This morning brings really encouraging news from South Korea, suggesting that those “reinfections” or “re-activations” that doctors in that country had previously reported “came because fragments of the virus remained in their bodies and showed up in test kits.” Apparently the tests the South Koreans were using were “so sensitive that [they] can still pick up parts of the small amount of RNA from a cell even after the person has recovered from COVID-19.”
If reinfection is not a possibility — at least for some period of time — then SARS-CoV-2 is a lot like most other viruses the medical world knows.
Good news is popping up all over. Oxford University and Pfizer Pharmaceuticals are cautiously optimistic about the early stages of their vaccine development. Gilead Sciences said today that “patients taking its drug remdesivir had a speedier recovery than patients taking placebo in a large government-funded study, but didn’t release detailed data showing the magnitude of the benefit.” As laid out in the Morning Jolt, testing production, distribution, and processing are increasing pretty quickly, although we’re still well short of where we would like to be.
And one of the nightmare scenarios, involving the virus mutating and evolving faster into new strains than treatments can be developed, thankfully appears unlikely.
How many strains are there? One analysis from last month identified eight different strains. Researchers at Zhejiang University in China released a paper saying they had identified more than 30 mutations and concluding “Sars-CoV-2 has acquired mutations capable of substantially changing its pathogenicity” — meaning some strains were more likely to kill the infected than others. Nextstrain.org is attempting to track and visualize the spread of different strains around the globe.
The next big question is how different those strains are. A study published earlier this month theorized that the reason some locations on the east coast, like New York City and northern New Jersey, have been hit so hard is because the strain there is more virulent than the one that hit the West Coast. “The G strain is predominantly on the East Coast of the United States, and the D strain is predominantly on the West Coast. . . . This observation may partially explain the discrepancy in predicted deaths from COVID-19 between the East Coast and West Coast, and possibly explain that other factors aside from social distance, such as competition between two strains of differing virulence, may be at play.”
Earlier this month, two medical schools in New York City came to a similar conclusion. By analyzing genomes from coronaviruses taken from New Yorkers starting in mid-March, they determined the viruses present in New Yorkers were “practically identical to viruses found around Europe.” But their study also noted that “the coronavirus has been moving from coast to coast for several weeks.”
In light of that troubling news, the next big questions would be, “Does catching and fighting off one strain protect you from the others?” and, “Would a vaccine for one strain work against others?”
The best answer right now is that a vaccine, treatment, or antibodies that work against one strain probably would work against the others.
The coronavirus is “all encoded on single RNA molecule,” whereas the influenza virus has eight different segments of RNA, [Richard Kuhn] noted. Two of these, hemagglutinin (HA) and neuraminidase (NA), are responsible for the annual variations that require new vaccines.
Kuhn expanded on these ideas of “shift and drift.” The former refers to genetic recombination that may lead to increases in infectivity and/or virulence, while “drift” is mutations in key proteins that may allow the virus to evade antiviral drugs and vaccine-induced immunity.
“A coronavirus has different mechanisms for recombination, but it’s not going to be as significant or as severe as the flu,” Kuhn said.
Similarly, those medical schools in New York City concluded, at least so far, “while the coronavirus mutations are useful for telling lineages apart, they don’t have any apparent effect on how the virus works.”
If catching one strain did not protect you from the others . . . we would all be in deep doo-doo. Cities could endure an outbreak of the D strain, and then get hit shortly thereafter by the G strain, with some people having to fight off multiple infections as the outbreak continued.
