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Updated: May 8, 2026

Measurement of γHV68 Infection in Mice
Published on: November 22, 2011
Promyelocytic leukemia protein modulates establishment and maintenance of latent gammaherpesvirus infection in
Jaturong Sewatanon1, Hao Liu, Paul D Ling
1Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
Abstract:
Promyelocytic leukemia protein (PML) is an essential organizer of PML nuclear bodies (NBs), which carry out a variety of activities, including antiviral functions. Herpesviruses from all subfamilies encode proteins that counteract PML NB-mediated antiviral defenses by multiple mechanisms. However, because of the species specificity of herpesviruses, only a limited number of in vivo studies have been undertaken to investigate the effect of PML or PML NBs on herpesvirus infection. To address this central issue in herpesvirus biology, we studied the course of infection in wild-type and PML⁻/⁻ mice using murine gammaherpesvirus 68 (MHV68), which encodes a tegument protein that induces PML degradation. While acute infection in PML⁻/⁻ mice progressed similarly to that in wild-type mice, the lytic reactivation frequency was higher in peritoneal exudate cells, due to both an increase of MHV68 genome-positive cells and greater reactivation efficiency. We also detected a higher frequency of persistent infection in PML⁻/⁻ peritoneal cells. These findings suggest that the PML protein can repress the establishment or maintenance of gammaherpesvirus latency in vivo. Further use of the PML⁻/⁻ mouse model should aid in dissecting the molecular mechanisms that underlie the role of PML in gammaherpesvirus latency and may yield clues for how PML modulates herpesvirus latency in general.
Insights
Promyelocytic leukemia protein (PML) represses gammaherpesvirus latency. PML-deficient mice showed increased MHV68 reactivation and persistent infection, suggesting PML
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Promyelocytic leukemia protein (PML) organizes nuclear bodies (NBs) with antiviral functions.
- Herpesviruses encode proteins to evade PML NB-mediated antiviral defenses.
- In vivo studies on PML's role in herpesvirus infection are limited due to species specificity.
Purpose of the Study:
- To investigate the in vivo effect of PML and PML NBs on gammaherpesvirus infection.
- To elucidate PML's role in the establishment and maintenance of herpesvirus latency.
Main Methods:
- Utilized wild-type and PML-deficient (PML⁻/⁻) mice.
- Infected mice with murine gammaherpesvirus 68 (MHV68).
- Analyzed acute infection, lytic reactivation, and persistent infection in peritoneal exudate cells.
Main Results:
- Acute MHV68 infection progressed similarly in wild-type and PML⁻/⁻ mice.
- PML⁻/⁻ mice exhibited higher lytic reactivation frequency in peritoneal cells.
- Increased MHV68 genome-positive cells and enhanced reactivation efficiency were observed in PML⁻/⁻ mice.
- A higher frequency of persistent infection was detected in PML⁻/⁻ peritoneal cells.
Conclusions:
- PML protein can repress the establishment or maintenance of gammaherpesvirus latency in vivo.
- The PML⁻/⁻ mouse model is valuable for dissecting molecular mechanisms of gammaherpesvirus latency.
- Findings may provide insights into how PML modulates herpesvirus latency generally.
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