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Without wanting to contribute to any more fear porn, I thought a look at the recent monkeypox theories would be interesting. Especially as cases are still rising, with an additional 82 infections in the UK over the last four days.
The most up-to-date analysis was from the National Institute of Health on 23 May.(Update - Robert Malone has also written about this as I have been typing). Since then, the University of Edinburgh has taken a further look at the findings.
However, I’ll begin by looking at a discussion started by Andrew Rambaut (from the University of Edinburgh) on 21 May.
Andrew thought that many of the mutations may have been caused by APOBEC3. APOBEC stands for Apolipoprotein B Editing Complex and these enzymes edit RNA or DNA, causing mutations in the viral genome. The mutations restrict viral replication, play an important role in controlling viruses and can be a potent inhibitor of HIV. APOBEC3, in particular, can contribute significantly to DNA mutagenesis in cancer and RNA editing in breast cancer leading to heightened immune activity and improved survival.
In the discussion, Andrew predicted that “all or most of these mutations arose in a single round of replication”. He thinks that this mutation occurred in a reservoir host, such as a rodent.
Gustave Palacios, from the Icahn School of Medicine at Mount Sinai replied with an interesting comment.
He thought the pattern of mutations were puzzling and non consistent with what had been observed in the past.
Next, the Portuguese analysis on 23 May concluded that “the multi-country outbreak most likely has a single origin, with all sequenced viruses released so far tightly clustering together”. The current virus is most closely related to viruses “associated with the exportation of monkeypox virus from Nigeria to several countries in 2018 and 2019, namely the United Kingdom, Israel and Singapore.”
However, what is interesting is that there have been 47 mutations from those 2018-2019 viruses which the authors say “is far more than one would expect considering the estimated substitution rate for Orthopoxviruses”.
Furthermore, they say that “as also mentioned by Rambaut, one cannot discard the hypothesis that the divergent branch results from an evolutionary jump (leading to a hypermutated virus) caused by APOBEC3 editing.”
Yesterday, Andrew Rambaut started a new thread concerning the the University of Edinburgh’s observations about the APOBEC3 theory.
In the thread it says that normally, in these types of viruses, there are 1-2 nucleotide changes per year. However, as mentioned above, this latest virus has had 47 substitutions in the space of 3-4 years. The authors say this is “an unexpectedly large number”.
After further analysis, they suggest that the patterns observed could mean “there has been sustained human to human transmission since at least 2017. An alternative theory (not suggested by the authors) is that circulation may have been occurring in non-human primates over the same time period.
So has there been sustained but undetected transmission in humans or primates over the last four years? With APOBEC3 editing driving short-term evolution? Maybe, but the “all or most of these mutations arose in a single round of replication” comment is still puzzling.
Some think this puzzle is explained by a lab origin for this latest strain of monkeypox. As well as the mutation, there has been a deletion which could indicate that serial passaging through a cell line has taken place.
Jikky also suggests that so many mutations, in a short space of time, could only happen by taking a lab strain of monkey pox and then passaging it through cells in the presence of a mutagen (APOBEC or molnupiravir).
It’s too early to reach any conclusions but, once again, the lab leak theory is not easily ruled out.
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Cue Bill Gates, "The next virus will get people's attention," smirking to himself and rubbing his hands.
Worth noting monkeypox pandemic exercise done last year had May 15, 2022 as the launch date. While we all stand in awe of Bill Gates psychic powers his funded ops are oddly predictive.