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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Stimulation via CD40 can substitute for CD4 T cell function in preventing reactivation of a latent herpesvirus.

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-gamma 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.[1]

References

  1. Stimulation via CD40 can substitute for CD4 T cell function in preventing reactivation of a latent herpesvirus. Sarawar, S.R., Lee, B.J., Reiter, S.K., Schoenberger, S.P. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
 
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