Human immunodeficiency virus type-1 (HIV-1) and human T lymphotropic virus type-1 (HTLV-1)
infections have complex effects on adaptive immunity, with specific tropism for, but contrasting effects on, CD4 T lymphocytes: depletion with HIV-1, proliferation with HTLV-1. Impaired T lymphocyte function occurs early in HIV-1
infection but
opportunistic infections (OIs) rarely occur in the absence of CD4
lymphopenia. In the unusual case where a HIV-1 infected individual with a high CD4 count presents with recurrent OIs, a clinician is faced with the possibility of a second underlying comorbidity. We present a case of pseudo-
adult T cell leukemia/lymphoma (
ATLL) in HIV-1/HTLV-1
coinfection where the individual fulfilled Shimoyama criteria for chronic
ATLL and had pulmonary Mycobacterium kansasii, despite a high CD4 lymphocyte count. However, there was no evidence of clonal T-cell proliferation by T-cell receptor gene rearrangement studies nor of monoclonal HTLV-1 integration by high-throughput sequencing. Mutually beneficial interplay between HIV-1 and HTLV-1, maintaining high level HIV-1 and HTLV-1
viremia and proliferation of poorly functional CD4 cells despite chronicity of
infection is a postulated mechanism. Despite good microbiological response to antimycobacterial
therapy, the patient remained systemically unwell with
refractory anemia. Subsequent initiation of combined antiretroviral
therapy led to paradoxical resolution of CD4 T
lymphocytosis as well as HIV-1 viral suppression and decreased HTLV-1 proviral load. This is proposed to be the result of attenuation of immune activation post-HIV virological control. This case illustrates the importance of screening for HTLV-1 in HIV-1 patients with appropriate clinical presentation and epidemiological risk factors and explores mechanisms for the complex interactions on HIV-1/HTLV-1 adaptive immunity.