| First Author | Lee BJ | Year | 2000 |
| Journal | J Virol | Volume | 74 |
| Issue | 6 | Pages | 2786-92 |
| PubMed ID | 10684295 | Mgi Jnum | J:127147 |
| Mgi Id | MGI:3763027 | Doi | 10.1128/jvi.74.6.2786-2792.2000 |
| Citation | Lee BJ, et al. (2000) Lymphotoxin-alpha-deficient mice can clear a productive infection with murine gammaherpesvirus 68 but fail to develop splenomegaly or lymphocytosis. J Virol 74(6):2786-92 |
| abstractText | Respiratory challenge with murine gammaherpesvirus 68 (MHV-68) leads to an acute productive infection of the lung and a persistent latent infection in B lymphocytes, epithelia, and macrophages. The virus also induces splenomegaly and an increase in the number of activated CD8 T cells in the circulation. Lymphotoxin- alpha-deficient (LTalpha(-/-)) mice have no lymph nodes and have disrupted splenic architecture. Surprisingly, in spite of the severe defect in secondary lymphoid tissue, LTalpha(-/-) mice could clear a productive MHV-68 infection, although with delayed kinetics compared to wild-type mice, and could control latent infection. Cytotoxic T-cell activity was comparable in the lungs and spleens of LTalpha(-/-) and wild-type mice. However, splenic gamma interferon responses were substantially reduced in LTalpha(-/-) mice. Furthermore, LTalpha(-/-) mice failed to develop splenomegaly or lymphocytosis. Although germinal centers were absent, LTalpha(-/-) mice were able to class switch and showed significant virus-specific antibody titers. This work demonstrates that organized secondary lymphoid tissue is not an absolute requirement for the generation of immune responses to viral infections. |
