Human T Lymphotropic Virus Type III Infection of Human Alveolar Macrophages

• Published in: Blood Vol. 68; no. 1; pp. 281 - 284
• Main Authors: Salahuddin, Syed Z., Rose, Richard M., Groopman, Jerome E., Markham, Phillip D., Gallo, Robert C.
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 01.07.1986; The Americain Society of Hematology
• Subjects: Acquired Immunodeficiency Syndrome - immunology; Acquired Immunodeficiency Syndrome - microbiology; AIDS/HIV; Biological and medical sciences; Deltaretrovirus - immunology; Fundamental and applied biological sciences. Psychology; Humans; In Vitro Techniques; Macrophages - immunology; Macrophages - microbiology; Microbiology; Phagocytosis; Pulmonary Alveoli - immunology; Pulmonary Alveoli - microbiology; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Rosette Formation; Virology; Virus; Human; Cell culture; Pulmonary alveolus; Persistent infection; Infectivity; Retroviridae; Human immunodeficiency virus; Macrophage
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.V68.1.281.281

The human T-cell lymphotropic virus type III (HTLV-III) is the etiologic agent of the acquired immunodeficiency syndrome (AIDS) and preferentially infects T4 lymphocytes. Other cell types, notably B lymphocytes and other nonlym-phoid cells, also have been reported to be infected in vitro by HTLV-III. We now report on the susceptibility of human pulmonary macrophages to infection with HTLV-III in vitro. Alveolar macrophages infected with HTLV-III produced low levels of virus that could be transferred to allogeneic human peripheral blood mononuclear leukocytes as long as 2 weeks after initiation of infection. Unlike HTLV-III infection of T lymphocytes, macrophages appeared more resis- tant to viral-mediated cytopathic effects. Primary cultures of pulmonary macrophages from two of four patients with AIDS spontaneously produced low levels of virus detected as precipitable reverse transcriptase activity, suggesting that these cells were infected in vivo. Because tissue macrophages are long-lived cells, they may act as a reservoir of HTLV-III, capable of transmitting the virus to other susceptible cells such as T lymphocytes, causing periodic low-level viremia. Macrophage infection with HTLV-III may be one mechanism for the establishment of viral persistence in infected hosts. © 1986 by Grune & Stratton, Inc.