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Stimulation Via CD40 Can Substitute for CD4 T Cell Function in Preventing Reactivation of a Latent Herpesvirus
Sally R. Sarawar, Bong Joo Lee, Su Khoh Reiter and Stephen P. Schoenberger
Proceedings of the National Academy of Sciences of the United States of America
Vol. 98, No. 11 (May 22, 2001), pp. 6325-6329
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/3055804
Page Count: 5
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Reactivation of latent herpesviruses is a particular problem in immunocompromised individuals, such as AIDS patients, who lack effective CD4 T helper cell function. An important question is whether residual immune defenses can be mobilized to combat such opportunistic infections, in the absence of CD4 T cells. In the present study, we used a mouse model of opportunistic infection to determine whether stimulation via CD40 could substitute for CD4 T cell function in preventing reactivation of a latent herpesvirus. Treatment with an agonistic antibody to CD40 was highly effective in preventing reactivation of latent murine gammaherpesvirus (MHV-68) in the lungs of CD4 T cell-deficient mice. CD8+ T cells were essential for this effect, whereas virus-specific serum antibody was undetectable and IFN-γ, production was unchanged. This demonstration that immunostimulation via CD40 can replace CD4 T cell help in controlling latent virus in vivo has potential implications for the development of novel therapeutic agents to prevent viral reactivation in immunocompromised patients.
Proceedings of the National Academy of Sciences of the United States of America © 2001 National Academy of Sciences