May I suggest that you don't understand the meaning/nature of direct evidence? Lay people (aka non attorneys) assume that direct is somehow synonymous with superior and that circumstantial means inferior; not really. An eyewitness is direct testimony, but eyewitnesses lie. A DNA test is circumstantial (it merely proves your DNA was at the crime scene, not that you did anything). DNA tests are harder to bribe/intimidate/fool than eyewitnesses, so I don't know about you, but I'd tend to believe the DNA that places you at the crime scene more than I'd believe an eyewitness, so - in that case - circumstantial is BETTER than direct..
So, here's my point: why don't we have DIRECT evidence of Wu Flu? Well, did you interview the eyewitnesses? Could you? Indeed, who can observe a secret lab's activity? What eyewitnesses would we expect to find?
Long and short, I would NOT expect direct evidence in this case, so it's absence is meaningless.
Well, now we are largely dealing with semantics, but that is fine, we don't have to change course. I merely need to point out that the "meaninglessness" of the absence is not magically confined to the area where circumstantial evidence does exist. So, Wuhan could have had a secret research project. But so could any building anywhere else in the entire world. What is more likely, that the secret research project was in one building in Wuhan where we have directed intense albeit choreographed scrutiny yielding no proof, or that it was somewhere else? It's the same as asking how likely that someone who says "I feel lucky, it's my birthday" before buying a lotto ticket is the winner the next day.
Have you already discussed his position? If I recall correctly, it does not rule out zoonotic origin but claims statistical likelihoods heavily indicate lab origin.
Essentially I would quibble with all the points of anyone's lab leak argument, including Washburne's, besides the argument that Wuhan emergence was unlikely which I embrace. I don't like the idea of trying to reinforce the Wuhan emergence point with a litany of weaker arguments that can't stand on their own, 1 because then the natural origin crew can just tear all the other stuff apart and appear victorious 2 because understanding the problems with the WIV leak theory lead to the argument for intentional release. So quibble-mode on the short case:
1 SC2 "unusual" because "emerged without a trace in animals, traces we’d expect if this was natural spillover" - I am far more skeptical of how likely we should expect to find the virus. Nuts and bolts the problem with considering this an argument for lab origin is that a hypothetical lab still has to source the genes from the wild, and the most likely scenario is that the hypothetical lab found a bat cov that pre-recombined a BANAL52-related spike protein with other genes we have seen in related covs, generating the (wild) "draft" genome that the hypothetical lab puts an FCS onto. And we haven't found this wild "draft" virus either. What is the argument for why we should not have expected to? Or you could say that some lab did their own DNA<>virus recomb, but either way we can't be precise in describing how SARS-CoV-2 was "engineered" yet, and the reason is because we don't have all the puzzle pieces in the wild. So not finding origin virus(es) = true regardless of natural or lab.
As a further note, there are still problems sorting out how the 1918 H1N1 genomes that were later recovered fit in the bird H1N1 phylogeny, in other words there seems to be missing steps that suggest the virus was already in humans before 1918, which begs the question of why no one was immune to it yet. So was 1918 a lab leak or is a puzzling natural origin actually not "unusual"?
2 "The Wuhan Institute of Virology took its database of coronaviruses offline." This one is *actual* misinfo. The database was *just launched* in June 2019, yes there is a gap in activity shortly afterward but this really doesn't demand any explanation since no gap in activity after June 2019 would not be "suspicious" in timing. Then there is the acknowledged take-down after Feb 2020, but if that was to hide something it would have happened earlier https://twitter.com/flodebarre/status/1577411921111748609
3 Sick worker stuff - ODNI report "some of the symptoms were not consistent with Covid-19 ... no indications that any of these researchers were hospitalized because of the symptoms consistent with Covid-19 ... early 2020 blood samples from WIV researchers all tested negative for SARS-CoV-2 antibodies." https://twitter.com/flodebarre/status/1672707221916995584
(How do these help argue for a WIV origin, really. If it originated at WIV there should be definitive evidence, therefore ambiguous evidence is worse than no evidence.)
4 "Every way in which SARS-CoV-2 is unusual was detailed in a 2018 research proposal for bioengineering work at the WIV" Mischaracterization of DEFUSE and the Ecohealth grant. WIV and Ecohealth intended to characterize a SARS-1-like backbone and put spikes on it. Because SARS-CoV-2's non-spike genes don't come from a published WIV backbone, they aren't like the proposal at all.
