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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.
Unlabelled:
Mason-Pfizer monkey virus (M-PMV) is a prototypical betaretrovirus responsible for simian AIDS (SAIDS) in rhesus macaques. It has been shown previously that mouse cells are resistant to infection by HIV-1 and other primate lentiviruses. However, the susceptibility of mouse cells to primate retroviruses such as M-PMV remains unexplored. In the present study, using single-round green fluorescent protein (GFP) reporter viruses, we showed that various mouse cell lines are unable to support the early stages of M-PMV replication. The block to infection occurs postentry and is independent of the viral envelope. Using quantitative real-time PCR, we showed that the block to infection occurs after reverse transcription but before formation of circular DNA or proviral DNA. Finally, we showed that the M-PMV block in mouse cells is not attributable to the previously characterized mouse restriction factor Fv1. Overall, these findings suggest that mouse cells exhibit a previously uncharacterized block to M-PMV infection.
Importance:
Here we document a novel postentry restriction to M-PMV infection in mouse cells. The block occurs after reverse transcription but before the formation of circular or proviral DNA and is independent of the previous characterized mouse restriction factor Fv1.
Insights
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.
