Lymphocyte subsets and viral load in patients with hiv-associated non-Hodgkin's lymphoma treated with anti-CD20 monoclonal antibody and chemotherapy

• Published in: Cancer Immunology, Immunotherapy Immunotherapy, 2001-05, Vol.50 (3), p.157-162
• Main Authors: DE PAOLI, P, VACCHER, E, TEDESCHI, R, CAFFAU, C, ZANUSSI, S, BORTOLIN, M. T, CREPALDI, C, SPINA, M, TIRELLI, U
• Format: Article
• Language: English
• Subjects: Adult; Antibodies, Monoclonal - therapeutic use; Antibodies, Monoclonal, Murine-Derived; Antigens, CD19 - biosynthesis; Antigens, CD20 - immunology; Antineoplastic agents; Antineoplastic Agents - therapeutic use; Biological and medical sciences; CD20 antigen; CD4 antigen; CD4-Positive T-Lymphocytes - metabolism; CD8-Positive T-Lymphocytes - metabolism; Chemotherapy; Female; Flow Cytometry; highly active antiretroviral therapy; HIV - metabolism; HIV Seropositivity - immunology; Human immunodeficiency virus; Humans; Leukocytes, Mononuclear - virology; Lymphocyte Subsets - metabolism; Lymphocyte Subsets - virology; Lymphoma, Non-Hodgkin - immunology; Lymphoma, Non-Hodgkin - therapy; Lymphoma, Non-Hodgkin - virology; Male; Medical sciences; Middle Aged; Original; Pharmacology. Drug treatments; Rituximab; RNA, Messenger - metabolism; Time Factors; viral load
• ISSN: 0340-7004; 1432-0851
• DOI: 10.1007/s002620100185

The anti-CD20 monoclonal antibody Rituximab is a novel antitumor agent used in association with chemotherapy (CT) for the treatment of high-grade/intermediate non-Hodgkin's lymphomas (NHL) in HIV-negative populations. This therapeutic combination is currently also being explored in HIV-positive patients with NHL (HIV-NHL). The objective of our study was to determine CD4 and CD8T cell counts, HIV plasma viremia and proviral load in patients with CD20-positive HIV-NHL treated with Rituximab plus CT and highly active antiretroviral therapy (HAART). We studied eight patients with HIV-NHL treated by anti-CD20 and CT before, after three, and after six cycles of therapy; CD4, CD8 and CD19 lymphocyte subsets were measured by monoclonal antibodies and flow cytometry. HIV plasma viremia was determined by the b-DNA assay, and proviral load by a quantitative competitive PCR. CD4T cell counts remained stable after three cycles of therapy, while a significant reduction of this subset was present at the end of therapy. HIV plasma viremia was significantly reduced after the third cycle, but returned to pretreatment levels at the end of therapy; we also observed individual fluctuations of proviral load during therapy, this marker being increased in two out of three patients at the end of therapy. These observations suggest that Rituximab plus CT accelerated the rate of CD4 depletion and of HIV replication in the peripheral blood of HIV-NHL patients and that HAART may be able to delay these effects.