5 "Restriction map of an infectious clone" as I mentioned in the previous post, I've cooled on the restriction map evidence since all the sites are found in related background covs, which is consistent with either natural origin or very elegant lab manipulation. Notably, WIV used a really ugly restriction map in their WIV1 construct (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936131/ Fig 1) So if the Bruttel et al. restriction map is really the product of lab manipulation of a (still missing) wild template virus then it shows different handiwork.
16 Dec 2019. First patient reported by Wuhan Jinyintan Hospital. 1 45% of cases prior to 1 Jan 2020 had no relation to the Seafood Market. 2 The Seafood Market doesn’t sell bats nor pangolins! The Chinese don’t eat raw civets 3 or raccoon dogs4 : animals used for eating either are immediately butchered or kept in cages in open air: it’s impossible to achieve a 1000 viral particle concentration. Correlation is not causation: if the first contagions of the disease originated close to that market, and people bought food there, the market only proves that the locals used it a lot… like all markets. It doesn’t prove the real origin. Likewise, most of first US COVID cases could have been linked to visiting a Walmart, McDonalds, etc.
26 Jul 2023 “No reports are known to be available for SARS-CoV-2 test results from these mammals at the Huanan market.” 1 Yet whore science kept repeating the zoonotic lie until 5 Apr 2023 when a Nature study2 confirmed with PCR testing, that in the seafood market, “SARS-CoV-2 was detected in 73 environmental samples, but none of the 457 animal samples.” 3 There were no bats, pangolins, civets or raccoon dogs in the Wuhan Seafood market, yet that lie was published and repeated ad nauseam of times starting from The Lancet !!! 4
16 laws we need to exit Prison Planet
Politics got us in, politics is the way out ... after prayers!
There were ~40 raccoon dogs per month per Xiao X. et al. 10 minks, which are known to be susceptible to SARS-CoV-2. Overall not a lot of susceptible species in a city with not a lot of wildlife of any type. So this just repeats the same point I have made about Wuhan being an implausible ground zero, I'm not in disagreement, and I didn't include anything about the wet market in my steelmanning case. Generally I do prefer comments to address the material in the post...
Nicely explained for the lay-thinker while still preserving the details. I hate to drive you on a tangentially related subject but I have been curious about HIV since reading Kennedy's Real Anthony Fauci. Have you done any reading or can recommend good reading on whether and how HIV kills T cells? Any general thoughts you wouldn't mind sharing?
Well I'm not Brian but I read about Peter Duesberg's ideas of AIDS as a syndrome caused by beat up immune systems of men who'd done poppers and other drugs and all night bathhouse bashes. Seeing how AZT was so toxic made it look like maybe AZT finished off men who were already in trouble, and caused rapid decline in men who weren't but were deemed "infected" with HIV. Kind of smells like similar marketing to the vaxxxes.
"Whether and how" - It seems moderately well-characterized, given apparent complexity
"The ability to directly lyse CD4+ T cells have been postulated to at least partially cause the reduction of these immune effecter cells which leads to the clinical condition of AIDS. Three additional mechanisms have been postulated for CD4+ T cell depletion including immune destruction of infected cells, apoptosis, and impaired lymphocyte regeneration. ... Selective depletion of CD4+ T cells is a hallmark of HIV infection and is accomplished, at least in part, due to direct cytopathic effects (CPE) of the virus [36]. The HIV replication cycle is complex and not completely understood. It is increasingly thought to begin via interaction with dendritic cells during transmission [37]. A protein present on dendritic cells, DC-SIGN, reversibly binds HIV, with or without internalizing it, and shuttles it to a regional lymph node, thought to be the primary site for replication and spread of HIV. When the virus encounters a macrophage or T cell with its primary CD4 receptor and a coreceptor, either CXCR4 or CCR5, conformational changes caused by the binding of SU expose the fusion peptide of TM triggering direct fusion of the HIV and host cell membranes. CD4 is expressed on many cells in the body, but is found in highest levels on T lymphocytes, macrophages, and in the brain, primarily astrocytes" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174939/ 2007
Note that the high sophistication of the HIV cycle - inter alia, a conformational change in the spike protein permits recognition of two additional receptors to complete the cycle - argues for a long-adapted human virus, not a recent spillover.
HIV is not the only virus to infect immune cells, including with DNA integration (latency) leading to lifelong presence in cell populations, e.g. Epstein-Barr infects B Cells, yet doesn't cause a big problem for most people.
