Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

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
Stable URL: http://www.jstor.org/stable/3055804
Page Count: 5
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Stimulation Via CD40 Can Substitute for CD4 T Cell Function in Preventing Reactivation of a Latent Herpesvirus
Preview not available

Abstract

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.

Page Thumbnails

  • Thumbnail: Page 
6325
    6325
  • Thumbnail: Page 
6326
    6326
  • Thumbnail: Page 
6327
    6327
  • Thumbnail: Page 
6328
    6328
  • Thumbnail: Page 
6329
    6329