Scientists all over the world are working to understand, contain and cure Covid-19. Here’s a quick look at four important advances that made headway this week.
A positive trial for an antiviral drug
Yesterday a rare bit of good news emerged from a clinical trial at the University of Chicago. STATnews reported that the antiviral drug Remdesivir appeared to have some fighting force against Covid-19. The trial included 125 people, 113 of them classified as having a severe case of the virus.
All got the drug; there was no placebo group. Most were released from the hospital less than a week later, and only 2 died – an unusually low number given how deadly the disease has been in those who get severely ill. Other trials around the world, if they go this well, should lead to quick FDA approval for the drug, manufactured by Gilead Sciences.
Long before the current Covid-19 pandemic, scientists at the University of North Carolina and Gilead began developing this drug in anticipation of new coronavirus epidemic. Two other deadly outbreaks that occurred this century, SARS and MERS, were both caused by coronaviruses from bats, as with Covid-19.
One of the developers of the drug, Timothy Sheahan of the University of North Carolina, told me in an interview last January that the drug was designed to interfere with enzymes SARS and MERS need to replicate themselves. At the time, his group had just started to see impressive results in animal studies of MERS.
The only human trials before the current outbreak were in Ebola patients in the Democratic Republic of Congo. While it didn’t work against Ebola as well as other therapies, it did pass basic safety standards.
The drug has been given sporadically for Covid-19. Anecdotal reports abound of people near death bouncing back after getting the drug. And even this clinical trial has to be viewed with cautious optimism, since it was small, and wasn’t compared with a placebo. But more trials are underway around the world – including 2,400 participants with severe disease and 1,600 patients whose symptoms are moderate.
New clues to how the virus spread from China
Genetic sleuths are digging deep into the origin and early spread of the Covid-19 virus, tracking small mutations in its genetic material. One surprise is that the virus had already branched into two subtypes by the time it was isolated from the first patient in Wuhan on December 23, and this patient seemed to have the second subtype – not the original. Peter Forster, a genetics professor from Cambridge University, has dubbed the original variant A, and the one found in that Wuhan patient variant B. (B carries two mutations not found in A.)
Strain A is more than 96% identical to samples isolated from horseshoe bats, which he believes harbored the virus before it jumped to humans. A molecular clock technique puts that leap between September 18 and December 7, 2019.
Forster said he and his colleagues, who published their work in the Proceedings of the National Academy of Sciences, used a collection of published viral sequences collected in an international database normally used to track influenza. The paper only included the first 160 viral genomes, but his group has now studied more than 1,000.
Looking at data from before January 17, which represents the earliest date people started travelling for Chinese New Year, Forster found that of 44 Wuhan samples, 42 were B and only 2 were A. There were more A strains in the Guangdong Province in southern China.
Some people have speculated that the virus escaped from the Wuhan Institute of Virology, which may have been experimenting on coronaviruses, but Forester says his data point to a jump from bats in Southern China that subsequently spread to Wuhan and other areas. The B strain might have branched off before it reached Wuhan, where the first major outbreak was noticed.
Meanwhile, he says, they find viruses from cluster A in Americans who’d travelled from China to the West Coast of the United States between January and early March. Before March 24th, most U.S. cases were A.
B, however, quickly became the dominant type in Wuhan and across China. Another mutation in B led to a strain C, which is nearly absent in China, but is still spreading across Europe. Europe has also shown a lot of sequences from the B cluster. (Whether these mutations affect the behavior or lethality of the virus is yet to be determined, since mutations don’t always lead to changes in function.)
Forster said the viral genetics show the first case in Italy in late January originated from an early spread in Germany, though Italian health authorities focused only on the patients’ possible connections to China. “Meanwhile the disease is spreading uncontrolled across Italy.”
Researchers at NYU and Mount Sinai used similar genetic information gathered later in the outbreak to determine that cases in New York City originated from multiple sources elsewhere in the U.S. and Europe, rather than directly from China, and that there had been local spread in New York for a month or so before it was officially first identified there at the end of February. Their paper is pending publication.
Forster hopes further work in sequencing genomes could help health authorities track new outbreaks without looking in the wrong place. And finding the true origin of the pandemic could help us avoid making the same mistake again.
Antibody studies are looking for more volunteers
Antibody tests have become a hot topic since people jumped to the conclusion that getting a positive test means you can’t get or spread Covid-19. While standard tests detect genetic material from the virus itself, antibody tests can detect proteins the body makes to fight the infections.
New York Times tech columnist Kara Swisher wrote this week that she got one, “because she knew a guy,” but found it a moral dilemma to take a test so many others need.
It would have presented no moral dilemma had the guy been the head of a legitimate research project, because scientists still can’t be sure antibodies from a previous infection always protect against a new one. Harvard epidemiologist Marc Lipsitch also warned that too little is yet known about post-infection immunity to assume people can’t get re-infected.
“It’s hard to know what immunity to this virus looks like since it’s only been in humans since, maybe late 2019,” says Harvard immunologist Duane Wesemann, who is collecting samples from volunteers to figure it out. Several other coronaviruses infect humans, causing a subset of common colds. Scientists want to know whether recent infection with these might affect the severity of Covid-19 infections.
The testing itself isn’t rocket science, says Wesemann. But understanding the complex relationship between the virus and the human immune system is.
So far only about 6% of volunteers from around the Boston area were positive in a preliminary data set. Some reported a cold or sore throat in February or March, while others recalled no symptoms at all. But the sample is still small, and in a follow-up email, Wesemann explained that it may not be representative.
Antibody-rich blood could help protect health care workers
If antibodies do work, and you test positive for them, you may be able to share your protection with several other people. Already, patients who’ve recovered from documented infections are donating their antibody-rich blood to others.
Doctors in China have treated small groups of patients and reported promising results in the Journal of the American Medical Association and the Proceeding of the National Academy of Sciences. In the United States, some severely ill patients get the same treatment under compassionate use guidelines.
But those are the cases where it’s least likely to work, says Johns Hopkins immunologist Arturo Casadevall. By then the virus has already done too much damage.
The rule of antibody therapy, he says, is it always works best if used early or prophylactically. Earlier this month, he and his fellow researchers at Johns Hopkins got approval for a clinical trial giving donated antibodies to front-line health care workers to protect them from getting sick.
Casadevall says he started pushing to develop the technology early, before the disease started spreading in the United States. His enthusiasm, he says, is based on his knowledge of medical history. Similar “convalescent serum” treatments have been used since the early 20th century to prevent or treat measles, mumps, and polio.
Unlike a vaccine, borrowed antibodies from recovered patients would confer only temporary protection – starting to fade after a half-life of about 20 days. Still, that’s long enough to help health care workers desperate to avoid getting infected.
The big limiting factor now is supply, he says. But that could change with more recovered patients and more antibody testing of people who had been only mildly ill. Donated blood can also be tested for antibodies.
Casadevall is optimistic that the biomedical research community will make quick inroads on this virus – between new treatments, new ways to speed up testing, and ways to protect people before a vaccine is close.
While this is the worst pandemic since 1918, and governments in many countries were slow to take precautions, he believes the international biomedical research community is a mighty force. “Humanity has never been better prepared.”
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