Thank you baker!
Getting in early with sum notable asf:
Robert W Malone MD: New data suggests monkeypox matches recent “war game” scenario, echoing Event 201 just prior to covid
This is his final summary, entire article is free to read and the comments are dating as well:
>So, at the risk of oversimplification:
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>1. Looks like the Monkeypox outbreak comes from a single original virus source. Following the teachings of the “Multiple working hypothesis” model for arriving at scientific “truth” (which was a core part of my education as a young scientist), a) this could be (for example) a “natural” single jump event from some infected animal into a single human somewhere in the world (who presumably had some relationship to the Maspalomas Gay Pride event). Or b) it could have come from an intentional release of a viral isolate. Mixed news - could be good or bad
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>2.The authors have confirmed that this new outbreak virus maps to the "(less disease-causing) West African group (clade) of Monkeypox viruses. Good news
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>3. This single source virus could have come from West Africa or could have come from United Kingdom, Israel or Singapore (consistent with either hypothesis a or b). Mixed news - could be good or bad
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>4. Despite the sequences indicating that the virus is most closely related to those isolated in 2018-2019, it is significantly different. This could be due to natural evolution or due to laboratory engineering/gain of function “research” (consistent with hypotheses a) and b). Generally bad news. Basically, the authors are indicating that they believe that genome of this virus is either evolving more rapidly than one would expect from a double stranded DNA poxvirus, (left unsaid, or somebody has been messing around with it).
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>5. The authors speculate that the pattern of mutations are consistent with the effects of a natural cellular protein with the abbreviated name of APOBEC3. For those who want to dive into the molecular virology of APOBEC3, here is a nice 2015 J Immunology review. For those seeking the “Cliff Notes” abridged version, see Wikipedia. For the obsessives or aficionados, note that APOBEC3 is associated with specific pattern of base changes- (C? U). On the basis of their hypothesis regarding the potential role for APOBEC3, I infer that the authors must have detected a statistically significant fraction of C? U changes in the current isolates relative to the 2018-2019 isolates. Mixed news - could be good or bad. Still does not differentiate between hypothesis a) or hypothesis b).
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>6. Here is the rub. While APOBEC3 is associated with cellular resistance (yet another form of “innate immunity” - isn’t molecular virology and cell biology amazing!) to HIV (and presumably other retroviruses), a quick pubmed search reveals that Poxviruses are resistant to the mutational effects of APOBEC3! For example, see this 2006 paper published in “Virology”. Frankly, whether through lack of curiosity or fear of attack from government controlled media and journals, the failure of the authors to even mention this Virology article is a major oversight at best. My inference and interpretation? On the basis of this sequence analysis report from the INSA team cited above, to me this is looking more like a laboratory manipulated strain than a naturally evolved strain. Bad news.
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>7. Furthermore, this double stranded DNA virus, infections by which have historically been self-limiting, appears to be evolving (during the last few days!) to a form that is more readily transmitted from human to human. Bad news.
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In conclusion, the preponderance of current evidence is pointing towards a hypothesis for the origin of this outbreak which is increasingly consistent with prior “war game” scenario planning, remarkably akin to that which occurred during Event 201, which posits emergence of an engineered Monkeypox virus into the human population during mid-May of 2022.
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>Draw your own conclusions, and do your own diligence.
https://rwmalonemd.substack.com/p/monkey-pox-update?sd=pf