For whatever reason, I am kind of fascinated by understanding the transmissibility and hardiness of infectious agents, especially respiratory ones like the coronavirus. It is a critical piece of knowledge for creating the most effective mitigation strategies. A study at Medrxiv gives some more thoughts on this. (Medrxiv Study) (One thing to note about these early release studies is that they have not been peer-reviewed yet, and are rushed to get the information to the public. So they may later be contradicted by other research, but they still tend to give timely insights.) This study was focused on the airborne and surface transmission of coronavirus and was done in a hospital in China. The primary methods of potential transmission of the virus are person to person through exhaled virus particles in droplets that another person literally inhales (I know, gross, right, OMG); aerosol or airborne in which the virus particles are exhaled and manage to stay in the air for some period of time; and surface transmission. Droplet transmission can’t last long because the droplets are heavy enough to fall, but the droplets can contaminate whatever surface they fall on. There has been some uncertainty about aerosol and surface transmission of the virus.
The researchers took air and surface samples from an ICU and a general ward where coronavirus patients had been treated in a Chinese hospital. Since the ICU housed sicker patients, as you might expect, there were higher levels of virus in that area, but there were some positive samples in the general ward as well. There were significant samples on the floor, likely where droplets had fallen. The floor samples in turn had been tracked by shoes to other areas in the hospital. Positive samples were obtained on several frequently touched surfaces, including bed rails, computer mice, trash cans and doorknobs. Gloves, masks and sleeves of staff also had some positive results. Significant positive results for the virus were also obtained from air samples and air outlets. Samples had spread to doctors’ offices. The researchers estimated that the virus was capable of spreading at least around 12 feet. The evidence is adding up that the virus can be transmitted by air and by surface contamination and that it can persist for some time.
Next up a couple of articles relating to immunity. One is a news story in Scientific American. (Sci. Am. Article) (As an aside, I started reading Scientific American as a child and read it for many years until they decided to print less science and become a popular and politicized journal. So now I have to read Nature and Science, which both are politicized but at least they still publish real science articles. Kind of sad if you love science.) The article does give a good general discussion of issues relating to antibodies and immunity. As the article notes, antibodies to seasonal coronaviruses don’t tend to last long. But the ones created to counter the earlier deadly forms of coronavirus, the original SARS and MERS, do last longer. This is consistent with the general rule that the greater the threat an infectious agent poses, the stronger the immune and antibody response. The body can’t keep track of every bad guy in town, so it tends to focus on the ones that really want to hurt it. And the story notes concerns about the difficulty of binding to the most dangerous part of the virus–the part it uses to gain access to the inside of a cell, which is partially masked by glycoproteins, which antibodies may have some trouble recognizing. I have however, read a couple of recent papers on Medrxiv which suggest that while this masking occurs, it does not appear to be sufficient to prevent antibody binding. I have also read papers in which the authors used antibodies recovered from blood to neutralize the virus, suggesting some potency.
A second paper follows up on the German study I mentioned in an earlier post. (German Paper) In this more detailed explanation of the study, it seems that in one town in Germany that had a high prevalence of coronavirus cases, the government did a study of the population to determine antibody, and therefore prior infection, levels. About 1000 people from 400 households had throat swabs and blood tests for antibodies. This paper presents interim results on 500 of the inhabitants. Around 14% of these people had antibodies, as determined by a test with a high rate of true positives. Another 2% had positive test results for current infection. There was some overlap, so the current total infection rate, past and present, was 15%. Based on this, the actual case fatality rate in the town, which is deaths to infections, was a very small .37%, whereas on the prior reported level of infections it was almost 2%. This supports the wide suspicion that there are a large number of unreported infections and in regard to all infections, the virus has a much smaller fatality rate than is typically reported. As the authors note, this is a significant step toward “herd” immunity.
And in the truly depressing column, but a reason why harms have to be balanced, a physician reader very kindly sent me a link to a piece of research exploring the links between recessions and suicide. (Suicide Study) The authors looked at suicide rates from 1928 through 2007. They compared the suicide rate both to overall economic performance–contraction versus expansion and to the unemployment rate. They also stratified rates by age bands. In general, suicide rates rose with recessions and fell with economic expansions and had a notable relationship to unemployment rates. As you would expect, the effect was strongest for the age groups from 25 to 64, which is the primary working population. Older people have some economic security with social security and Medicare, so may feel less stress. But the study reminds us that measures that create joblessness are not cost free in terms of lives either.