During the pandemic, Ars has done its best to keep you on top of the most important news. But there are definitely gaps in our coverage: small updates to stories we’ve covered, or news that we’ve decided wasn’t worth the time to report deeply. Focusing on breaking news also limits our opportunity to provide bigger-picture perspective. To make up for this, we’re going to try doing a series of Monday updates to help keep you informed.
Current counts: 4.1 million confirmed cases globally; 1.33 million of those in the United States. 285,000 deaths attributed to COVID-19; 80,000 deaths in the US.
While the focus of attention has been on the respiratory impact of COVID-19, there have been clear indications that the virus attacks other tissues, with intestinal distress being a commonly reported symptom. Over the weekend, The Washington Post looked at all the organs that seem to have problems in people with SARS-CoV-2 infections. The virus triggers a systemic immune response, and it can be difficult to tell which symptoms are a product of this response and which are caused by the virus directly infecting these tissues.
Unfortunately, it’s easy to get a virus to infect cells in culture dishes but much harder to see what it’s doing inside a human body. However, some progress has already been made in studying the virus’s spread in miniature versions of tissues called “organoids.” Organoids were only developed as a model system within the last decade, largely in response to progress in studying stem cells. Now they’ve been used to show which cells within the small intestine can be infected by the virus.
At the start of the month, we covered how the federal government had cut the funding for a group that studies how viruses transfer from animals to humans. It turns out that 60 Minutes had interviewed the head of that research group over a decade ago, and he said things that seem positively prophetic in retrospect. The program also traces how conspiracy theories about the research went from a Florida congressman through Fox News and to the president shortly before funding was cut.
Remdesivir is the first drug to have emerged successfully from a huge array of clinical trials for COVID-19 therapies, as it shortens the recovery time in patients. That was quickly followed by the FDA allowing its use in patients prior to its approval as a therapy. Now, we’re on to having to plan how to allocate limited supplies of the drug as its maker ramps up production capacity. The current plan is to allocate it to the states, which can then decide which hospitals will get it.
Coronaviruses produce some proteins that are inactive until they are cut into smaller pieces. Like a number of other viruses, coronaviruses carry specialized enzymes called proteases that do this cutting. Inactivating these proteases would block viral infection, which makes them a good target for drugs (this approach produced some of the most effective HIV therapies). As a result, many protease inhibitors designed for other viruses were screened against SARS-CoV-2’s enzymes. One of those, carmofur, turned out to be effective, and a new study shows how it’s able to bind the SARS-CoV-2 protease and inactivate it. We don’t yet have data on whether it has any activity in patients, though.
Another bit of research could fit in a number of categories here. As early as March, when there were very few recovered COVID-19 patients, hospitals were already planning to determine whether the antibodies contained in patients’ blood plasma are an effective treatment in patients with active infections. Now, less than two months later, there are organized networks of donors who are ready to help keep the trials supplied with antibodies.
The new research angle attempts to ensure we’re not limited by a supply of willing blood donors. Researchers have identified an antibody that blocks both SARS-CoV-1 and -2 from infecting cells in culture and have already obtained the DNA that encodes this specific antibody and have made a human version of it. Hopefully, the clinical trials with patient plasma will tell us whether antibodies block the virus’s spread in infected patients; if that turns out to be true, then we can test this specific antibody to see if it works in the human body.
Some good news before we get to the full policy trainwreck. Illinois has published a short description of its plan for handling the pandemic going forward. The plan breaks the state up into regions and relies on tracking infections and hospitalizations to determine which of five phases the pandemic is in within each region. Different businesses will be allowed to reopen depending on the pandemic status at their location. And critically, it realistically accepts that things won’t completely return to pre-pandemic activity until there’s an effective therapy or vaccine. Guidelines for moving between different status levels are also described.
The plan itself seems reasonable, but the clarity with which it’s presented—it’s sufficient for most people to understand where things stand, what might come next, and why decisions are being made—should make it a model for other governments.
The plan relies on extensive testing, something the US has fallen well short of achieving. But last week, President Trump indicated he’s OK with low levels of testing, saying, “So the media likes to say we have the most cases, but we do, by far, the most testing. If we did very little testing, we wouldn’t have the most cases. So, in a way, by doing all of this testing, we make ourselves look bad.” Trump’s comments are consistent with a New York Times report that indicates downplaying the number of infections has become a strategic political strategy meant to boost the election chances of those who have made comments that minimized the pandemic, including Trump himself.
The report makes clear that the boundary between political strategy and conspiratorial thinking ranges from pretty thin to nonexistent. Unfortunately, that’s having impacts well beyond the US, as evidenced by anti-lockdown protesters in Australia chanting “arrest Bill Gates.”