So is it not actually particular (Duesberg / RFK), particular because it infects T Cells (mainstream story), or particular for another reason?
In favor of 'another reason' especially for the initial US outbreak are circumventing of mucosal immunity and network effects. If you just directly inject a virus, you don't have a chance to build an immune response in the mucosal replication and surveillance phase. Homosexual partner exchange increases background STIs which degrade mucosal immunity - "The various mucosal surfaces possess specific mechanisms that help prevent the transmission of virus. Yet, HIV manages to cross these barriers to establish infection, and this is enhanced in the presence of physical trauma or pre-existing sexually transmitted infections." https://link.springer.com/article/10.1007/s11904-007-0005-x And similar issues may prevail in African heterosexual populations. And then network effects - if it's 1981 and your first infection is actually seven first infections with different preexisting antigenic makeups, your T Cells get floored before antibodies kick in.
I lean toward the other reasons above, but the research is so vast and no one seems to address the gestalt (where's the money in that). Basically, if you have a fast antibody response, then yes the virus gets a lifetime hold in your T Cells but it's only in a small portion of them. This baseline foothold writes the destiny of the ensuing reactivation cycle. So what we saw of HIV in the 80s was unnatural. Simian SIV: "Unlike HIV-1 and HIV-2 infections in humans, SIV infections in their natural simian non-human hosts appear in many cases to be non-pathogenic due to evolutionary adaptation of the hosts to the virus." "Because host evolution" makes no sense since we have plenty of immune countermeasures to HIV. More parsimonious is that SIV shows what HIV would look like with normal mucosal immunity tempering the first infection.
Note to self need to incorporate inefficacy of vaccines into this model. Maybe ironically vaccines work (prevent out-of-control initial infection) but the success is not recognized because mere HIV+ is taken as proxy for failure.
I'll have to think more about this, but if you run out of interesting things to say about covid then I know a lot of people would like to hear your thoughts. I think it was Montagnier who always insisted that HIV had been in humans for a very long time. It seems to me that even if the virus destroys T cells that its mere presence is not the proximate cause. I would have to learn an entire field though to even begin to answer that question. SIV is a very good datapoint though. It seems to suggest that the difference between HIV positive and AIDS is a preexisting immunocompromised condition, like you mention in mucus membranes. Of course, if you just give everyone with a positive test massive doses of experimental drugs it will all turn out good. No wonder this strikes some people as familiar...
I always mean to pivot to researching either HIV or Polio more exhaustively, been on my to-do list since late 2021...
As for the Fauci drugs, I don't think it's a big part of the problem because in the end not many heterosexual people (proportionally) wound up being diagnosed. Either they don't get infected or if they are infected, they never get tested because the virus is contained when it has only a pre-pathogenic foothold. The ones who do get tested were high partner unsafe sex havers, and maybe wound up with a pathogenic infection for the same reasons as above.
So I think the majority of people who ever tested + were probably on a course to AIDS, in which case the drugs are not responsible for most symptoms even if they worsened them. And this is also what I would say holds for Remdesivir and ventilation in SARS-CoV-2, they did not generate the severe disease even if they worsened it (as opposed to suppression of early treatment, which is responsible for severe disease).
I am still struggling to keep my notes organized now that Apple has ruined spotlight search but somewhere I have a study which follows HIV+ Africans, mortality is very high. I think you can think of humanity as a house that, after the 1980s, let some cockroaches get a foothold in one really dirty apartment, and now any apartment in the house that spends a long time being dirty will get infested. I mean this in the intuitive way where you can have one bug going through and it's not a problem, but there is a certain point where you can't get rid of the things. That's how the network effects of multiple-partner dating markets amplifies viral dosage, like putting a bunch of hot coals together which leads to a fire. We might see Western heterosexuals have a big outbreak of full-on AIDS soon now that prophylactics are uncool and the winner-take-all sexual market means anyone who *is* having sex has a 100 body count.
I mean to comment this, and maybe I have mentioned it before, but I recall a hypothesis in which it was argued that HIV may have occurred at some point in the past to explain the prevalence of the CCR5 mutation among European populations. I'd have to look and see if I can find that hypothesis. My original comment confused that hypothesis with another hypothesis that suggested the black plague was possibly of viral etiology rather than bacterial.
