could recognize and attack the coronavirus. “T-cell responses may be more sensitive indicators of exposure to SARS-Co-V-2 than antibodies,” the researchers said Monday in an article not yet peer-reviewed. “Our results indicate that epidemiological data based solely on the detection of antibodies to SARS-CoV-2 may lead to a substantial underestimation of previous exposure to the virus.” (bit.ly/2Yt2Frl)

Details of dexamethasone study showing reduced risk of death released

Last week’s announcement that cheap and widely used steroid dexamethasone significantly reduced deaths in seriously ill patients with COVID-19 generated both enthusiasm and skepticism, because British researchers announced the result without publishing all the details. On Monday, they released their data online, before the full peer review. They compared 2,104 coronavirus patients who received dexamethasone with 4,321 patients who did not receive it. Overall, 21.6% of patients who received dexamethasone and 24.6% of those who received standard care died within 28 days. But the effect on mortality rates varied depending on how sick the patients were when they entered the study. Dexamethasone reduced the death rate by one third in patients who needed a ventilator to help them breathe (from 40.7% to 29.0%) and by a fifth in patients who received supportive oxygen without an invasive ventilator (from 25.0% to 21.5%). The steroid did not reduce deaths in patients who did not receive respiratory support. The World Health Organization has said that dexamethasone should be reserved for severe cases of COVID-19 where it has been shown to provide benefits. (bit.ly/2Yuc7L9; reut.rs/2BFVm6H)

Open here in an external browser for a Reuters chart of vaccines and treatments in development.

(This story has been filled in to correct the name of the first item in the post)