Just one quick note, in the last two days, Minnesota has reported a very high number of deaths. Until I see the CDC data by week of death I don’t know when those deaths actually occurred. In the past, large jumps in deaths reported are typically reflective of reporting of deaths that occurred several weeks or more ago. The predominance of deaths among long-term care residents and in the very old continues to be very noticeable. The rate of deaths seems much higher than the rise in hospitalizations would suggest. I need to update my place of death work, because I again wonder if we are seeing the effect of high prevalence of advance directives which preclude any aggressive treatment of the disease.
This paper from the English Public Health authority looks at the adequacy of antibody tests and the results of some surveys of adaptive immune response. (English Paper) It reports on an ongoing study of antibody levels in England. There is a critique of some types of tests used and their ability to detect lower levels of antibodies. One interesting part of the discussion is the high level of responsive T cells in people who have not been infected, again suggesting some pre-existing response in the population.
Understanding the likely values for certain parameters relevant to the epidemic is still going on. This paper from the United Kingdom makes estimates from data in that country. (Medrxiv Paper) The best estimate for the generation interval, the time between sequential infections, is 4.8 days. The best estimate for the serial interval, the time between appearance of symptoms in sequential infections is 5.6 days and the incubation period, generally thought of as the time from infection to appearance of symptoms in an individual, is estimated at 5.5 days. Each of these obviously has a range, and both the average and the range can be important in understanding how the epidemic might proceed and where interventions can be most effectively targeted.
Equally important is understanding the contribution of asymptomatic individuals, since many people never develop them and that serial interval and incubation period are over 5 days and represent a time when people can be infectious but not aware that they are infected. This Nature article examines the nature and extent of asymptomatic spread. (Nature Article) According to the author, around 20% of people are truly asymptomatic throughout their infection and these people are much less likely to spread the virus. Quantifying this is difficult at best, but estimates are that asymptomatic people have about 25% the risk of transmitting as symptomatic ones.
Amid growing concern in the United States around depriving children of an actual in-person education, especially minority and low-income children, a study from UNICEF asserts that schools are not a major source of transmission among children. (UNICEF Study) While children account for over 10% of cases, they aren’t getting infected at school. And they are missing health, nutrition and other social services that they often receive at school.
Another study from India, and these seem to be coming daily now, on the adaptive immune response, and on pre-existing cross-reactive responses. There has been concern especially about the durability of the immune response for those with mild infections. The paper looked at patients with mild disease and those who were uninfected. (Medrxiv Paper) In the mild disease group they found detectable T cell and B cell responses up to five months after infection. Interestingly they found a cross-reactive T cell response in about 70% of uninfected individuals. It could be that Indians have a much higher rate of exposure to seasonal coronavirus than people in other countries, and therefore are more resistant to at least serious infection.
This study attempted to assess factors associated with nosocomial CV-19 outbreaks in hospitals, or situations where the patient or a staff member gets infected in the facility. This happens with some regularity. (Medrxiv Paper) The authors found that most such infections appeared to be spread by health care workers and that social distancing measures in the community were the major factor leading to a reduction of these infections.
This is kind of an interesting study finding that viral loads decreased as the epidemic proceeded in Detroit. (Medrxiv Paper) From April 4 to early June, the initial PCR results found this decline, which was reflected in lower mortality among hospitalized patients. A variety of explanations for the change were given, while a likely one, a seasonal change in environmental favorability for the virus, was ignored. This could also reflect more widespread testing finding patients earlier in their infection, although you would assume the criteria for hospitalization would be the same.
Finally I am not going to go into much detail on this, but people are trying to figure out actual prevalence of infection in a situation where testing strategies and rates varied so greatly over time both within and across countries. The authors examined nine countries in Europe and came up with their own method for determining what they call the “genuine virus prevalence.” (Medrxiv Paper)
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At Minnesota around 10 minutes: https://www.youtube.com/watch?v=8PAwc8nlE_Q Evil Governor.
Dr. Clare Craig has a reasonable hypothesis as to the rise in deaths vs. hospitalizations/ITC (ICU).
*U.K. specific, but may still be useful.
I just don’t understand why so much credibility is given to the PCR test when the inventor, Kary Mullis, said in 1993,
“It doesn’t tell you that you’re sick and it doesn’t tell you that the thing you ended up with was going to hurt you or anything like that.”
The video is commentary by Kary Mullis: https://www.brighteon.com/72d824c2-4aa9-42fd-834d-0c9bb4a292ad
If a person doesn’t have a large enough load of any virus, he’s not going to get sick, and he’s not going to be contagious.
I think this is all political and money driven.
P.S. That was in reference to Dr. Craig’s praise of PCR as a test.