Interesting idea - I am generally skeptical of these kind of evolutionary stories because humans and viruses have built up a million weapons from our ancient conflict, so a mutation adding one weapon is probably not going to redefine the host-virus relationship.
In the SIV wikipedia page I quoted above, I found "Therefore, it is theorized that SIV may have previously crossed the species barrier into human hosts multiple times throughout history, but it was not until recently, after the advent of modern transportation and global commuterism, that it finally took hold, spreading beyond localized decimations of a few individuals or single small tribal populations." - I mean it's not surprising if someone is putting the obvious clues together, just hard to find. Citations are https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935100/ 2010 and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289907/ 2015, going to give them a look.
I suppose a justification for this hypothesis will relate to HIV variants which don't rely on CCR5, but then that has to look at when these variants emerged. I'd have to look back and see what exact argument was made.
Following along with your response to John I'm curious if the supposed "sudden emergence" of HIV may be due to increased life expectancy (taking into account the mortality bias that skewed the age younger in prior centuries), the increase in population density, sexual activities, etc. There's a lot of human behavioral factors that seem to work well for viruses. I mean, we argue that modern farming practices are dangerous due to crowding and putting animals so close together.
I've heard the poppers/amyl nitrate story with respect to AIDS (Steven Crowder brought it up once in one of his streams), but I've never heard of the actual way in which amyl nitrate damages the immune system, so I'm curious if you ever researched that. A quick glance appears to suggest that it's a vasodilator, and so I'm not exactly sure how that ties with deterioration of the immune system.
More food for thought Brian! It is something worth considering when we argue that SARS-COV2 and other viruses would get weaker over time because otherwise they would kill off their hosts. I don't find this argument compelling, but if one were to follow this line of reasoning it would extend to other animal models as well. It's not like we can act as if we are so distinct from other animals.
I actually find a lot of fascination with steelmanning other hypotheses, otherwise we wouldn't be able to tell what arguments are out there. Irrespective of what position we fall into it's good to at least see other possibilities, otherwise we sort of gate ourselves into a narrow mode of thinking.
"Bats are not required to license their viruses with some federal agency; what we haven’t found today, we can at any point find tomorrow; and we have no very good idea how much of the genetic territory in question is still unexplored. No biological principle argues we should extrapolate from a lack of currently-known exceptions to suppose an impossibility of exception."
This was great with much needed clarity for many components. Lots of the science is way over my head but enough basics stick to put the key mystery puzzle pieces together. Your point here seems to apply to so much of the official positions that assume select experts know all that needs to be known & what they measure has all the information required for certainty.
Princess Cruise had enough people who never got sick the idea of some natural immunity seemed obvious & theory of also being completely novel seemed impossible. Given years observing the tracking abilities of our public health institutions any idea they could be ahead of the curve tracking anything makes novel virus story even more or a long shot.
16 Dec 2019. First patient reported by Wuhan Jinyintan Hospital. 1 45% of cases prior to 1 Jan 2020 had no relation to the Seafood Market. 2 The Seafood Market doesn’t sell bats nor pangolins! The Chinese don’t eat raw civets 3 or raccoon dogs4 : animals used for eating either are immediately butchered or kept in cages in open air: it’s impossible to achieve a 1000 viral particle concentration. Correlation is not causation: if the first contagions of the disease originated close to that market, and people bought food there, the market only proves that the locals used it a lot… like all markets. It doesn’t prove the real origin. Likewise, most of first US COVID cases could have been linked to visiting a Walmart, McDonalds, etc.
26 Jul 2023 “No reports are known to be available for SARS-CoV-2 test results from these mammals at the Huanan market.” 1 Yet whore science kept repeating the zoonotic lie until 5 Apr 2023 when a Nature study2 confirmed with PCR testing, that in the seafood market, “SARS-CoV-2 was detected in 73 environmental samples, but none of the 457 animal samples.” 3 There were no bats, pangolins, civets or raccoon dogs in the Wuhan Seafood market, yet that lie was published and repeated ad nauseam of times starting from The Lancet !!! 4
16 laws we need to exit Prison Planet
Politics got us in, politics is the way out ... after prayers!
