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

[Jon_Tradicionali]

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

 

[heapsreal]

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

 

[Jon_Tradicionali]

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

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?)

 

[heapsreal]

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?)

Opposite of dr learners findings??

 

[natasa778]

on the other hand valtrex and acyclovir have been used successfully for controlling HIV infection - still not entirely clear if they works by just quieting EBV and/or other herpes viruses (that might be 'helping' HIV) or by actually slowing down HIV directly through RV inhibition


Acyclovir Is Activated into a HIV-1 Reverse Transcriptase Inhibitor in Herpesvirus-Infected Human Tissues