After infection with HIV, there is an initial increase in patient viral load, followed by marked, but not permanent, decrease in viral load. If you were to examine the patients lymphocyte populations during this period of viral load decrease, what would you expect to find?
A. Lowered CD4+ and CD8+ T cells; CD4/CD8 ratio greater than 1 B. Raised CD4+ and CD8 + T cells; CD4/CD8 ratio greater than 1 C. CD4+ T cells within the normal range, CD8+ T cells raised; CD4/CD8 ratio less than 1 D. Lowered CD4+, raised CD8+ T cells; CD4/CD8 ratio less than 1
Lowered cd4+, raised cd8+ t cells; cd4/cd8 ratio less than 1-the disease process in untreated hiv-infected individuals occurs in three stages: the acute phase, the chronic (or asymptomatic) phase and the aids (or end-stage, also referred to as the symptomatic phase). during the acute phase, initial infection with hiv results in viral dissemination to the lymphoid tissue and numerous other sites. during this phase, viremia (number of viruses found in blood, also referred to as the viral load) peaks and then drops when the cd8+ ctl response is initiated (hiv-specific ctls; th1 response). this response takes a couple of weeks to a month to arise. during this phase, the observed depletion of cd4+ t-lymphocytes in peripheral blood (cd4+ cell count) is not only due to the cytopathic effects of viral infection (direct viral cytopathic effects), but also to the destruction of infected cd4+ cells by cd8+ cytotoxic t-lymphocytes, as well as sequestration of high numbers of both cd4+ and cd8+ cells in lymphoid tissues (which explains the lymphadenopathy associated with hiv primo-infection). after another few weeks, an efficient neutralizing antibody response develops. consequently, the viral load decreases and the cd4+ counts increase again. this phase induces a febrile illness (mononucleosis-like syndrome) that lasts 3 to 4 months, and is characterized by fever, malaise, pharyngitis, lymphadenopathy, headache, arthralgias, diarrhea, maculopapular rash, and meningoencephalitis. however, partly due to poor reverse transcriptase proofreading activity, escape mutants to ctls and neutralizing antibodies rapidly arise (refer to the section on escape mutants in the htlv-1 part) and the infection slides into the chronic phase. although this phase, which can last years, is asymptomatic, it is characterized by a steady-state level of hiv replication as well as a slow and steady decline in circulating cd4+ cells, potentially driven by viral reservoirs such as memory lymphocytes and macrophages. the end-stage phase (full-blown aids) lasts months to years, and is characterized by the appearance of severe, signature (aids-defining) opportunistic diseases such as candida albicans, pneumocystis jirovecii, cryptococcus neoformans, mycobacterium avium, toxoplasma gondii, or isospora belli infections among others, reactivation of herpesviruses such as vzv, ebv and hcmv, as well as malignancies such as kaposis sarcoma, before death ultimately occurs.