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Murphy Edward
JAIDS Journal of Acquired Immune Deficiency Syndromes: January 2016
doi: 10.1097/01.qai.0000479616.17150.2a
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HTLV-1, HTLV-2 and HCV cause chronic infections of humans, are transmitted parenterally and cause serious outcomes after long latencies. It is interesting to compare and contrast the characteristics of these viruses in several domains. Both HTLV-2 and HCV are highly prevalent among injection drug users (IDUs) in the United States and Europe and show age and sex prevalences consistent with a birth cohort effect due to epidemics of IDU in the 1960s and 1970s. HCV is broadly prevalent at 1% to 2% in many countries, with foci of hyper-endemicity due to presumed iatrogeneic transmission. In contrast, HTLV-1 is also globally prevalent but with a more spotty distribution linked to human migrations. HTLV-1 and HTLV-2 are clearly transmitted sexually whereas HCV is not. All three viruses have long periods of viral latency. In the case of HTLV-1 and HTLV-2, there is integration of pro-virus into the host genome and clonal expansion of CD4+ and CD8+ lymphocytes, respectively, but little production of cell free viral RNA. For HCV, 20%–50% of those infected resolve the infection with maintenance of antibody but resolution of plasma viremia while the remainder has chronic viremia. HTLV-1 infection leads to adult T-cell leukemia/lymphoma (ATL) in 2%–4% of those infected after 40–50 years of latency and acquisition of infection during infancy carries greater risk. Both HTLV-1 and HTLV-2 cause a myelopathy in 4% and 1% of those infected, respectively, again after long latency except for rare cases of with acute onset following transfusion acquired HTLV infection. HCV causes cirrhosis and hepatocellular carcinoma but again in only a small fraction of those infected and better prognostic indicators are needed for HCV.

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