Vaccinia virus lacking the Bcl-2-like protein N1 induces a stronger natural killer cell response to infection.

[en] The vaccinia virus (VACV) N1 protein is an intracellular virulence factor that has a Bcl-2-like structure and inhibits both apoptosis and signalling from the interleukin 1 receptor, leading to nuclear factor kappa B activation. Here, we investigated the immune response to intranasal infection with a virus lacking the N1L gene (vDeltaN1L) compared with control viruses expressing N1L. Data presented show that deletion of N1L did not affect the proportion of CD4+ and CD8+ T cells infiltrating the lungs or the cytotoxic T-cell activity of these cells. However, vDeltaN1L induced an increased local natural killer cell activity between days 4 and 6 post-infection. In addition, in the absence of N1 the host inflammatory infiltrate was characterized by a reduced proportion of lymphocytes bearing the early activation marker CD69. Notably, there was a good correlation between the level of CD69 expression and weight loss. The implications of these findings are discussed.

Disciplines :

Immunology & infectious disease

Author, co-author :

Jacobs, Nathalie ; Université de Liège - ULiège > Département des sciences biomédicales et précliniques > Anatomie et cytologie pathologiques

Bartlett, Nathan W

Clark, Richard H

Smith, Geoffrey L; Imperial College London

Language :

English

Title :

Vaccinia virus lacking the Bcl-2-like protein N1 induces a stronger natural killer cell response to infection.

Publication date :

2008

Journal title :

Journal of General Virology

ISSN :

0022-1317

eISSN :

1465-2099

Publisher :

Society for General Microbiology, London, United Kingdom

Volume :

Issue :

Pt 11

Pages :

2877-81

Peer reviewed :

Peer Reviewed verified by ORBi

Funders :

Wellcome Trust

Available on ORBi :

since 22 December 2008

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Bibliography

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