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Journal of Virology, June 2007, p. 5628-5636, Vol. 81, No. 11
0022-538X/07/$08.00+0     doi:10.1128/JVI.01152-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Synergistic Roles of Antibody and Interferon in Noncytolytic Clearance of Sindbis Virus from Different Regions of the Central Nervous System{triangledown}

Rebeca Burdeinick-Kerr, Jennifer Wind, and Diane E. Griffin*

W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205

Received 3 June 2006/ Accepted 9 March 2007

Sindbis virus (SINV) is an alphavirus that causes infection of neurons and encephalomyelitis in adult immunocompetent mice. Recovery can occur without apparent neurological damage. To better define the factors facilitating noncytolytic clearance of SINV in different regions of the central nervous system (CNS) and the roles of innate and adaptive immune responses at different times during infection, we have characterized SINV infection and clearance in the brain, brain stem, and spinal cords of severe combined immunodeficiency (SCID) and C57BL/6 (wild-type [WT]) mice and mice deficient in beta interferon (IFN-ß) (BKO), antibody (µMT), IFN-{gamma} (GKO), IFN-{gamma} receptor (GRKO), and both antibody and IFN-{gamma} (µMT/GKO). WT mice cleared infectious virus by day 8, while SCID mice had persistent virus replication at all sites. For 3 days after infection, BKO mice had higher titers at all sites than WT mice, despite similar IFN-{alpha} production, but cleared virus similarly. GKO and GRKO mice cleared infectious virus from all sites by days 8 to 10 and, like WT mice, displayed transient reactivation at 12 to 22 days. µMT mice did not clear virus from the brain, and clearance from the brain stem and lumbar spinal cord was delayed, followed by reactivation. Eighty-one days after infection, µMT/GKO mice had not cleared virus from any site, but titers were lower than for SCID mice. These studies show that IFN-ß is independently important for early control of CNS virus replication, that antiviral antibody is critical for clearance from the brain, and that both antibody and IFN-{gamma} contribute to prevention of reactivation after initial clearance.

* Corresponding author. Mailing address: W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD 21205. Phone: (410) 955-3459. Fax: (410) 955-0105. E-mail: dgriffin{at}jhsph.edu

{triangledown} Published ahead of print on 21 March 2007.

Journal of Virology, June 2007, p. 5628-5636, Vol. 81, No. 11
0022-538X/07/$08.00+0     doi:10.1128/JVI.01152-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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