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Epstein-Barr virus-driven lymphomagenesis in the context of HIV1 infection

Discussion in 'Latest ME/CFS Research' started by Jon_Tradicionali, Apr 27, 2014.

  1. Jon_Tradicionali

    Jon_Tradicionali Senior Member

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    Zogor-Ndreaj, Shkodër, Albania
    Epstein-Barr virus-driven lymphomagenesis in the context of human immunodeficiency virus type 1 infection.
    Authors
    Petrara MR, et al. Show all
    Journal
    Front Microbiol. 2013 Oct 18;4:311. doi: 10.3389/fmicb.2013.00311.

    Affiliation
    Abstract

    Epstein-Barr virus (EBV) is a ubiquitous human γ-herpes virus which establishes a life-long asymptomatic infection in immunocompetent hosts. In human immunodeficiency virus type 1 (HIV-1) infected patients, the impaired immunosurveillance against EBV may favor the development of EBV-related diseases, ranging from lymphoproliferative disorders to B cell non-Hodgkin's lymphomas (NHL). Antiretroviral therapy (ART) has significantly modified the natural course of HIV-1 infection, resulting in decreased HIV-1 plasmaviremia, increased CD4 lymphocytes, and decreased opportunistic infections, indicating a restoration of immune functions. However, the impact of ART appears to be less favorable on EBV-related malignancies than on other AIDS-defining tumors, such as Kaposi's sarcoma, and NHL remains the most common cancer during the ART era. EBV-driven tumors are associated with selective expression of latent oncogenic proteins, but uncontrolled lytic cycle with virus replication and/or reactivation may favor cell transformation, at least in the early phases. Several host's factors may promote EBV reactivation and replication; besides immunodepression, inflammation/chronic immune stimulation may play an important role. Microbial pathogen-associated molecular patterns and endogenous damage-associated molecular patterns, through Toll-like receptors, activate the immune system and may promote EBV reactivation and/or polyclonal expansion of EBV-infected cells. A body of evidence suggests that chronic immune stimulation is a hallmark of HIV-1 pathogenesis and may persist even in ART-treated patients. This review focuses on lymphomagenesis driven by EBV both in the context of the natural history of HIV-1 infection and in ART-treated patients. Understanding the mechanisms involved in the expansion of EBV-infected cells is a premise for the identification of prognostic markers of EBV-associated malignancies.

    "Microbial pathogen-associated molecular patterns and endogenous damage-associated molecular patterns, through Toll-like receptors, activate the immune system and may promote EBV reactivation and/or polyclonal expansion of EBV-infected cells."

    http://www.ncbi.nlm.nih.gov/m/pubmed/24151490/?i=2&from=herpes persist
     
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  2. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    So i guess they have thought of using valtrex or famvir for ebv, especially if ART isnt fully working on ebv??
     
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  3. Jon_Tradicionali

    Jon_Tradicionali Senior Member

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    Zogor-Ndreaj, Shkodër, Albania
    If I can remember to do it, I'll post the link to another study which answered exactly your question. It basically sated just how ineffective Valtrex was in suppressing EBV on someone with an abnormally stimulated immune system (us?)
     
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  4. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Opposite of dr learners findings??
     
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  5. natasa778

    natasa778 Senior Member

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    NK17, heapsreal and maryb like this.

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