MicroRNA-155 plays a critical role in the establishment of latency in murine γ-herpesvirus infection (VIR1P.1148)

• Published in: The Journal of immunology (1950) 2015-05, Vol.194 (1_Supplement), p.74-74.25
• Main Authors: Crepeau, Rebecca, Usherwood, Edward
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.194.Supp.74.25

Gammaherpesvirus infection in immunosuppressed populations is associated with severe disease. MicroRNA-155 (miR155) has been shown to play significant roles in the immune response, including in the formation of germinal centers (GC) and the development and maturation of T follicular helper cells (Tfh). We sought to determine the relative contribution of miR-155 in the T and B cell compartments to latent murine gammaherpesvirus infection. Mice deficient in miR-155 had a 100-fold decrease in latent viral load, measured by qPCR, and exhibited decreases in both follicular helper cells and germinal center B cells. However, infection of mixed bone marrow chimeric mice showed a similar latent viral burden in both WT and miR-155 deficient B cells. Therefore the role of miR-155 may not be B cell intrinsic, but is likely mediated in part due to the regulation that miR155 exerts on the T follicular helper cell population. Studies using a YFP marker virus also address roles for miR-155 in virus reactivation and maintenance of latency. Further elucidating the relative role of miR155 on these cell populations will provide key insights into the development of latency in this model system.