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Roseolovirus-associated encephalitis in immunocompetent and immunocompromised individuals

Discussion in 'Other Health News and Research' started by JaimeS, Aug 23, 2016.

  1. JaimeS

    JaimeS Senior Member

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    So, it seems to be a day for HHV-s.

    Citation:
    Ongrádi, J., Ablashi, D.V., Yoshikawa, T. et al. J. Neurovirol. (2016). doi:10.1007/s13365-016-0473-0
    Link:

    http://link.springer.com/article/10.1007/s13365-016-0473-0

    Abstract:

    The roseoloviruses, human herpesvirus (HHV)-6A, HHV-6B, and HHV-7, can cause severe encephalitis or encephalopathy. In immunocompetent children, primary HHV-6B infection is occasionally accompanied by diverse clinical forms of encephalitis.

    Roseolovirus coinfections with heterologous viruses and delayed primary HHV-7 infection in immunocompetent adults result in very severe neurological and generalized symptoms. Recovery from neurological sequelae is slow and sometimes incomplete. In immunocompromised patients with underlying hematological malignancies and transplantation, frequent single or simultaneous reactivation of roseoloviruses elicit severe, lethal organ dysfunctions, including damages in the limbic system, brain stem, and hippocampus.

    Most cases have been due to HHV-6B with HHV-6A accounting for 2–3%. The most severe manifestation of HHV-6B reactivation is post-transplantation limbic encephalitis. Seizures, cognitive problems, and abnormal EEG are common.

    Major risk factors for HHV-6B-associated encephalitis include unrelated cord blood cell transplantation and repeated hematopoietic stem cell transplantation. Rare genetic disorders, male gender, certain HLA constellation, and immune tolerance to replicating HHV-6 in persons carrying chromosomally integrated HHV-6 might also predispose an individual to roseolovirus-associated brain damage.

    At this time, little is known about the risk factors for HHV-7-associated encephalitis. Intrathecal glial cell destruction due to virus replication, overexpression of proinflammatory cytokines, and viral mimicry of chemokines all contribute to brain dysfunction.

    High virus load in the cerebrospinal fluid, hippocampal astrogliosis, and viral protein expression in HHV-6B-associated cases and multiple microscopic neuronal degeneration in HHV-7-associated cases are typical laboratory findings. Early empirical therapy with ganciclovir or foscarnet might save the life of a patient with roseolovirus-associated encephalitis.

    Keywords
    Human herpesvirus 6 and 7Post-transplant limbic encephalitisGlial cell destructionIntrathecal overexpression of proinflammatory cytokinesMonitoring CSF viral loadEmpirical ganciclovir and foscarnet therapy


    ....broke up that giant abstract into smaller chunks, otherwise unaltered.

    -J
     
  2. Avengers26

    Avengers26 Senior Member

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    @JaimeS I just wanted to take a moment to say thank you, for posting all this research/studies. I don't post a whole lot but try to read when ever I get a chance.
     
    Groggy Doggy and sarah darwins like this.
  3. JaimeS

    JaimeS Senior Member

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    You're very welcome! It seems so weird that two came up to do with HHVs today; and both discuss CFS.
     
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  4. Avengers26

    Avengers26 Senior Member

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    Every "Positive" & "Negative" results is a Plus. IMO, it narrows the field & makes it less of a looking for a needle in a haystack.

    My Positiv-o-meter has been going up slowly over the last few months. Hopefully, it's a parabolic curve but I will take a linear one, too.
     
    sarah darwins and JaimeS like this.

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