WASHINGTON: The new coronavirus is quickly destroyed by sunlight, according to new research announced by a senior US official on Thursday, though the study has not yet been made public and awaits external evaluation. William Bryan, science and technology advisor to the Department of Homeland Security secretary, told reporters at the White House that government scientists had found ultraviolet rays had a potent impact on the pathogen, offering hope that its spread may ease over the summer.
“Our most striking observation to date is the powerful effect that solar light appears to have on killing the virus, both surfaces and in the air,” he said. “We’ve seen a similar effect with both temperature and humidity as well, where increasing the temperature and humidity or both is generally less favorable to the virus.” But the paper itself has not yet been released for review, making it difficult for independent experts to comment on how robust its methodology was.
It has long been known that ultraviolet light has a sterilizing effect, because the radiation damages the virus’s genetic material and their ability to replicate. A key question, however, will be what the intensity and wavelength of the UV light used in the experiment was and whether this accurately mimics natural light conditions in summer.
“It would be good to know how the test was done, and how the results were measured,” Benjamin Neuman, chair of biological sciences at Texas A&M University-Texarkana, told AFP. “Not that it would be done badly, just that there are several different ways to count viruses, depending on what aspect you are interested in studying.”
Bryan shared a slide summarizing major findings of the experiment that was carried out at the National Biodefense Analysis and Countermeasures Center in Maryland. It showed that the virus’s half-life – the time taken for it to reduce to half its amount – was 18 hours when the temperature was 21 to 24 degrees Celsius with 20 percent humidity on a non-porous surface. This includes things like door handles and stainless steel.
But the half-life dropped to six hours when humidity rose to 80 percent – and to just two minutes when sunlight was added to the equation. When the virus was aerosolized – meaning suspended in the air – the half-life was one hour when the temperature was 21 to 24 degrees Celsius with 20 percent humidity. In the presence of sunlight, this dropped to just one and a half minutes.
Bryan concluded that summer-like conditions “will create an environment (where) transmission can be decreased”. He added, though, that reduced spread did not mean the pathogen would be eliminated entirely and social distancing guidelines cannot be fully lifted. “It would be irresponsible for us to say that we feel that the summer is just going to totally kill the virus and then if it’s a free-for-all and that people ignore those guides,” he said.
Previous work has also agreed that the virus fares better in cold and dry weather than it does in hot and humid conditions, and the lower rate of spread in southern hemisphere countries where it is early fall and still warm bear this out. Australia, for example, has had just under 7,000 confirmed cases and 77 deaths – well below many northern hemisphere nations.
The reasons are thought to include that respiratory droplets remain airborne for longer in colder weather, and that viruses degrade more quickly on hotter surfaces, because a protective layer of fat that envelops them dries out faster. US health authorities believe that even if COVID-19 cases slow over summer, the rate of infection is likely to increase again in fall and winter, in line with other seasonal viruses like the flu.
Meanwhile, the experimental coronavirus treatment remdesivir has failed in its first randomized clinical trial, inadvertently released results showed Thursday, dampening expectations for the closely watched drug. A draft summary went online briefly on the website of the World Health Organization (WHO) and was first reported by the Financial Times and Stat, which posted a screenshot. But Gilead Sciences, the company behind the medicine, disputed how the now-deleted post had characterized the findings, saying the data showed a “potential benefit”.
The summary said the Chinese trial involved 237 patients, with 158 on the drug and 79 in a control group. Remdesivir was stopped early in 18 patients because of side effects. The authors said remdesivir was “not associated with a difference in time to clinical improvement” compared to the control. After a month, 13.9 percent of the patients on remdesivir had died compared to 12.8 percent of those in the control group. The difference is not statistically significant. The WHO told the Financial Times that the draft is undergoing peer review and was published early in error.
A spokesman for Gilead told AFP: “We believe the post included inappropriate characterizations of the study,” saying it was terminated early due to low enrollment and was therefore not statistically meaningful. “As such, the study results are inconclusive, though trends in the data suggest a potential benefit for remdesivir, particularly among patients treated early in disease,” the spokesman added. The study does not represent the final word on the matter, and there are several large-scale trials in advanced stages that should soon provide a clearer picture.
Remdesivir, which is administered intravenously, was among the first drugs suggested as a treatment for the novel coronavirus and as such has great hopes riding on it. Stephen Evans, a professor of pharmacoepidemiology at the London School of Hygiene & Tropical Medicine, who was not involved in the research, said “the trial was too small in numbers recruited” to detect either benefit or risk. But he added: “If the drug only works well when given very early after infection, it may be much less useful in practice.”
Last week, Stat reported it had shown significant efficacy at a Chicago hospital where patients who are part of one of the major trials are being treated. The US National Institutes for Health also reported it had proven effective in a small experiment on monkeys. Remdesivir, which previously failed in trials against Ebola, belongs to a class of drugs that act on the virus directly – as opposed to controlling the abnormal and often lethal autoimmune response it causes.
It mimics one of the four building blocks of RNA and DNA and gets absorbed into the virus’s genome, which in turn stops the pathogen from replicating. The antimalarial drugs hydroxychloroquine and chloroquine are also being widely used on COVID-19 on a so-called “compassionate basis” pending results from large trials, with early studies decidedly mixed. Other therapies that are being studied include collecting antibodies from COVID-19 survivors and injecting them in patients, or harvesting antibodies from genetically-engineered mice that were deliberately infected. – Agencies