Interleukin-1 Inhibitor Activity Induced by Respiratory Syncytial Virus: Abrogation of Virus-Specific and Alternate Human Lymphocyte Proliferative Responses
Document Type
Article
Language
eng
Format of Original
7 p.
Publication Date
1-1991
Publisher
Oxford University Press
Source Publication
Journal of Infectious Diseases
Source ISSN
0022-1899
Original Item ID
doi: 10.1093/infdis/163.1.71
Abstract
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.
Recommended Citation
Salkind, Alan R.; McCarthy, Donna O.; Nichols, Joan E.; Domurat, Frank M.; Walsh, Edward E.; and Roberts, Norbert J. Jr, "Interleukin-1 Inhibitor Activity Induced by Respiratory Syncytial Virus: Abrogation of Virus-Specific and Alternate Human Lymphocyte Proliferative Responses" (1991). College of Nursing Faculty Research and Publications. 223.
https://epublications.marquette.edu/nursing_fac/223
Comments
Journal of Infectious Diseases, Vol. 163, No. 1 (January, 1991): 71-77. DOI.