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Flu virus can activate HERV: implications for MS and other diseases

Discussion in 'Other Health News and Research' started by natasa778, Feb 20, 2014.

  1. natasa778

    natasa778 Senior Member

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    Transcriptional de-repression of ERVWE1 following influenza A virus infection.

     
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  2. anciendaze

    anciendaze Senior Member

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    Please note that they are only saying that transcription is activated. They are not claiming that replication-competent retroviruses are being resurrected. That may happen, but so far researchers are taking few chances of provoking a counter-attack.

    To save others confusion, I will add that in medicine the adjective ectopic is used to indicate something out of its normal place, as in ectopic pregnancy, which can happen in, e.g. fallopian tubes instead of the uterus.

    Just transcribing retroviral genes and generating the corresponding proteins can cause problems for immune response. Here is a relevant paper on such antibodies in the gut of ME/CFS patients.
     
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  3. Ecoclimber

    Ecoclimber Senior Member

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    J Virol. 2014 Jan 29. [Epub ahead of print]
    Transcriptional de-repression of ERVWE1 following influenza A virus infection.
    Li F1, NellÄker C, Sabunciyan S, Yolken RH, Jones-Brando L, Johansson AS, Owe-Larsson B, Karlsson H.
    Author information
    Abstract

    Syncytin-1, a fusogenic protein encoded by a human endogenous retrovirus (HERV-W) element (ERVWE1), is expressed in the syncytiotrophoblast layer of the placenta. This locus is transcriptionally repressed in adult tissues through promoter CpG methylation and suppressive histone modifications.

    Whereas syncytin-1 appears crucial for the development and functioning of the human placenta, its ectopic expression has been associated with pathological conditions such as multiple sclerosis and schizophrenia.

    We previously reported on the transactivation of HERV-W elements, including ERVWE1, during influenza A/WSN/33 virus infection in a range of human cell-lines. We here report qPCR analyses of transcripts encoding syncytin-1 in both cell-lines and primary fibroblast cells. We observed that spliced ERVWE1 transcripts and those encoding the transcription factor glial cells missing 1 (GCM1), acting as an enhancer element upstream of ERVWE1, are prominently up-regulated in response to influenza A/WSN/33 virus infection in non-placental cells. Knock-down of GCM1 by siRNA, followed by infection suppressed the transactivation of ERVWE1. While the infection had no influence on CpG methylation in the ERVWE1 promoter, chromatin immunoprecipitation assays detected decreased H3K9 trimethylation (H3K9me3) and histone methytransferase SETDB1 levels along with viral proteins associated with ERVWE1 and other HERV-W loci in infected CCF-STTG1 cells.

    The present findings suggest that an exogenous influenza virus infection can transactivate ERVWE1 by increasing transcription of GCM1 and reducing H3K9me3 in this region and in other regions harboring HERV-W elements.Importance Syncytin-1, a protein encoded by the env gene in the HERV-W locus ERVWE1 appears crucial for the development and functioning of the human placenta and is transcriptionally repressed in non-placental tissues.

    Nevertheless, its ectopic expression has been associated with pathological conditions such as multiple sclerosis and schizophrenia.

    In the present paper we report findings suggesting that an exogenous influenza A virus infection can transactivate ERVWE1 by increasing transcription of GCM1 and reducing the repressive histone mark H3K9me3 in this region and in other regions harboring HERV-W elements. These observations have implications of potential relevance for viral pathogenesis and for conditions associated with aberrant transcription of HERV-W loci.

    Since many of the patients onset of ME/CFS is followed by a post viral infection (typically infuenza A, the flu), it would be an interesting avenue for Dr. Huber to investigate,
     
    Last edited: Feb 26, 2014
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  4. natasa778

    natasa778 Senior Member

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    there is already a thread on this, could someone merge?
     
  5. Daffodil

    Daffodil Senior Member

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    I didn't realize influenza A triggered many CFS cases...I thought it was most often EBV infection

    very very interesting article.
     
  6. SOC

    SOC

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    Can you point to the other thread?
     
  7. natasa778

    natasa778 Senior Member

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    it was what ecoclimber posted above, now merged here
     
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  8. natasa778

    natasa778 Senior Member

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    EBV can do the same thing, or very similar ...

    full paper

    and another one by the same group
     
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  9. natasa778

    natasa778 Senior Member

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  10. Daffodil

    Daffodil Senior Member

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    this probably doesn't bode too well for treatment to come in timely fashion, but i really believe HERV is the answer.

    perhaps diet modification and co-infection treatment is it the best we can do for the time being?
     
  11. anciendaze

    anciendaze Senior Member

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    Before anyone gets too excited about this causing a radical shift in medical thinking, you should read this paper by Karl Menninger on increased admission rates to mental hospitals for schizophrenia and depression after the "Spanish flu" following WWI.
     
  12. Bob

    Bob

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    That's interesting, because schizophrenia has been linked to HERVs. (I haven't read the paper that you've linked to yet.)
     
    Last edited: Mar 3, 2014
  13. anciendaze

    anciendaze Senior Member

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    I believe you mean HERV-W, and yes it has been found expressed in cerebrospinal fluid of people with schizophrenia, including those with recent onset.

    Can anyone tell me what this paper says about the role of bovine leukemia virus (BLV)? I'm confused about whether this was a finding in patients or part of the laboratory procedures.
     
  14. Bob

    Bob

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    I was actually thinking of HERV-K, but it seems that various HERVs have been linked to schizophrenia. Perhaps HERV-W has the most research literature in relation to schizophrenia, but I don't follow this research closely.
     
    Last edited: Mar 3, 2014
  15. anciendaze

    anciendaze Senior Member

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    HERV-K, or at least the most common types of HERV-K in human cells, appears to be derived from an ancestral beta retrovirus. HERV-W appears to be derived from a gamma retrovirus. So too do HERV-E, HERV-Fc1, HERV-Fc2, HERV-H, HERV-I and HERV-T. A number of these defective proviruses consist of full-length copies with small defects. This means they could likely be resurrected by a helper virus. Chimeric retroviruses are well-known, so these classifications should not be considered hard and fast.

    There are active beta retrovirus infections in mice (MMTV), sheep (JSRV) and monkeys (MPMV), and active gamma retrovirus infections in mice (MLV), cats (FLV), pigs (PLV), apes (GALV) and fowl (REV). REV appears to have evolved and been very active in the 20th century. There is no question that humans are currently exposed to these, but the common assumption that such a virus would breed true in a cellular environment dominated by copies of similar retroviral sequences has not been tested carefully. I've written a blog post or two on the idea that recombination would quickly convert a similar exogenous retrovirus into something resembling an ERV, which conventional virology would then ignore as harmless. Disease states in which HERV activation is common are well-known, and are not confined to mental illnesses.
     
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