Advertisement

Research Article Free access | 10.1172/JCI114672

Productive infection of isolated human alveolar macrophages by respiratory syncytial virus.

J R Panuska, N M Cirino, F Midulla, J E Despot, E R McFadden Jr, and Y T Huang

Airway Disease Center, University Hospitals of Case Western Reserve University, Cleveland, Ohio 44106.

Find articles by Panuska, J. in: JCI | PubMed | Google Scholar

Airway Disease Center, University Hospitals of Case Western Reserve University, Cleveland, Ohio 44106.

Find articles by Cirino, N. in: JCI | PubMed | Google Scholar

Airway Disease Center, University Hospitals of Case Western Reserve University, Cleveland, Ohio 44106.

Find articles by Midulla, F. in: JCI | PubMed | Google Scholar

Airway Disease Center, University Hospitals of Case Western Reserve University, Cleveland, Ohio 44106.

Find articles by Despot, J. in: JCI | PubMed | Google Scholar

Airway Disease Center, University Hospitals of Case Western Reserve University, Cleveland, Ohio 44106.

Find articles by McFadden, E. in: JCI | PubMed | Google Scholar

Airway Disease Center, University Hospitals of Case Western Reserve University, Cleveland, Ohio 44106.

Find articles by Huang, Y. in: JCI | PubMed | Google Scholar

First published July 1, 1990 - More info

Published in Volume 86, Issue 1 (July 1, 1990)
J Clin Invest. 1990;86(1):113–119. doi:10.1172/JCI114672.
Copyright © 1990, The American Society for Clinical Investigation.

Published July 1, 1990 Accepted: date unavailable
Abstract

Respiratory syncytial virus (RSV) is a significant cause of lower respiratory tract disease in children and individuals with cell-mediated immunodeficiencies. Airway epithelial cells may be infected with RSV, but it is unknown whether other cells within the lung permit viral replication. We studied whether human alveolar macrophages supported RSV replication in vitro. Alveolar macrophages exposed to RSV demonstrated expression of RSV fusion gene, which increased in a time-dependent manner and correlated with RSV protein expression. RSV-exposed alveolar macrophages produced and released infectious virus into supernatants for at least 25 d after infection. Viral production per alveolar macrophage declined from 0.053 plaque-forming units (pfu)/cell at 24 h after infection to 0.003 pfu/cell by 10 d after infection and then gradually increased. The capability of alveolar macrophages to support prolonged RSV replication may have a role in the pulmonary response to RSV infection.

Images
Browse pages

Click on an image below to see the page. View PDF of the complete article

Version history
  • Version 1 (July 1, 1990): No description
Advertisement
Advertisement