May I suggest that you don't understand the meaning/nature of direct evidence? Lay people (aka non attorneys) assume that direct is somehow synonymous with superior and that circumstantial means inferior; not really. An eyewitness is direct testimony, but eyewitnesses lie. A DNA test is circumstantial (it merely proves your DNA was at the crime scene, not that you did anything). DNA tests are harder to bribe/intimidate/fool than eyewitnesses, so I don't know about you, but I'd tend to believe the DNA that places you at the crime scene more than I'd believe an eyewitness, so - in that case - circumstantial is BETTER than direct..
So, here's my point: why don't we have DIRECT evidence of Wu Flu? Well, did you interview the eyewitnesses? Could you? Indeed, who can observe a secret lab's activity? What eyewitnesses would we expect to find?
Long and short, I would NOT expect direct evidence in this case, so it's absence is meaningless.
Well, now we are largely dealing with semantics, but that is fine, we don't have to change course. I merely need to point out that the "meaninglessness" of the absence is not magically confined to the area where circumstantial evidence does exist. So, Wuhan could have had a secret research project. But so could any building anywhere else in the entire world. What is more likely, that the secret research project was in one building in Wuhan where we have directed intense albeit choreographed scrutiny yielding no proof, or that it was somewhere else? It's the same as asking how likely that someone who says "I feel lucky, it's my birthday" before buying a lotto ticket is the winner the next day.
I didn't see explicit mention of Alex Washburne in your piece
https://alexwasburne.substack.com/p/the-case-for-a-lab-origin-of-sars
https://alexwasburne.substack.com/p/the-short-case-for-a-lab-origin
Have you already discussed his position? If I recall correctly, it does not rule out zoonotic origin but claims statistical likelihoods heavily indicate lab origin.
Essentially I would quibble with all the points of anyone's lab leak argument, including Washburne's, besides the argument that Wuhan emergence was unlikely which I embrace. I don't like the idea of trying to reinforce the Wuhan emergence point with a litany of weaker arguments that can't stand on their own, 1 because then the natural origin crew can just tear all the other stuff apart and appear victorious 2 because understanding the problems with the WIV leak theory lead to the argument for intentional release. So quibble-mode on the short case:
1 SC2 "unusual" because "emerged without a trace in animals, traces we’d expect if this was natural spillover" - I am far more skeptical of how likely we should expect to find the virus. Nuts and bolts the problem with considering this an argument for lab origin is that a hypothetical lab still has to source the genes from the wild, and the most likely scenario is that the hypothetical lab found a bat cov that pre-recombined a BANAL52-related spike protein with other genes we have seen in related covs, generating the (wild) "draft" genome that the hypothetical lab puts an FCS onto. And we haven't found this wild "draft" virus either. What is the argument for why we should not have expected to? Or you could say that some lab did their own DNA<>virus recomb, but either way we can't be precise in describing how SARS-CoV-2 was "engineered" yet, and the reason is because we don't have all the puzzle pieces in the wild. So not finding origin virus(es) = true regardless of natural or lab.
As a further note, there are still problems sorting out how the 1918 H1N1 genomes that were later recovered fit in the bird H1N1 phylogeny, in other words there seems to be missing steps that suggest the virus was already in humans before 1918, which begs the question of why no one was immune to it yet. So was 1918 a lab leak or is a puzzling natural origin actually not "unusual"?
2 "The Wuhan Institute of Virology took its database of coronaviruses offline." This one is *actual* misinfo. The database was *just launched* in June 2019, yes there is a gap in activity shortly afterward but this really doesn't demand any explanation since no gap in activity after June 2019 would not be "suspicious" in timing. Then there is the acknowledged take-down after Feb 2020, but if that was to hide something it would have happened earlier https://twitter.com/flodebarre/status/1577411921111748609
3 Sick worker stuff - ODNI report "some of the symptoms were not consistent with Covid-19 ... no indications that any of these researchers were hospitalized because of the symptoms consistent with Covid-19 ... early 2020 blood samples from WIV researchers all tested negative for SARS-CoV-2 antibodies." https://twitter.com/flodebarre/status/1672707221916995584
(How do these help argue for a WIV origin, really. If it originated at WIV there should be definitive evidence, therefore ambiguous evidence is worse than no evidence.)
4 "Every way in which SARS-CoV-2 is unusual was detailed in a 2018 research proposal for bioengineering work at the WIV" Mischaracterization of DEFUSE and the Ecohealth grant. WIV and Ecohealth intended to characterize a SARS-1-like backbone and put spikes on it. Because SARS-CoV-2's non-spike genes don't come from a published WIV backbone, they aren't like the proposal at all.
