I noticed that they estimated the infection fatality rate as 0.37% based on their initial numbers.
In Iceland, where they have been conducting widespread testing not limited to people with symptoms, the mortality rate seems to lie between 0.35 - 0.85%. The data there indicate about half of infected people are asymptomatic, whereas in that German town it seems to be much greater. Of the 14% with Abs, 2% (1/7) tested positive for the virus, though some of the negatives might have been people who recovered from symptoms, Conversely, there could have been positives in that group who hadn't developed Abs yet. I don't know if any data on this were furnished.
By the way, Fauci, apparently reversing course, now says Ab testing will begin soon.
Streeck seems to think transmission was more through parties and festivals with more closer contact and less through surfaces and casual encounters.
That makes sense to me. While getting the virus from surfaces is no doubt possible, I think it's probably been exaggerated as a main source of transmission.
the number of severe diseases could be minimized by having people infected with a lower dose of the virus (which I hadn't heard about before).
That could be very risky. We still don't know know how strong the relationship is between size of dose and intensity/duration of symptoms. In one of those articles Aphro posted a while back, there was a description of how that did work with smallpox, but not all viruses are necessarily the same in that regard.
"logically, the larger amount of virus should trigger more severe disease by prompting a brisker inflammatory response. But that is still speculative. The relationship between initial viral dose and severity remains to be seen.”
https://www.newyorker.com/magazine/2020/04/06/how-does-the-coronavirus-behave-inside-a-patient
The American Throracic Society has now given its approval for the use of hydroxychloroquine (HCQ) in treatment of COVID-19. In doing this, they acknowledge that evidence from studies of this drug is “contradictory”, and basically acknowledge or imply that this is a nothing-to-lose situation. The NIH just announced it 's beginning a blinded, randomized trial involveding 500 volunteers, but it seems that the study is expected to take more than year to complete. So we will be depending on doctors's reports for a while. I want to delve into this a little more, using some simple statistics.
Start with the assumption that the mortality rate from COVID-19 is about 1%. This figure could be off by a factor of two or three in either direction, but that doesn’t affect much the argument that I’m going to make. Next, we know that about 20% of COVID-19 cases are hospitalized. Since almost all the people who die from the virus are hospitalized, this means that the mortality rate of people who are hospitalized is about 5%. This neglects the fact that some people may die at home, without ever having been hospitalized, but taking into account this would actually make my argument even stronger, so I won’t even bother with it.
So about 95% of the people who are hospitalized with COVID-19 recover. These are the people that many doctors are currently treating with HCQ. It follows that almost all patients given HCQ are going to recover, anyway. Coupled with the fact that most of these treatments don’t use controls—the emphasis is on possibly saving lives at this point, not getting rigorous data on how effective the drug is—it’s clear that even doctors who report that all of their patients treated with the drug recovered are not providing much evidence for the drug’s effectiveness. I think some doctors are claiming that the recovery is faster. Again, without controls, this is hard to confirm, but even assuming this is the case, it doesn’t mean that the drug is saving lives. Faster recovery could be very important, to be sure, because it would mean patients would get out of hospitals more quickly, making room for new patients. But that’s a separate issue.
Let’s consider critical patients, those who end up in the ICU, and usually need a ventilator. The original data from China indicated that all patients who died were critical cases—again, this ignores the people who may have died at home, without ever going to the hospital—and their figures indicated about a 50% mortality rate. About half of all critical patients died.
First, note that in light of these numbers, anecdotal evidence that HCQ has helped a few critical patients doesn’t mean much. A couple of days ago, there was a report that some woman said the drug saved her life. Maybe it did, but with a 50% chance of recovering, we can’t conclude this with any certainty. Another report, from an ex-NFL player, described how he was on a ventilator, and was sure he was going to die, and how relieved he was that he survived. Had he been treated with HCQ, no doubt he would have attributed his recovery to that, when in fact he would have survived, anyway. Another example is Boris Johnson, who has just been moved out of the ICU. While he remains hospitalized, it seems pretty safe to say he's going to recover.
Suppose, though, many such patients are studied. For example, a doctor treats half a dozen critical patients with HCQ, and all of them survive. The odds of this appear to be about 1.5%, which is fairly significant. The problem though, is that this is just one study. If many such studies are run, the odds are that some study will find all six patients recovering just by chance. E.g., if about 45 such studies of six critical patients were conducted, the odds are about 50% that one such study would result. If a much larger group of critical patients was studied, evidence of an effect could be potentially greater, but I’m not sure how many such patients most doctors see. In the U.S. currently, there are about 10,000 cases classified as serious/critical. There are about 6000 hospitals in the entire country. Even the largest ones, in the areas where the virus has spread the most, will see a limited number of such cases, and they presumably will be divided among several or more doctors.
So unless large studies with many controls are run, we may have difficulty concluding anything with certainty about the effectiveness of HCQ. Another problem with HCQ is that we really don’t know how it would work, even assuming it does. While empirical evidence rules supreme in science, evidence is rarely slam dunk, and when it isn’t, a case can be greatly strengthened when a plausible mechanism for the result can be envisioned.
This is where zinc may come in. There is solid evidence that zinc can inhibit the replicase enzyme that catalyzes the process by which viruses make copies of their RNA. The problem is that it’s very difficult to get zinc into the cells, which the virus has infected. So it’s of great interest that a study showed that chloroquine—which differs from HCQ by a single atom—is a zinc ionophore, i.e., it transports the metal ion into cells. This was reported several years ago, long before the current coronavirus had infected any people, in a study of CQ as a possible anti-cancer agent.
So assuming HCQ does have an effect, it might be through its ability to get zinc into cells. This could also explain why the effects of HCQ on COVID-19 patients so far seem to be inconsistent. Some patients, because of diet, genetics, and other factors, may have more zinc in their bodies, available for uptake into cells, than others. Thus HCQ would potentially help them more than patients with less available zinc. Studies combining HCQ and zinc can help see if there is anything to this hypothesis. If there is, there are other substances, more readily available than HCQ and with fewer potential side effects, that may accomplish the same end.
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