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Purpose of Review: Human T-lymphotropic virus (HTLV)/HIV co-infections are often undiagnosed, with important clinical implications. The literature is relatively sparse with key observations derived in the pre-highly-active antiretroviral therapy era., Recent Findings: The epidemiology of co-infection, the impact of each virus on the other, with particular reference to clinical manifestations and the impact of antiretroviral therapy on HTLVs are described., Summary: Important clinical effects of HTLV/HIV co-infection include the higher rates of myelopathy and other neurological disorders and the poor predicative value of CD4+ cell counts as a surrogate for immune suppression. Current antiretroviral therapies in isolation have no proven effect on HTLV-1/2 proviral load.

Background: Human T lymphotropic virus types 1 (HTLV-1) and 2 (HTLV-2) are frequent copathogens among individuals infected with human immunodeficiency virus type 1 (HIV-1). The long-term effects of coinfection are unknown, and little information exists regarding how levels of HTLV-1/2 viral burden are affected by antiretroviral medications., Methods: Factors associated with HTLV-1/2 viral burden were examined in patients with HIV-HTLV-1/2 coinfection. A total of 72 subjects were evaluated. The variables analyzed included HTLV-1/2 proviral load, HTLV-1/2 tax/rex mRNA expression, HIV load, HTLV-1/2 viral antigen detection in peripheral blood mononuclear cell (PBMC) cultures, T cell subsets, demographic variables (age, race, sex, and reported use of injection drugs), and administration of highly active antiretroviral therapy., Results: An HTLV-1/2 proviral DNA copy number >20,000 copies/10(6) PBMCs was significantly associated with the following variables: (1) a positive HTLV-1 Western blot test result, (2) a positive HTLV-1/2 PBMC culture result, (3) a positive tax/rex mRNA result, (4) an HIV load <10,000 copies/mL, and (5) higher CD4 cell counts among subjects with HIV-HTLV-1 coinfection. There was no correlation between HTLV-1/2 proviral copy number or HTLV-1/2 tax/rex mRNA detection and administration of antiretroviral therapy., Conclusions: HTLV-1/2 proviral burden was significantly higher among patients with HIV-HTLV-1 coinfection than among patients with HIV-HTLV-2 coinfection. Highly active antiretroviral therapy may be of limited value in controlling virus expression of HTLV-1/2 in patients with HIV-HTLV-1/2 coinfection.

Objective: Human T-cell leukemia virus types I (HTLV-I) and II (HTLV-II) are closely related human retroviruses. HTLV-I has been implicated in a chronic progressive myelopathy, known as tropical spastic paraparesis (TSP) or HTLV-I-associated myelopathy (HAM). We sought to determine whether autoantibodies to brain antigens were present in the cerebrospinal fluid (CSF) of a patient with chronic progressive spastic myelopathy with evidence of both HIV-1 infection and HTLV-I/II seropositivity., Design: A 54-year-old bisexual man with clinical features of HAM/TSP of over 20 years' duration was followed., Methods: We applied discriminatory DNA amplification (polymerase chain reaction) to distinguish HTLV-I from HTLV-II and to verify co-infection with HIV-1. The patient's CSF was used to screen a human brain cDNA expression library to identify antibodies directed against brain antigens. Autoreactive bacteriophage clones were isolated and sequenced., Results: The patient was found to be co-infected with both HIV-1 and HTLV-II, but not with HTLV-I. HTLV-II proviral levels in the peripheral blood remained relatively constant, despite therapy with zidovudine. Prominent oligoclonal banding of immunoglobulins was present in the patient's CSF. A single repeatedly reactive cDNA clone was identified, by screening with CSF antibody, sequenced, and found to be the human homologue of the rat insulinoma gene, rig., Conclusions: HTLV-II infection may predispose to development of a HAM/TSP-like illness. Autoimmune mechanisms, such as autoantibody formation, may play a role in pathogenesis.