Murine gammaherpesvirus-68 expands,but does not activate,CD11b + gr-1 + splenocytes in vivo

Background: murine gammaherpesvirus 68 (hv-68) is an efficient pathogen,capable of infecting and establishing lifelong latency in rodents. while many studies have demonstrated the ability of this viral infection to modulate immune responses,a unifying mechanism for hv-68-induced subversion of a protective host response remains elusive. we questioned whether infection with hv-68 could expand a population of myeloid derived suppressor cells (mdsc) as one mechanism for altering protective immunity. methods: mice were infected with hv-68,with viral latency being established in these animals. at varying times post-infection,cells were isolated for detection of viral genomes,phenotyping of myeloid cell populations,and ex vivo analysis of suppressor activity of myeloid cells. results: cd11b + gr-1+ myeloid cells accumulated in the spleens,but not the bone marrow,of hv-68 infected mice. these cells were predominantly gr-1+ ly-6 g+,and could be found to contain viral genomes. increased levels of serum s100a8/a9 produced during viral infection were consistent with the expansion of these cd11b + gr-1+ myeloid cells. despite their expansion,these cells exhibited no increased arginase 1 or inos activity,and did not have the ability to suppress anti-cd3 antibody activated t lymphocyte responses. conclusions: we concluded that hv-68 infection was capable of expanding a population of myeloid cells which were phenotypically similar to mdsc. however these cells were not sufficiently activated during the establishment of viral latency to actively suppress t cell responses. © 2012 nelson et al.; licensee biomed central ltd.