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Updated: May 30, 2026
Measurement of γHV68 Infection in Mice
Published on: November 22, 2011
De novo infection of B cells during murine gammaherpesvirus 68 latency
Michael L Freeman1, Claire E Burkum, Eric J Yager
1Trudeau Institute, 154 Algonquin Avenue, Saranac Lake, NY 12983, USA.
Insights
Gammaherpesvirus (GHV) latency is controlled by both T cells and antibodies. These immune components prevent the spread of GHV to new B cells, even during viral reactivation.
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Gammaherpesviruses (GHVs) establish lifelong latent infections.
- The precise mechanisms governing GHV latency maintenance remain largely unknown.
Purpose of the Study:
- To investigate the role of the immune system in controlling gammaherpesvirus latency and reactivation.
- To elucidate the mechanisms of viral spread during latent infection.
Main Methods:
- Utilized a murine gammaherpesvirus (MHV) model in immunocompetent mice.
- Employed in vivo T cell depletion strategies.
- Assessed viral loads and viral transfer to naive B cells.
Main Results:
- Previously uninfected B cells acquired virus during latency in immunocompetent mice.
- T cell depletion led to viral reactivation but not enhanced viral spread to new cells.
- Absence of both T cells and antibodies resulted in robust infection of new B cells from latently infected cells.
Conclusions:
- Both T cells and antibodies are critical for controlling gammaherpesvirus latency.
- Immune surveillance effectively limits viral reactivation and spread during latent infection.
- Understanding these mechanisms is key to developing strategies against persistent viral infections.
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.