5 "Restriction map of an infectious clone" as I mentioned in the previous post, I've cooled on the restriction map evidence since all the sites are found in related background covs, which is consistent with either natural origin or very elegant lab manipulation. Notably, WIV used a really ugly restriction map in their WIV1 construct (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936131/ Fig 1) So if the Bruttel et al. restriction map is really the product of lab manipulation of a (still missing) wild template virus then it shows different handiwork.
16 Dec 2019. First patient reported by Wuhan Jinyintan Hospital. 1 45% of cases prior to 1 Jan 2020 had no relation to the Seafood Market. 2 The Seafood Market doesn’t sell bats nor pangolins! The Chinese don’t eat raw civets 3 or raccoon dogs4 : animals used for eating either are immediately butchered or kept in cages in open air: it’s impossible to achieve a 1000 viral particle concentration. Correlation is not causation: if the first contagions of the disease originated close to that market, and people bought food there, the market only proves that the locals used it a lot… like all markets. It doesn’t prove the real origin. Likewise, most of first US COVID cases could have been linked to visiting a Walmart, McDonalds, etc.
26 Jul 2023 “No reports are known to be available for SARS-CoV-2 test results from these mammals at the Huanan market.” 1 Yet whore science kept repeating the zoonotic lie until 5 Apr 2023 when a Nature study2 confirmed with PCR testing, that in the seafood market, “SARS-CoV-2 was detected in 73 environmental samples, but none of the 457 animal samples.” 3 There were no bats, pangolins, civets or raccoon dogs in the Wuhan Seafood market, yet that lie was published and repeated ad nauseam of times starting from The Lancet !!! 4
16 laws we need to exit Prison Planet
Politics got us in, politics is the way out ... after prayers!
https://scientificprogress.substack.com/p/laws-to-exit-planet-prison
There were ~40 raccoon dogs per month per Xiao X. et al. 10 minks, which are known to be susceptible to SARS-CoV-2. Overall not a lot of susceptible species in a city with not a lot of wildlife of any type. So this just repeats the same point I have made about Wuhan being an implausible ground zero, I'm not in disagreement, and I didn't include anything about the wet market in my steelmanning case. Generally I do prefer comments to address the material in the post...
Nicely explained for the lay-thinker while still preserving the details. I hate to drive you on a tangentially related subject but I have been curious about HIV since reading Kennedy's Real Anthony Fauci. Have you done any reading or can recommend good reading on whether and how HIV kills T cells? Any general thoughts you wouldn't mind sharing?
Well I'm not Brian but I read about Peter Duesberg's ideas of AIDS as a syndrome caused by beat up immune systems of men who'd done poppers and other drugs and all night bathhouse bashes. Seeing how AZT was so toxic made it look like maybe AZT finished off men who were already in trouble, and caused rapid decline in men who weren't but were deemed "infected" with HIV. Kind of smells like similar marketing to the vaxxxes.
I have read a lot of the same things and had the same thoughts.
"Whether and how" - It seems moderately well-characterized, given apparent complexity
"The ability to directly lyse CD4+ T cells have been postulated to at least partially cause the reduction of these immune effecter cells which leads to the clinical condition of AIDS. Three additional mechanisms have been postulated for CD4+ T cell depletion including immune destruction of infected cells, apoptosis, and impaired lymphocyte regeneration. ... Selective depletion of CD4+ T cells is a hallmark of HIV infection and is accomplished, at least in part, due to direct cytopathic effects (CPE) of the virus [36]. The HIV replication cycle is complex and not completely understood. It is increasingly thought to begin via interaction with dendritic cells during transmission [37]. A protein present on dendritic cells, DC-SIGN, reversibly binds HIV, with or without internalizing it, and shuttles it to a regional lymph node, thought to be the primary site for replication and spread of HIV. When the virus encounters a macrophage or T cell with its primary CD4 receptor and a coreceptor, either CXCR4 or CCR5, conformational changes caused by the binding of SU expose the fusion peptide of TM triggering direct fusion of the HIV and host cell membranes. CD4 is expressed on many cells in the body, but is found in highest levels on T lymphocytes, macrophages, and in the brain, primarily astrocytes" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174939/ 2007
Note that the high sophistication of the HIV cycle - inter alia, a conformational change in the spike protein permits recognition of two additional receptors to complete the cycle - argues for a long-adapted human virus, not a recent spillover.
