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B cells regulate murine gammaherpesvirus 68 latency
K E Weck1, S S Kim, I V Virgin HW
1Center for Immunology and Departments of Pathology and Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Journal of Virology
|May 11, 1999
Summary
B cells are not essential for establishing gammaherpesvirus 68 (gammaHV68) latency but are crucial for controlling its reactivation and chronic infection in mice. This study quantifies gammaHV68 latency dynamics and highlights B cell roles in viral regulation.
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Gammaherpesviruses establish latent infections, but the dynamics of latency establishment and reactivation in natural hosts are not well understood.
- Murine gammaherpesvirus 68 (gammaHV68) is a model virus genetically related to primate gammaherpesviruses, establishing latent infections in mice.
Purpose of the Study:
- To quantitatively analyze the establishment and reactivation dynamics of gammaherpesvirus 68 (gammaHV68) latency in a natural host.
- To compare gammaHV68 latency and reactivation in normal (C57BL/6) and B-cell-deficient (MuMT) mice.
Main Methods:
- Utilized limiting dilution reactivation and limiting dilution PCR assays to quantify gammaHV68 genome-carrying cells and reactivation frequency.
- Compared latency establishment and reactivation efficiency in spleen, bone marrow, and peritoneal cells following intraperitoneal (i.p.) or intranasal (i.n.) inoculation.
Main Results:
- B cells are not required for gammaHV68 latency establishment in peritoneal cells, but splenic latency establishment is less efficient in B-cell-deficient mice.
- Splenic cells showed lower reactivation efficiency than peritoneal cells, irrespective of mouse strain or inoculation route.
- B-cell-deficient mice exhibited 10- to 100-fold higher gammaHV68 reactivation efficiency from 28 to 250 days post-infection, with increased genome-positive peritoneal cells at 7 weeks.
Conclusions:
- B cells are dispensable for gammaHV68 latency establishment but play a critical role in regulating viral reactivation from latency.
- Organ-specific differences in reactivation efficiency exist, with peritoneal cells reactivating more efficiently than splenic cells.
- B cells are vital for controlling chronic gammaHV68 infection, as B-cell-deficient mice showed increased mortality due to dysregulated infection.