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Clinical characteristics of patients with Epstein Barr virus in cerebrospinal fluid

Discussion in 'Other Health News and Research' started by heapsreal, Nov 30, 2014.

  1. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    I will pluck a few interesting things that caught my eye and then post the link to the research article and a few of my thoughts in brackets.

    We identified 32 patients with EBV DNA in CSF. 11 had history of allogeneic hematopoietic stem cell transplantation, 7 solid organ transplantation and 5 HIV/AIDS. 5 patients had no preceding immunodeficiency.
    (sounds abit like cfs/me)

    In 8 of the cases, another pathogen was identified in CSF. These were M. tuberculosis (2), T. gondii (2), Aspergillus (1), Herpes simplex virus 1 (1), C. neoformans (1) and Human herpesvirus 6 (1). Altogether in 15/32 (47%) of the cases the clinician had a strong suspicion of cause other than EBV for the patients' CNS symptoms/findings.
    (possibly why Dr lerner looks for other pathogens and also could be why some who are positive to EBV may not respond to antivirals due to other co-infections)


    Central nervous system (CNS) complications of Epstein-Barr virus (EBV) infection occur in 1 to 18% of patients with infectious mononucleosis and include encephalitis, meningitis, cerebellitis, polyradiculomyelitis, transverse myelitis, cranial and peripheral neuropathies, and psychiatric abnormalities.
    (uniformed researchers on cfs/me mentioning psychiatric abnormalities??)
    (The dubbo studies indicate 10% of those who get glandular fever went on to get cfs/me, not to different to the 1-18% of the those with some type of cns infection)


    Most hospital patients with EBV DNA in CSF are immunosuppressed
    Of the 32 patients 26 (81%), had an immunosuppressive condition: 11 had history of allogeneic hematopoietic stem cell transplantation, 7 solid organ transplant and 5 HIV/AIDS. In addition 2 patients had hematological malignancy without stem cell transplantation, and one had IgG subclass deficiency. One patient had a suspicion of lymphoma at the time of EBV finding and died of pneumocystis infection and sepsis. 5/32 (16%) patients had no preceding immunodeficiency. Two of these had a clinical picture consistent with mononucleosis and one patient had multiple sclerosis diagnosed at the time of EBV DNA positivity in CSF. (16% with no proceeding immunodefiency, close to the 10% Dubbo study again)


    Among the, 7 stem cell transplant patients with encephalitis, 4 had normal MRI at the time of CSF EBV DNA positivity. One had only computed tomography performed initially. One had unenhancing patchy changes both supra- and infratentorially, compatible with encephalitis. Another patient had a hemorrhagic lesion in the cerebellum and small changes supratentorially, suggesting mold infection. Despite broad spectrum antibiotics and voriconazole the patient recovered only after rituximab.
    ( cool and ebv recovery with rituximab)


    Serology
    EBV antibodies had been studied in 25 of the 32 patients. Only 2 had positive IgM and low IgG avidity indicating primary EBV infection. These were previously immunocompetent patients with mononucleosis. Two more had borderline IgM. One of these was a solid organ transplant recipient with persistently negative EBV IgG and prolonged viremia, diagnosed later with EBER-positive PTLD.

    The remaining patients were EBV IgG positive and IgM negative indicating existing EBV immunity and reactivation rather than primary infection.
    ( Always seem to be people/doctors saying that their ebv is a past infection as they dont have a positive IGM, this seems to show one doesnt need igm antibodies to show that ebv has reactivated)


    Most of our patients had serology consistent with past EBV immunity and reactivation. This could imply that other infections in the CNS may trigger EBV reactivation.
    ( interesting, so not having an ebv onset for cfs/me doesnt rule out that ebv reactivation after the initial trigger as it seems other infections can cause ebv to reactivate and possibly other viral infections)


    Unfortunately, at present no simple way seems to exist to determine whether EBV is the cause of an individual patient's CNS disease.
    (yes, dont we know this already)


    Inpatients with EBV DNA in the CSF a consideration of reduction of immunosuppression, if feasible, is warranted. Rituximab is well established in treatment of EBV associated lymphoproliferative disease 12]. However its role in EBV-associated encephalitis is unclear. The same is true for antiviral agents and i.v. immunoglobulin.
    ( maybe this could be a good reason to research rituximab with antivirals and or ivig, i think rituximab can hit the ebv infected B cells, maybe the other treatments can go after the ebv throughout the rest of the body that rituximab cant get at. This could also explain relapses in responders to rituximab as well as antivirals??)


    I
    ndications to test CSF for EBV DNA include suspicion of CNS PTLD or lymphoma in solid organ- and stem cell transplant patients and HIV patients. Encephalitis in stem cell transplant patients propably warrants EBV testing of CSF, among other tests. In other patient groups the indications are less clear but in general, profound deficiency of T-cell mediated immunity predisposes to complications of EBV infection.
    ( profound defiency in T cells increasing of complications of ebv infections. Could this be why Griffith university have found low nk function as well as low cd8 t cell function??)

    I know this article is about cfs/me specifically but it present alot of questions in regards to EBV in cfs/me. A few things worth thinking about??

    http://www.biomedcentral.com/1471-2334/11/281

    Interesting to note that this work was done by a Scandinavian country who havent just closed the book on EBV and keeping an open view of things as research technology hopefully improves and not just dismissing this virus.
     
    zzz, natasa778, minkeygirl and 3 others like this.

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