Those who oppose the, admittedly, drastic strategy of social distancing have generally relied on the notion of 'herd' immunity. In the context of SARS-CoV-2, for which there is no vaccine at this time, what that means is: Going about business more or less as usual, treating the sick--whether through palliative care or perhaps with something like HCQ+ therapy--and assuming that as more and more of the population becomes infected and recovers they will develop an immunity to the virus and at a certain point the virus will begin failing to spread because there will be fewer and fewer non-immune victims left. For a virus like SARS-CoV-2 that point is generally calculated to be achievable when about 60% of the population has been infected. As for the necessary deaths entailed in this process, well, those would have been mostly "old" people--like, people over 60--or people with other health problems, or oddballs who refused to develop an immunity.
Various experts have made the argument that we probably already reached that point long ago--that the virus has probably spread like wildfire and infected just about everybody. We can all go back to work. The virus has done its damnedest and we've sailed through it.
Naturally, policy makers and public health officials would like just a bit of assurance that that is in fact the case before recommending or acting on what is, after all, speculation. (I have in the past expressed strong--not to say extreme--skepticism about this whole theory.) The only way to obtain that sort of assurance is through widespread antibody testing, since an immunity will be evidenced by antibodies specific to the virus in the blood. If this theory of developing 'herd' immunity is true, then widespread serological testing should reveal that a very large percentage of the population will have developed antibodies to the virus.
Scientists and public health officials have begun acting to discover the extent of acquired immunity in populations that have been or may have been exposed to the virus. While these efforts are still at an early stage, the findings have been somewhat disturbing thus far.
Earlier this week I recounted--Herd Immunity In Northern Italy? Not So Much--the experience of Italian officials in a definite "hot zone" of northern Italy. If the theory was true, the testing should have revealed a high percentage of the population having antibodies to the virus. Unfortunately, only 13-14% of those tested--about a third of the population of the town--had antibodies in their blood. Far, far below the level needed for 'herd' immunity.
There are some ongoing antibody testing efforts here in the US, and Steve Sailer explains the results of one, in Telluride, CO. The testing is incomplete, but the results so far are also very disappointing:
1,631 tests have been processed
8 were positive
25 were indeterminate (borderline)
1,598 were negative
If that's any indication of how widely the virus has spread in the US in a geographic sense, the answer has to be: not very far.
What's going on with these tests? Is there a problem with reliability? Are there a lot of false negatives? We've also heard, 'anecdotally' as it were, from South Korea, that a fair number of people who have 'recovered' have somehow been 'reinfected.' Had they truly recovered? Why didn't they develop an immunity. Well, as I've repeatedly reminded people, immunity isn't a given.
The South China Morning Post has reported on a study conducted by Fudan University in Shanghai that may shed some very disturbing light on this whole question. The study hasn't been peer reviewed and was limited to 175 persons. On the other hand, all of the persons tested for antibodies were persons known to have been infected by the SARS-CoV-2 virus and hospitalized, and the selection process appears to have been quite careful. The antibody levels in a third of those tested were low enough that any actual immunity would have been questionable. But these findings also had serious implications for developing an effective vaccine. Check this out:
Researchers in Shanghai hope to determine whether some recovered coronavirus patients have a higher risk of reinfection after finding surprisingly low levels of Covid-19 antibodies in a number of people discharged from hospital.
A team from Fudan University analysed blood samples from 175 patients discharged from the Shanghai Public Health Clinical Centre and found that nearly a third had unexpectedly low levels of antibodies.
In some cases, antibodies could not be detected at all. [10 out of 175.]
Although the study was preliminary and not peer-reviewed, it was the world’s first systematic examination of antibody levels in patients who had recovered from Covid-19, the disease caused by the coronavirus, the researchers said.
All of the patients had recently recovered from mild symptoms of the disease and most of those with low antibody levels were young. The researchers excluded patients who had been admitted to intensive care units because many of them already had antibodies from donated blood plasma.
Antibodies are generated by the immune system and have unique chemical structures to inhibit specific pathogens. The coronavirus antibody intercepts the spike protein on the viral envelope to prevent it from binding with human cells.
The researchers said they were surprised to find that the antibody “titer” value in about a third of the patients was less than 500, a level that might be too low to provide protection.
