title: Immune Compromise in HIV-1/HTLV-1 Coinfection With Paradoxical Resolution of CD4 Lymphocytosis During Antiretroviral Therapy: A Case Report.
abstract: 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.
authors.affiliation: From the Department of HIV, Chelsea and Westminster Hospital, London, United Kingdom (NR, SB, AP); Division of Infectious Diseases, Department of Medicine, Imperial College London, London, United Kingdom (NR); National Centre for Human Retrovirology, Imperial College Healthcare NHS Trust, London, United Kingdom (LC, HK, GT); and Section of Virology, Department of Medicine, Imperial College London, London, United Kingdom (LC, HK, CB, GT).
authors.forename: N
authors.initials: N
authors.lastname: Rockwood
authors.forename: L
authors.initials: L
authors.lastname: Cook
authors.forename: H
authors.initials: H
authors.lastname: Kagdi
authors.forename: S
authors.initials: S
authors.lastname: Basnayake
authors.forename: C R M
authors.initials: CRM
authors.lastname: Bangham
authors.forename: A L
authors.initials: AL
authors.lastname: Pozniak
authors.forename: G P
authors.initials: GP
authors.lastname: Taylor
mesh_terms: D044966:Anti-Retroviral Agents / Q000627:therapeutic use*; D018791:CD4 Lymphocyte Count; D060085:Coinfection; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy* / Q000276:immunology*; D015497:HIV-1; D015490:HTLV-I Infections / Q000150:complications / Q000276:immunology* / Q000628:therapy; D006801:Humans; D008218:Lymphocytosis / Q000150:complications / Q000276:immunology* / Q000628:therapy; D008297:Male; D008875:Middle Aged
chemical_list: D044966:Anti-Retroviral Agents