Interleukin-1-Inhibitor Activity Induced by Respiratory Syncytial Virus: Abrogation of Virus-Specific and Alternate Human Lymphocyte Proliferative Responses

• Published in: The Journal of infectious diseases 1991-01, Vol.163 (1), p.71-77
• Main Authors: Salkind, Alan R., McCarthy, Donna O., Nichols, Joan E., Domurat, Frank M., Walsh, Edward E., Roberts, Norbert J.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Cell Cycle; Cell growth; Cell Survival; Cells, Cultured; Flow Cytometry; Fundamental and applied biological sciences. Psychology; HLA-DR Antigens - biosynthesis; Human respiratory syncytial virus; Humans; Infections; Influenza A virus - immunology; influenza virus; Interleukin-1 - antagonists & inhibitors; Leukocytes, Mononuclear - cytology; Leukocytes, Mononuclear - immunology; Leukocytes, Mononuclear - microbiology; Lymphocyte Activation; Lymphocytes; Macrophages - cytology; Macrophages - immunology; Macrophages - microbiology; Major Articles; Microbiology; Monocytes - cytology; Monocytes - immunology; Monocytes - microbiology; Orthomyxoviridae; Receptors, Interleukin-2 - biosynthesis; Receptors, Transferrin - biosynthesis; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Respiratory syncytial viruses; Respiratory Syncytial Viruses - immunology; T lymphocytes; Thymocytes; Virology; Viruses
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/163.1.71

Respiratory syncytial virus (RSV) infection has been shown to induce human mononuclear leukocyte(MNL)production of net interleukin-1 (IL-1)-inhibitor activity. In the current studies of IL-1-inhibitor effects, RSV-exposed cells were compared with autologous MNL that were shamexposed or exposed to inactivated RSV or influenza virus (which induces net IL-1 activity and commonly elicits effective homotypic immunity). Exposure of MNL to influenza virus or inactivated RSV resulted in increased expression of human leukocyte antigen-DR, the IL-2 receptor, and the transferrin receptor and increased progression through the cell cycleby 3 days. In contrast, exposure to infectious RSV resulted in decreased marker expression and cell cycle arrest, with abrogation of proliferation in response to the virus or other stimuli. These data raise the possibility that a contributing mechanism for recurrence of RSV infection is early suppression of the clonal expansion of virus-specific lymphocytes due to net IL-1-inhibitor activity.