“About 30 per cent of patients failed to develop high titers of neutralising antibodies after Covid-19 infection. However, the disease duration of these patients compared to others was similar," they said.
The team also found that antibody levels rose with age, with people in the 60-85 age group displaying more than three times the amount of antibodies as people in the 15-39 age group.
The low amounts of antibodies could affect herd immunity, resistance to the disease among the general population to stop its spread.
“Vaccine developers may need to pay particular attention to these patients,” Huang said. If the real virus could not induce antibody response, the weakened version in the vaccine might not work in these patients either.
Have I mentioned recently that Covid19 is NOT the flu? Ah--I think I did yesterday. But it bears repeating--often. Take all the happy talk about imminent developments of vaccines with a grain of salt. That's the best case scenario, but--and I'm fully aware that I'm repeating myself again--it's not a given. There's a lot still to learn.
It may not be the flu, but going to hell isn't much of an antidote.ReplyDelete
Fauci’s main event was HIV. Many sophisticated antivirals have been developed since that outbreak began to emerge in the early 80s and that virus was identified. And now fewer meds are required to control the virus than were back then. Many afflicted with HIV have thus survived and are still alive and reasonably well. There is still no vaccine for HIV but behavior modification and antivirals have controlled it.ReplyDelete
Anti-virus vaccines are apparently the most difficult to develop. Even the annual flu vaccines are “best guesses” based upon the nature of the strain(s) that prevailed the previous year.
Fauci is in another world… He talks, but I don’t believe our pragmatic
President is listening...
Why has nobody just asked Tom Friedman already if we're going to be okay?!ReplyDelete
There was a unique report on a blog that was subsequently taken down explaining that, yes, the Chinese Virus was not the flu, but also not SARS. The post describe s process similar to malaria, but worked a bit differently in which your blood could not bond with oxygen.ReplyDelete
That may explain why malaria meds seem to work very well and ventilators not soo much and that last is appearing to be a vast understatement.
The yahoo reporting flirts, but does not delve into the information from that blog.
"What we’re doing now is not working, and I think making the same mistake over and over is a sign of stupidity,” Dr. Paul Marik told Yahoo News. “If it’s not working, we’ve got to look for something else.”
"Marik is promoting a treatment of his own devising, a combination of corticosteroids and high-dose ascorbic acid, or vitamin C, as a first-line therapy for patients hospitalized with COVID-19. Marik is a respected clinician, chief of Pulmonary and Critical Care Medicine at Eastern Virginia Medical School."
"Marik’s theory is based on an idea that is becoming widespread among researchers: that the cause of death for a significant number of COVID-19 patients, especially younger ones, is severe inflammation of the lungs resulting from an overly vigorous immune-system response."
(The blog noted that this is the body's response to the virus)
"In a video posted to YouTube on March 31, which has been widely circulated and discussed among doctors on the front lines of fighting COVID-19, Cameron Kyle-Sidell, an emergency medicine doctor at Maimonides Medical Center in Brooklyn, explains how, like most health care workers around the U.S., when he first started providing critical care for coronavirus patients in March, he was under the impression that he would be treating patients with a “viral pneumonia infection that would progress into acute respiratory distress syndrome.” It’s based on this understanding, he explained, that doctors in New York and elsewhere have been using ventilators to treat coronavirus patients who suddenly become unable to breath on their own, in the same way that they would treat respiratory failure in people with ARDS.
However, over the course of nine days, Kyle-Sidell says he concluded that the lung disease developing in patients with COVID-19 was nothing like the typical presentation of ARDS.
COVID-19 lung disease, as far as I can see, is not a pneumonia and should not be treated as one,” said Kyle-Sidell. “Rather, it appears as if some kind of viral-induced disease most resembling high altitude sickness."
(Again, this is what that blog stated and I believe made the same comparison. I just do not have the link to a saved copy of it.)
"Other doctors in the U.S. and Italy have made similar observations about the difference between typical ARDS and loss of oxygen that appears to develop rapidly in COVID-19 patients."
(A loss of oxygen due to the fact blood cannot bind to oxygen)
That was all discussed--including the views of Kyle-Sidell--in the second "must read" at:Delete
Oh, the post I went postal on.Delete
Sorry, couldn't resist that. :-)Delete
Well played. :)Delete