HIV- and EBV-infection

The purpose is to understand the basis for increased risk of lymphomatous malignancies in HIV-carriers. We are in particular interested in the interaction with other viruses, such asEBV and HHV-8. Four studies have been completed and are under publication: 1) EBV genome load in blood B-lymphocyte populations increase increase after HIV-infection, but decrease upon development of AIDS. The individual span of virus load is conspicuously wide ranging. 2) Immunostimulatory treatment such as vaccine adjuvant (alun) contributes to considerable increase of EB virus load in HIV-carriers, further enhanced by history of symtoms upon primary HIV-infection. 3) Primary HIV-infection without adjuvant treatment as above results in no significant increase compared to a group of long term survivors (> 10 years). HIV-RNA levels and EBV-DNA levels in B-cells correlate before treatment with HAART, while the decrease of HIV-RNA after HAART treatment does not correlate to a decerase of EBV genomes after short term observation. 4) Long term follow up of EBV-DNA load for more than three years of HIV-carriers reveals a correlation between high genome levels and various complications. The correlation to lymphoma risk is still being evaluated. We have also shown that in healthy individuals EBV is most predominantly in IgA-positive B-cells of memory type in blood. This is now being compared with the situation in HIV-carriers. We have established a test system for specific response of CD4 positive cells to EBV-infected B-cells, which is now evaluated in HIV-carriers, as a function that hypothetically may be affected upon HIV-infectio

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