Greetings Brian - long time no see! Why? Because my email started sending your posts to spam beginning July 27. All this time I thought you were taking a break! 😠 Did ya miss me? 😄 Oh well, plenty of good stuff to read while doing the laundry.
Many different species of primates were co-housed at Lindi Camp. The organs of these primates were used to amplify batches of the oral polio vaccine, which were then given to millions of Africans. This gave SIV/HIV three different opportunities to mutate and recombine at a vastly accelerated rate, which would explain why phylogenetic dating methods appear to show a early-20th-century crossover.
1. Because the primates were co-housed, ate together, played together, fought together, etc at Lindi Camp, their different strains of SIV/HIV had many opportunities to recombine and mutate
2. Different strains of SIV/HIV had even more opportunity to recombine and mutate when primate organs/blood were mixed together in vitro in order to facilitate amplification of the OPV vaccine
3. Millions of Africans who received the oral polio vaccine had many opportunities to exchange different strains of HIV amongst themselves before anybody knew it even existed
This, combined with the lack of evidence of a single case of HIV/AIDS before the late 1950s, makes me extremely suspicious that Worobey's (and others') earlier dating of the crossover was a result of ulterior motives and not honest scientific methods.
*edit: This comment is marred again in terms of my misunderstanding of the timing for spread beyond Congo area; once again leaving as stands but this comment is basically revoked.
3 If then saying polio vaccine -> human nursing of 1M diversity, "millions" isn't satisfactory. This post's point that we can measure the shallowness of growth of 1M diversity from 1980-2000 to appreciate the depth of the growth before 1980 explicitly advances a novel, non-clock based argument for why there would need to be more than 2/3 decades of transmission, no matter what there were way more transmissions in 1980-2000 than 1950-1980 in any polio theory model, so the polio theory model doesn't satisfy.
The remark about "exchanging strains" I think further points to a misconception of the significance of the 1M subgroups and non-appreciation of the need for long-term geographic isolation, and so on that I repeat the argument made in the other comment above.
Finally, this fails to approach the problem as one of relative plausibility. No matter what if you argue that the Koprowski-1980 is (purported as) plausible, "just grew in humans after crossing from chimps decades earlier than that" is *more* plausible to explain the extreme depth of genetic diversity.
1, A Camp Lindi shenanigans theory offers an answer for the distance on the 1M tree but fails to satisfactorily explain the subgroups. Quite the opposite, you want geographic isolation *edit: I have misunderstood the case for the spread of HIV out of Congo area, so it was all isolated to there until probably 80s. Anyway the rest of the comment is too unwieldy to edit, just assume a version that replaces reference to geographic on continent scale with geographic within Congo area
of the strains so they can build all this distance from each-other with just a truly very modest level of recombination in the meanwhile. And if you say, "well that's just how swarms work, you get a lot of variety, tissue tropism and intra-host evolution being so rampant in HIV" - not so much, there are transmission bottlenecks, clonal interference, and die-off of individual strains (because of clonal interference and because within a given environment HIV is boom or bust in terms of R on an individual level). And even saying that still fails to explain lack of recomb. You really just need geographical isolation, there's no getting around it.
Then you have the tropism problem. HIV 1M has a very important adaptation to restore inhibition of human tetherin (the other HIV families don't), so it's human-adapted (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2779047/). If the subgroups of 1M developed in chimps then you wouldn't expect preservation of this adaptation, and certainly wouldn't be able to explain widespread adaptation across these diverse subgroups (in chimps or in human crossover infections) as opposed to just one that crosses over and dominates the globe (as the 1M group has done), given that HIV-1N/O and HIV-2 have failed to achieve the same adaptation to human tetherin despite being in actual humans.
So the 1M subgroups probably were grown in humans after 1Mancenstral gained this adaptation, it's once again not plausible that chimps nursed their genetic diversity.
Then you have the question of whether the answer RE distance is actually very good. Would there be effective "candle carrying" in such a situation or would you have, again a lot of loser infections which don't propagate their mutations, strains thus dying out, and new infections are for whatever reason from a minority of chimps that stay in the camp longer. Similar to how swine flu is antigenically very stable due to the annual slaughter of pigs, you can retard viral evolution when you move animals around unnaturally, rather than advancing it.
Then you have the question of why camp chimp strains of HIV fail to reeneter the wild chimp population. If they still have chimp tropism (despite also developing and keeping human tropism implausibly early and long in the case of 1M), then once humans start to spread them as well, they should go back into chimps, and then when we look at viruses in chimps we find these proto-1Ms in many of the different subgroups, because after all the claim is that 1M was grown in chimps, it would spread in chimps. As said in this post footnote 7, we would essentially just see HIV in chimps, and 1M would fall into different parts of the chimpanzee HIV tree. But we haven't found that.
Oct 3, 2023·edited Oct 3, 2023Liked by Brian Mowrey
Most Australians my age remember it as it originating in bowling alleys or something like that. It could be prevented by always using condoms when bowling. Well that’s how I remember it.
As the cold war waged, high level communist biowarfare research sought many ways to vectorize bowling, the West's one remaining past-time; officially none were ever perfected.
Greetings Brian - long time no see! Why? Because my email started sending your posts to spam beginning July 27. All this time I thought you were taking a break! 😠 Did ya miss me? 😄 Oh well, plenty of good stuff to read while doing the laundry.
I see - glad to have you back!
