J Gen Virol Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Gen Virol 66 (1985), 2533-2538; DOI 10.1099/0022-1317-66-12-2533
© 1985 Society for General Microbiology

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Taylor, G.
Right arrow Articles by Hayle, A. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Taylor, G.
Right arrow Articles by Hayle, A. J.
Agricola
Right arrow Articles by Taylor, G.
Right arrow Articles by Hayle, A. J.

Cytotoxic Lymphocytes in the Lungs of Mice Infected with Respiratory Syncytial Virus

G. Taylor, E. J. Stott and A. J. Hayle

AFRC, Institute for Research on Animal Diseases, Compton, Nr. Newbury, Berks, RG16 0NN, U.K.

Mice infected with respiratory syncytial virus (RSV) developed cytotoxic lymphocytes in the lungs, which lysed RSV-infected, but not uninfected cells. Cytotoxic activity was greatest 7 to 9 days after infection, was virus-specific, MHC-restricted and abolished by treatment of lymphocytes with anti-Thy 1.2 or with anti-Lyt 2.2 sera and complement. There was a close temporal relationship between the appearance of these cytotoxic lymphocytes in the lung and clearance of virus. In contrast, RSV persisted in the lungs of athymic (nude) mice and such animals failed to develop RSV-specific cytotoxic lymphocytes. Thus, cytotoxic T-cells may have an important role in recovery from RSV infection.

Keywords: RSV, cytotoxic lymphocytes, lung

Received 3 April 1985; accepted 16 August 1985.


This article has been cited by other articles:


Home page
Arch. Dis. Child.Home page
P S McNamara, P Ritson, A Selby, C A Hart, and R L Smyth
Bronchoalveolar lavage cellularity in infants with severe respiratory syncytial virus bronchiolitis
Arch. Dis. Child., October 1, 2003; 88(10): 922 - 926.
[Abstract] [Full Text] [PDF]


Home page
J. Gen. Virol.Home page
S. Jiang, N. J. Borthwick, P. Morrison, G. F. Gao, and M. W. Steward
Virus-specific CTL responses induced by an H-2Kd-restricted, motif-negative 15-mer peptide from the fusion protein of respiratory syncytial virus
J. Gen. Virol., February 1, 2002; 83(2): 429 - 438.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
G. P. Bembridge, J. A. Lopez, R. Bustos, J. A. Melero, R. Cook, H. Mason, and G. Taylor
Priming with a Secreted Form of the Fusion Protein of Respiratory Syncytial Virus (RSV) Promotes Interleukin-4 (IL-4) and IL-5 Production but Not Pulmonary Eosinophilia following RSV Challenge
J. Virol., December 1, 1999; 73(12): 10086 - 10094.
[Abstract] [Full Text]


Home page
Clin. Microbiol. Rev.Home page
J. B. Domachowske and H. F. Rosenberg
Respiratory Syncytial Virus Infection: Immune Response, Immunopathogenesis, and Treatment
Clin. Microbiol. Rev., April 1, 1999; 12(2): 298 - 309.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
G. P. Bembridge, J. A. Lopez, R. Cook, J. A. Melero, and G. Taylor
Recombinant Vaccinia Virus Coexpressing the F Protein of Respiratory Syncytial Virus (RSV) and Interleukin-4 (IL-4) Does Not Inhibit the Development of RSV-Specific Memory Cytotoxic T Lymphocytes, whereas Priming Is Diminished in the Presence of High Levels of IL-2 or Gamma Interferon
J. Virol., May 1, 1998; 72(5): 4080 - 4087.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 1985 by the Society for General Microbiology.