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

• Published in: Journal of inflammation (London, England) England), 2012-04, Vol.9 (1), p.14-14, Article 14
• Main Authors: Nelson, Daniel A, Chauhan, Vinita S, Tolbert, Melanie D, Bost, Kenneth L
• Format: Article
• Language: English
• Subjects: Analysis; Autoimmune diseases; B cells; Deoxyribonucleic acid; Disease; DNA; Gammaherpesvirus; Genomics; Health aspects; Herpes; Herpesvirus diseases; Immune response; Infection; Infections; Myeloid derived suppressor cells; Physiological aspects; Proteins; Rodents; Spleen; Studies; T cells; Virus diseases
• ISSN: 1476-9255; 1476-9255
• DOI: 10.1186/1476-9255-9-14

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. 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. 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. 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.