title: De novo infection of B cells during murine gammaherpesvirus 68 latency.
abstract: The mechanisms by which gammaherpesviruses maintain latency are unclear. Here we used a murine gammaherpesvirus model to show that previously uninfected B cells in immunocompetent mice can acquire virus during latency. In vivo depletion of T cells allowed viral reactivation, as measured by increased viral loads, but not enhanced transfer of virus to new cells. In the absence of both immune T cells and antibody following the transfer of latently infected cells into naïve animals, there was robust infection of new B cells. These data confirm that both T cells and antibody contribute to the control of gammaherpesvirus latency, reactivation, and spread.
authors.affiliation: Trudeau Institute, 154 Algonquin Avenue, Saranac Lake, NY 12983, USA.
authors.forename: Michael L
authors.initials: ML
authors.lastname: Freeman
authors.forename: Claire E
authors.initials: CE
authors.lastname: Burkum
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Yager
authors.forename: David L
authors.initials: DL
authors.lastname: Woodland
authors.forename: Marcia A
authors.initials: MA
authors.lastname: Blackman
mesh_terms: D000818:Animals; D000914:Antibodies, Viral / Q000276:immunology; D001402:B-Lymphocytes / Q000821:virology*; D008212:Lymphocyte Depletion; D051379:Mice; D020297:Mice, Congenic; D018144:Rhadinovirus / Q000472:pathogenicity*; D013601:T-Lymphocytes / Q000276:immunology; D019562:Viral Load; D014775:Virus Activation; D053586:Virus Internalization; D017735:Virus Latency
chemical_list: D000914:Antibodies, Viral