By coincidence all my posts since July have been Chinese bot-generated weightloss promotionals.
See this "one new trick"! 😀
Many different species of primates were co-housed at Lindi Camp. The organs of these primates were used to amplify batches of the oral polio vaccine, which were then given to millions of Africans. This gave SIV/HIV three different opportunities to mutate and recombine at a vastly accelerated rate, which would explain why phylogenetic dating methods appear to show a early-20th-century crossover.
1. Because the primates were co-housed, ate together, played together, fought together, etc at Lindi Camp, their different strains of SIV/HIV had many opportunities to recombine and mutate
2. Different strains of SIV/HIV had even more opportunity to recombine and mutate when primate organs/blood were mixed together in vitro in order to facilitate amplification of the OPV vaccine
3. Millions of Africans who received the oral polio vaccine had many opportunities to exchange different strains of HIV amongst themselves before anybody knew it even existed
This, combined with the lack of evidence of a single case of HIV/AIDS before the late 1950s, makes me extremely suspicious that Worobey's (and others') earlier dating of the crossover was a result of ulterior motives and not honest scientific methods.
*edit: This comment is marred again in terms of my misunderstanding of the timing for spread beyond Congo area; once again leaving as stands but this comment is basically revoked.
3 If then saying polio vaccine -> human nursing of 1M diversity, "millions" isn't satisfactory. This post's point that we can measure the shallowness of growth of 1M diversity from 1980-2000 to appreciate the depth of the growth before 1980 explicitly advances a novel, non-clock based argument for why there would need to be more than 2/3 decades of transmission, no matter what there were way more transmissions in 1980-2000 than 1950-1980 in any polio theory model, so the polio theory model doesn't satisfy.
The remark about "exchanging strains" I think further points to a misconception of the significance of the 1M subgroups and non-appreciation of the need for long-term geographic isolation, and so on that I repeat the argument made in the other comment above.
Finally, this fails to approach the problem as one of relative plausibility. No matter what if you argue that the Koprowski-1980 is (purported as) plausible, "just grew in humans after crossing from chimps decades earlier than that" is *more* plausible to explain the extreme depth of genetic diversity.
1, A Camp Lindi shenanigans theory offers an answer for the distance on the 1M tree but fails to satisfactorily explain the subgroups. Quite the opposite, you want geographic isolation *edit: I have misunderstood the case for the spread of HIV out of Congo area, so it was all isolated to there until probably 80s. Anyway the rest of the comment is too unwieldy to edit, just assume a version that replaces reference to geographic on continent scale with geographic within Congo area
of the strains so they can build all this distance from each-other with just a truly very modest level of recombination in the meanwhile. And if you say, "well that's just how swarms work, you get a lot of variety, tissue tropism and intra-host evolution being so rampant in HIV" - not so much, there are transmission bottlenecks, clonal interference, and die-off of individual strains (because of clonal interference and because within a given environment HIV is boom or bust in terms of R on an individual level). And even saying that still fails to explain lack of recomb. You really just need geographical isolation, there's no getting around it.
Then you have the tropism problem. HIV 1M has a very important adaptation to restore inhibition of human tetherin (the other HIV families don't), so it's human-adapted (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2779047/). If the subgroups of 1M developed in chimps then you wouldn't expect preservation of this adaptation, and certainly wouldn't be able to explain widespread adaptation across these diverse subgroups (in chimps or in human crossover infections) as opposed to just one that crosses over and dominates the globe (as the 1M group has done), given that HIV-1N/O and HIV-2 have failed to achieve the same adaptation to human tetherin despite being in actual humans.
So the 1M subgroups probably were grown in humans after 1Mancenstral gained this adaptation, it's once again not plausible that chimps nursed their genetic diversity.
Then you have the question of whether the answer RE distance is actually very good. Would there be effective "candle carrying" in such a situation or would you have, again a lot of loser infections which don't propagate their mutations, strains thus dying out, and new infections are for whatever reason from a minority of chimps that stay in the camp longer. Similar to how swine flu is antigenically very stable due to the annual slaughter of pigs, you can retard viral evolution when you move animals around unnaturally, rather than advancing it.
Then you have the question of why camp chimp strains of HIV fail to reeneter the wild chimp population. If they still have chimp tropism (despite also developing and keeping human tropism implausibly early and long in the case of 1M), then once humans start to spread them as well, they should go back into chimps, and then when we look at viruses in chimps we find these proto-1Ms in many of the different subgroups, because after all the claim is that 1M was grown in chimps, it would spread in chimps. As said in this post footnote 7, we would essentially just see HIV in chimps, and 1M would fall into different parts of the chimpanzee HIV tree. But we haven't found that.
HIV was present in the Congo in 1959
https://pubmed.ncbi.nlm.nih.gov/9468138/
HIV infection in a 16 yo in St Louis in 1968
https://jamanetwork.com/journals/jama/article-abstract/374422
HIV was present before the homosexual revolution, gay bars and bath houses. It was not widely spread until the change in social norms.
Most Australians my age remember it as it originating in bowling alleys or something like that. It could be prevented by always using condoms when bowling. Well that’s how I remember it.
https://youtu.be/_lhFc_9U_UY?si=1rPrQQ-NNJJEy3od
As the cold war waged, high level communist biowarfare research sought many ways to vectorize bowling, the West's one remaining past-time; officially none were ever perfected.