Facial recognition has become more widespread and accurate in recent years, as an artificial intelligence technology called deep learning made computers much better at interpreting images. Governments and private companies use facial recognition to identify people at workplaces, schools, and airports, among other places, although some algorithms perform less well on women and people with darker skin tones. Now the facial-recognition industry is trying to adapt to a world where many people keep their faces covered to avoid spreading disease. [...] “We can identify a person wearing a balaclava, or a medical mask and a hat covering the forehead,” says Artem Kuharenko, founder of NtechLab, a Russian company whose technology is deployed on 150,000 cameras in Moscow. He says that the company has experience with face masks through contracts in southeast Asia, where masks are worn to curb colds and flu. US Customs and Border Protection, which uses facial recognition on travelers boarding international flights at US airports, says its technology can identify masked faces. But Anil Jain, a professor at Michigan State University who works on facial recognition and biometrics, says such claims can’t be easily verified. [WIRED]
Does the amount of virus exposure affect disease severity? It looks that way. Many health care workers have become seriously ill with COVID-19, despite being young and healthy. Various reports have suggested it’s because they were exposed to more virus than a typical COVID-19 patient. This is consistent with experimental studies of porcine respiratory coronavirus (PRCV). Scientists found pigs that were inoculated with it developed more severe cases than the pigs that caught the disease naturally. This makes logical sense, since the higher the amount of virus infecting you, the harder it is for your body to control its replication and spread. [...] One outcome: The disease could become milder with time. This may have happened with HCoV-OC43, which appears to have diverged from its ancestral virus BCoV around 1890, when it jumped from cattle to humans. Coincidentally, that was also the year of a nasty influenza epidemic — though it may very well have been a coronavirus outbreak, like today’s. The increased mildness of HCoV-OC43 may have been facilitated in part by the deletion of 290 base pairs of the virus’s RNA near the spike gene, which allows a virus to penetrate and infect its host’s cells. This deletion likely hindered its ability to bind effectively, making it harder to produce severe infections. Such evolution by deletion is actually a common feature of these viruses. [...] Another possible outcome if SARS-CoV-2 never goes away: recombination, where the virus mixes and matches its genetic material with those of other circulating coronaviruses. These events are frequent, and they can result in the emergence of entirely new viruses. [Quanta]
Four coronaviruses cause around a quarter of all common colds, but each was probably deadly when it first made the leap to humans. What four coronaviruses from history can tell us about covid-19
In the early 1950s, psychiatrists began treating schizophrenia with a new drug called chlorpromazine. Seven decades later, the drug is still used as an anti-psychotic.
But now scientists have discovered that the drug, also known as Thorazine, can do something entirely different. It can stop the new coronavirus that causes Covid-19 from invading cells. Driven by the pandemic’s spread, research teams have been screening thousands of drugs to see if they have this unexpected potential to fight the coronavirus. [...] The researchers determined that the virus manipulates our cells by locking onto at least 332 of our own proteins. By manipulating those proteins, the virus gets our cells to make new viruses. Dr. Krogan’s team found 69 drugs that target the same proteins in our cells the virus does. They published the list in a preprint last month, suggesting that some might prove effective against Covid-19. [...] Most of the 69 candidates did fail. But both in Paris and New York, the researchers found that nine drugs drove the virus down. [...] “The things we’re finding are 10 to a hundred times more potent than remdesivir,” Dr. Krogan said. [...] Dr. Frieman and Dr. Chanda also found that chloroquine-related drugs worked fairly well in slowing the virus in cell cultures. But Dr. Chanda found they didn’t work as well as the six compounds at the top of his list. [NY Times]
Even assuming that immunity is long-lasting, a very large number of people must be infected to reach the herd immunity threshold required. Given that current estimates suggest roughly 0.5 percent to 1 percent of all infections are fatal, that means a lot of deaths. Perhaps most important to understand, the virus doesn’t magically disappear when the herd immunity threshold is reached. That’s not when things stop — it’s only when they start to slow down.