| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
The Department of Virology, The School of Pathological Sciences, The Medical School, The University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne NE2 4HH, U.K.
Pulmonary A2 strain respiratory syncytial virus infection of BALB/c laboratory mice persisted for up to 7 days after initial infection with peak virus titres being recovered on day 4. Virus antigen within the lungs was found to be restricted essentially to the alveolar regions. Similarly, pulmonary histopathological changes remained confined to the peri-alveolar regions being consistent with mild pneumonia. Infection was found to elicit a pulmonary major histocompatibility complex-restricted cytotoxic T lymphocyte (CTL) response which was first detectable 6 days after infection and optimal 7 to 9 days after infection. This local CTL response was preceded by a rapid transient virus-specific lymphocyte transformation response which was detectable only 3 days after intranasal infection. In addition, infection induced rapid interferon production within the lungs which was accompanied by an equally rapid rise in pulmonary natural killer (NK) cell cytotoxic activity. Enhanced NK cell cytotoxicity could be detected after only 1 day post-infection and continued to rise to maximum levels on day 3. This response like the acute CTL response was found to be restricted to the lower respiratory tract. IgG was the first class of virus-specific immunoglobulin to be detected in the lungs of infected animals after experimental infection. However, IgG was not detected until day 10 post-infection, 5 days after the initial decline of virus shedding. Virus-specific IgA although detectable did not appear in the lung until day 24.
Present address: The Departments of Immunology and Bacteriology, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne, U.K.
Received 7 July 1989;
accepted 28 February 1990.
This article has been cited by other articles:
|
|
 |
|
  R. Janssen, J. Pennings, H. Hodemaekers, A. Buisman, M. van Oosten, L. de Rond, K. Ozturk, J. Dormans, T. Kimman, and B. Hoebee Host Transcription Profiles upon Primary Respiratory Syncytial Virus Infection J. Virol., June 1, 2007; 81(11): 5958 - 5967. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Kotelkin, I. M. Belyakov, L. Yang, J. A. Berzofsky, P. L. Collins, and A. Bukreyev The NS2 Protein of Human Respiratory Syncytial Virus Suppresses the Cytotoxic T-Cell Response as a Consequence of Suppressing the Type I Interferon Response. J. Virol., June 1, 2006; 80(12): 5958 - 5967. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Bukreyev, I. M. Belyakov, G. A. Prince, K. C. Yim, K. K. Harris, J. A. Berzofsky, and P. L. Collins Expression of Interleukin-4 by Recombinant Respiratory Syncytial Virus Is Associated with Accelerated Inflammation and a Nonfunctional Cytotoxic T-Lymphocyte Response following Primary Infection but Not following Challenge with Wild-Type Virus J. Virol., August 1, 2005; 79(15): 9515 - 9526. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Cianci, E. V. Genovesi, L. Lamb, I. Medina, Z. Yang, L. Zadjura, H. Yang, C. D'Arienzo, N. Sin, K.-L. Yu, et al. Oral Efficacy of a Respiratory Syncytial Virus Inhibitor in Rodent Models of Infection Antimicrob. Agents Chemother., July 1, 2004; 48(7): 2448 - 2454. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. R. Johnson, S. Hong, L. Van Kaer, Y. Koezuka, and B. S. Graham NK T Cells Contribute to Expansion of CD8+ T Cells and Amplification of Antiviral Immune Responses to Respiratory Syncytial Virus J. Virol., March 27, 2002; 76(9): 4294 - 4303. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Bukreyev, I. M. Belyakov, J. A. Berzofsky, B. R. Murphy, and P. L. Collins Granulocyte-Macrophage Colony-Stimulating Factor Expressed by Recombinant Respiratory Syncytial Virus Attenuates Viral Replication and Increases the Level of Pulmonary Antigen-Presenting Cells J. Virol., December 15, 2001; 75(24): 12128 - 12140. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. SCHWARZE, G. CIESLEWICZ, A. JOETHAM, T. IKEMURA, M. J. MAKELA, A. DAKHAMA, L. D. SHULTZ, M. C. LAMERS, and E. W. GELFAND Critical Roles for Interleukin-4 and Interleukin-5 during Respiratory Syncytial Virus Infection in the Development of Airway Hyperresponsiveness after Airway Sensitization Am. J. Respir. Crit. Care Med., August 1, 2000; 162(2): 380 - 386. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 J. Schwarze, G. Cieslewicz, A. Joetham, T. Ikemura, E. Hamelmann, and E. W. Gelfand CD8 T Cells Are Essential in the Development of Respiratory Syncytial Virus-Induced Lung Eosinophilia and Airway Hyperresponsiveness J. Immunol., April 1, 1999; 162(7): 4207 - 4211. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Schwarze, G. Cieslewicz, E. Hamelmann, A. Joetham, L. D. Shultz, M. C. Lamers, and E. W. Gelfand IL-5 and Eosinophils Are Essential for the Development of Airway Hyperresponsiveness Following Acute Respiratory Syncytial Virus Infection J. Immunol., March 1, 1999; 162(5): 2997 - 3004. [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 | |
