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Postentry restriction of Mason-Pfizer monkey virus in mouse cells
1Integrated Program in Cellular, Molecular and Biophysical Studies, Columbia University, New York, New York, USA Medical Scientist Training Program, Columbia University College of Physicians and Surgeons, New York, New York, USA.
Journal of Virology
|December 26, 2014
Summary
Mouse cells resist Mason-Pfizer monkey virus (M-PMV) infection due to a novel postentry block. This restriction occurs after reverse transcription and is not due to the Fv1 factor, revealing a new cellular defense mechanism against betaretroviruses.
Area of Science:
- Virology
- Retroviruses
- Cellular Biology
Background:
- Mason-Pfizer monkey virus (M-PMV) causes simian AIDS (SAIDS) in macaques.
- Mouse cells are known to resist primate lentiviruses like HIV-1.
- Susceptibility of mouse cells to M-PMV, a betaretrovirus, was previously unknown.
Purpose of the Study:
- To investigate the susceptibility of mouse cells to M-PMV infection.
- To characterize the stage and mechanism of M-PMV restriction in mouse cells.
- To determine if the restriction is related to the known mouse restriction factor Fv1.
Main Methods:
- Utilized single-round green fluorescent protein (GFP) reporter viruses for M-PMV.
- Employed quantitative real-time PCR to track viral DNA formation.
- Tested for involvement of the Fv1 restriction factor.
Main Results:
- Mouse cell lines were unable to support early M-PMV replication.
- The infection block occurred postentry and was independent of the viral envelope.
- Restriction happened after reverse transcription but before circular or proviral DNA formation.
- The M-PMV block was not due to the Fv1 restriction factor.
Conclusions:
- Mouse cells possess a previously uncharacterized restriction mechanism against M-PMV.
- This restriction acts post-reverse transcription and is distinct from Fv1.
- Findings suggest a novel cellular defense against betaretroviral infection in mice.