HIV is not the only virus to infect immune cells, including with DNA integration (latency) leading to lifelong presence in cell populations, e.g. Epstein-Barr infects B Cells, yet doesn't cause a big problem for most people.
So is it not actually particular (Duesberg / RFK), particular because it infects T Cells (mainstream story), or particular for another reason?
In favor of 'another reason' especially for the initial US outbreak are circumventing of mucosal immunity and network effects. If you just directly inject a virus, you don't have a chance to build an immune response in the mucosal replication and surveillance phase. Homosexual partner exchange increases background STIs which degrade mucosal immunity - "The various mucosal surfaces possess specific mechanisms that help prevent the transmission of virus. Yet, HIV manages to cross these barriers to establish infection, and this is enhanced in the presence of physical trauma or pre-existing sexually transmitted infections." https://link.springer.com/article/10.1007/s11904-007-0005-x And similar issues may prevail in African heterosexual populations. And then network effects - if it's 1981 and your first infection is actually seven first infections with different preexisting antigenic makeups, your T Cells get floored before antibodies kick in.
I lean toward the other reasons above, but the research is so vast and no one seems to address the gestalt (where's the money in that). Basically, if you have a fast antibody response, then yes the virus gets a lifetime hold in your T Cells but it's only in a small portion of them. This baseline foothold writes the destiny of the ensuing reactivation cycle. So what we saw of HIV in the 80s was unnatural. Simian SIV: "Unlike HIV-1 and HIV-2 infections in humans, SIV infections in their natural simian non-human hosts appear in many cases to be non-pathogenic due to evolutionary adaptation of the hosts to the virus." "Because host evolution" makes no sense since we have plenty of immune countermeasures to HIV. More parsimonious is that SIV shows what HIV would look like with normal mucosal immunity tempering the first infection.
Note to self need to incorporate inefficacy of vaccines into this model. Maybe ironically vaccines work (prevent out-of-control initial infection) but the success is not recognized because mere HIV+ is taken as proxy for failure.
I'll have to think more about this, but if you run out of interesting things to say about covid then I know a lot of people would like to hear your thoughts. I think it was Montagnier who always insisted that HIV had been in humans for a very long time. It seems to me that even if the virus destroys T cells that its mere presence is not the proximate cause. I would have to learn an entire field though to even begin to answer that question. SIV is a very good datapoint though. It seems to suggest that the difference between HIV positive and AIDS is a preexisting immunocompromised condition, like you mention in mucus membranes. Of course, if you just give everyone with a positive test massive doses of experimental drugs it will all turn out good. No wonder this strikes some people as familiar...
I always mean to pivot to researching either HIV or Polio more exhaustively, been on my to-do list since late 2021...
As for the Fauci drugs, I don't think it's a big part of the problem because in the end not many heterosexual people (proportionally) wound up being diagnosed. Either they don't get infected or if they are infected, they never get tested because the virus is contained when it has only a pre-pathogenic foothold. The ones who do get tested were high partner unsafe sex havers, and maybe wound up with a pathogenic infection for the same reasons as above.
So I think the majority of people who ever tested + were probably on a course to AIDS, in which case the drugs are not responsible for most symptoms even if they worsened them. And this is also what I would say holds for Remdesivir and ventilation in SARS-CoV-2, they did not generate the severe disease even if they worsened it (as opposed to suppression of early treatment, which is responsible for severe disease).
I am still struggling to keep my notes organized now that Apple has ruined spotlight search but somewhere I have a study which follows HIV+ Africans, mortality is very high. I think you can think of humanity as a house that, after the 1980s, let some cockroaches get a foothold in one really dirty apartment, and now any apartment in the house that spends a long time being dirty will get infested. I mean this in the intuitive way where you can have one bug going through and it's not a problem, but there is a certain point where you can't get rid of the things. That's how the network effects of multiple-partner dating markets amplifies viral dosage, like putting a bunch of hot coals together which leads to a fire. We might see Western heterosexuals have a big outbreak of full-on AIDS soon now that prophylactics are uncool and the winner-take-all sexual market means anyone who *is* having sex has a 100 body count.
I mean to comment this, and maybe I have mentioned it before, but I recall a hypothesis in which it was argued that HIV may have occurred at some point in the past to explain the prevalence of the CCR5 mutation among European populations. I'd have to look and see if I can find that hypothesis. My original comment confused that hypothesis with another hypothesis that suggested the black plague was possibly of viral etiology rather than bacterial.
