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

Nathalie Jacobs

Nathan W. Bartlett

Richard H. Clark

Department of Virology, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK

Correspondence
Geoffrey L. Smith
glsmith{at}imperial.ac.uk

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 (vN1L) 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, vN1L 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.

Present address: Department of Pathology, Faculty of Medicine, University of Liège, 4000 Liège, Belgium.

Present address: Department of Respiratory Medicine, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK.

Present address: Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK.

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