The human gammaherpesviruses Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus and murine gammaherpesvirus-68 (gHV68) are associated with B-cell lymphomas. The establishment of a chronic infection in B-cells is a critical step in the ability of these viruses to establish a life-long infection that may put infected cells at risk for transformation. gHV68 represents a small tractable animal model for gammaherpesvirus latency. These studies aim to utilize gHV68 as a model for understanding the role of NFkappaB in the establishment of chronic infection by gammaherpesviruses. NF-kB is necessary for the survival of B-cells infected with gHV68. In addition, NF-kappaB is required for achieving normal levels of chronic gHV68 infection in B-cells of mice. Here, two aspects of NF-kappaB signaling in B-cells upon infection with gHV-68 will be investigated: the specific NF-kappaB signaling pathways and subunits that are activated and the viral proteins that modulate these pathways. Characterization of these critical virus-cell interactions will provide a greater understanding of gammaherpesvirus-associated lymphoproliferative disorders and may thereby lead to novel therapeutic targets.
| Krug, Laurie T; Torres-González, Edilson; Qin, Qianhong et al. (2010) Inhibition of NF-kappaB signaling reduces virus load and gammaherpesvirus-induced pulmonary fibrosis. Am J Pathol 177:608-21 |
| Krug, Laurie T; Collins, Christopher M; Gargano, Lisa M et al. (2009) NF-kappaB p50 plays distinct roles in the establishment and control of murine gammaherpesvirus 68 latency. J Virol 83:4732-48 |
| Krug, Laurie T; Moser, Janice M; Dickerson, Shelley M et al. (2007) Inhibition of NF-kappaB activation in vivo impairs establishment of gammaherpesvirus latency. PLoS Pathog 3:e11 |