Interesting idea - I am generally skeptical of these kind of evolutionary stories because humans and viruses have built up a million weapons from our ancient conflict, so a mutation adding one weapon is probably not going to redefine the host-virus relationship.
In the SIV wikipedia page I quoted above, I found "Therefore, it is theorized that SIV may have previously crossed the species barrier into human hosts multiple times throughout history, but it was not until recently, after the advent of modern transportation and global commuterism, that it finally took hold, spreading beyond localized decimations of a few individuals or single small tribal populations." - I mean it's not surprising if someone is putting the obvious clues together, just hard to find. Citations are https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935100/ 2010 and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289907/ 2015, going to give them a look.
I suppose a justification for this hypothesis will relate to HIV variants which don't rely on CCR5, but then that has to look at when these variants emerged. I'd have to look back and see what exact argument was made.
Following along with your response to John I'm curious if the supposed "sudden emergence" of HIV may be due to increased life expectancy (taking into account the mortality bias that skewed the age younger in prior centuries), the increase in population density, sexual activities, etc. There's a lot of human behavioral factors that seem to work well for viruses. I mean, we argue that modern farming practices are dangerous due to crowding and putting animals so close together.
I've heard the poppers/amyl nitrate story with respect to AIDS (Steven Crowder brought it up once in one of his streams), but I've never heard of the actual way in which amyl nitrate damages the immune system, so I'm curious if you ever researched that. A quick glance appears to suggest that it's a vasodilator, and so I'm not exactly sure how that ties with deterioration of the immune system.
More food for thought Brian! It is something worth considering when we argue that SARS-COV2 and other viruses would get weaker over time because otherwise they would kill off their hosts. I don't find this argument compelling, but if one were to follow this line of reasoning it would extend to other animal models as well. It's not like we can act as if we are so distinct from other animals.
I actually find a lot of fascination with steelmanning other hypotheses, otherwise we wouldn't be able to tell what arguments are out there. Irrespective of what position we fall into it's good to at least see other possibilities, otherwise we sort of gate ourselves into a narrow mode of thinking.
"Bats are not required to license their viruses with some federal agency; what we haven’t found today, we can at any point find tomorrow; and we have no very good idea how much of the genetic territory in question is still unexplored. No biological principle argues we should extrapolate from a lack of currently-known exceptions to suppose an impossibility of exception."
This was great with much needed clarity for many components. Lots of the science is way over my head but enough basics stick to put the key mystery puzzle pieces together. Your point here seems to apply to so much of the official positions that assume select experts know all that needs to be known & what they measure has all the information required for certainty.
Princess Cruise had enough people who never got sick the idea of some natural immunity seemed obvious & theory of also being completely novel seemed impossible. Given years observing the tracking abilities of our public health institutions any idea they could be ahead of the curve tracking anything makes novel virus story even more or a long shot.
There's zero chance it's natural. Here's the absolute proof:
https://scientificprogress.substack.com/p/the-real-covid-timeline
16 Dec 2019. First patient reported by Wuhan Jinyintan Hospital. 1 45% of cases prior to 1 Jan 2020 had no relation to the Seafood Market. 2 The Seafood Market doesn’t sell bats nor pangolins! The Chinese don’t eat raw civets 3 or raccoon dogs4 : animals used for eating either are immediately butchered or kept in cages in open air: it’s impossible to achieve a 1000 viral particle concentration. Correlation is not causation: if the first contagions of the disease originated close to that market, and people bought food there, the market only proves that the locals used it a lot… like all markets. It doesn’t prove the real origin. Likewise, most of first US COVID cases could have been linked to visiting a Walmart, McDonalds, etc.
26 Jul 2023 “No reports are known to be available for SARS-CoV-2 test results from these mammals at the Huanan market.” 1 Yet whore science kept repeating the zoonotic lie until 5 Apr 2023 when a Nature study2 confirmed with PCR testing, that in the seafood market, “SARS-CoV-2 was detected in 73 environmental samples, but none of the 457 animal samples.” 3 There were no bats, pangolins, civets or raccoon dogs in the Wuhan Seafood market, yet that lie was published and repeated ad nauseam of times starting from The Lancet !!! 4
16 laws we need to exit Prison Planet
Politics got us in, politics is the way out ... after prayers!
https://scientificprogress.substack.com/p/laws-to-exit-planet-prison