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Resurrection of endogenous retroviruses during aging reinforces senescence, 2023, Liu et al

Discussion in 'Other health news and research' started by SNT Gatchaman, Jan 15, 2023.

  1. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    Resurrection of endogenous retroviruses during aging reinforces senescence
    Liu X, Liu Z, Wu Z, Ren J, Fan Y, Sun L, Cao G, Niu Y, Zhang B, Ji Q, Jiang X, Wang C, Wang Q, Ji Z, Li L, Esteban CR, Yan K, Li W, Cai Y, Wang S, Zheng A, Zhang YE, Tan S, Cai Y, Song M, Lu F, Tang F, Ji W, Zhou Q, Belmonte JCI, Zhang W, Qu J, Liu GH. R

    Whether and how certain transposable elements with viral origins, such as endogenous retroviruses (ERVs) dormant in our genomes, can become awakened and contribute to the aging process is largely unknown.

    In human senescent cells, we found that HERVK (HML-2), the most recently integrated human ERVs, are unlocked to transcribe viral genes and produce retrovirus-like particles (RVLPs). These HERVK RVLPs constitute a transmissible message to elicit senescence phenotypes in young cells, which can be blocked by neutralizing antibodies. The activation of ERVs was also observed in organs of aged primates and mice as well as in human tissues and serum from the elderly. Their repression alleviates cellular senescence and tissue degeneration and, to some extent, organismal aging.

    These findings indicate that the resurrection of ERVs is a hallmark and driving force of cellular senescence and tissue aging.

    Link | PDF (Cell)
     
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  2. Hutan

    Hutan Moderator Staff Member

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    Thanks for posting this @SNT Gatchaman. In the context of what we were talking about the other day, about how similar ME/CFS symptoms are to those of our very eldest relatives, I think the idea of human endogenous retrovirus reactivation makes for an intriguing hypothesis.

    I need to read it again carefully, with a list of deciphered acronyms readily to hand.

    I think it makes sense that these endogenous retroviruses might awaken when a pathogen acts to reduce the body's capacity to control viruses. We've seen evidence that various pathogens do actively disable the body's immunity defences, and many of us have experienced latent viruses such as HSV-1 reactivating during PEM.

    It seems that the human endogenous retroviruses produce retrovirus-like particles that are able to make healthy cells become senescent.
    (SC_CM is senescent-cell conditioned medium; hMPC are a type of human cell)

    Could these particles be the 'something in the blood'?

    There have been and are some studies on HERV's in ME/CFS (click on the HERV tag above to see some of them).
     
    Last edited: Jan 16, 2023
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  3. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    See also the thread on Temelimab, a monoclonal antibody against a HERV-W glycoprotein, which the Swiss are trialling in long COVID (also being evaluated for MS).
     
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  4. SNT Gatchaman

    SNT Gatchaman Senior Member (Voting Rights)

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    A little more on HERVs in MS, which I'll put here in this non-ME thread. Please see also threads tagged with herv.

    These are a few background papers relating to the cascade as a hypothetical mechanism in MS. (I think it might be summarised as: "some-virus" or immune challenge -> immune dysregulation -> loss of immune control of latent virus -> EBV/HHV (trans)activation <-> HERV expression -> "badness").

    These papers all relate to multiple sclerosis. The first (2021) paper is a comprehensive overview, containing the following —

    There's also the interesting suggestion that MS ± various autoimmune conditions could have their female predisposition explained by a pathological HERV incompletely encoded on the X chromosome.

    I wonder whether this MS-related research could relate to ME/LC. Conceivably that MS end-point might be a genetically or otherwise determined fork in the road (maybe depending on things like HLA or the specific HERV), where an alternative result could be ME/CFS (or ALS or Parkinson's or glioblastoma etc).
     
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