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Journal of Virology, May 2006, p. 4538-4545, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4538-4545.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Sendai Virus Infection Induces Efficient Adaptive Immunity Independently of Type I Interferons

Carolina B. López, Jacob S. Yount, Tamar Hermesh, and Thomas M. Moran*

Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029

Received 20 December 2005/ Accepted 16 February 2006

Adaptive immunity in response to virus infection involves the generation of Th1 cells, cytotoxic T cells, and antibodies. This type of immune response is crucial for the clearance of virus infection and for long-term protection against reinfection. Type I interferons (IFNs), the primary innate cytokines that control virus growth and spreading, can influence various aspects of adaptive immunity. The development of antiviral immunity depends on many viral and cellular factors, and the extent to which type I IFNs contribute to the generation of adaptive immunity in response to a viral infection is controversial. Using two strains (Cantell and 52) of the murine respiratory Sendai virus (SeV) with differential abilities to induce type I IFN production from infected cells, together with type I IFN receptor-deficient mice, we examined the role of type I IFNs in the generation of adaptive immunity. Our results show that type I IFNs facilitate virus clearance and enhance the migration and maturation of dendritic cells after SeV infection in vivo; however, soon after infection, mice clear the virus from their lungs and efficiently generate cytotoxic T cells independently of type I IFN signaling. Furthermore, animals that are unresponsive to type I IFN develop long-term anti-SeV immunity, including CD8+ T cells and antibodies. Significantly, this memory response is able to protect mice against challenge with a lethal dose of virus. In conclusion, our results show that primary and secondary anti-SeV adaptive immunities are developed normally in the absence of type I IFN responsiveness.

* Corresponding author. Mailing address: Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029. Phone: (212) 241-6401. Fax: (212) 987-3653. E-mail: Thomas.Moran{at}mssm.edu.

Journal of Virology, May 2006, p. 4538-4545, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4538-4545.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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