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The Use of Mouse Mammary Tumor Cells in an In Vitro Invasion Assay as a Measure of Oncogenic Cell Behavior
Published on: June 12, 2019
Moderate sensitivity of mouse mammary tumour virus to inhibition by human APOBEC3G
Constantine James Konstantoulas1, Benedikt Hagen1, Stanislav Indik1
1Institute of Virology, University of Veterinary Medicine, Veterinaerplatz 1, 1210 Vienna, Austria.
Abstract:
Infectivity of the mouse mammary tumour virus (MMTV) is inhibited by mouse APOBEC3 (mA3) which is efficiently packaged into virions. As the inhibition is only partial, the virus can replicate in tissues expressing mA3 and complete its replication cycle. Here, we have examined the sensitivity of MMTV to inhibition by a human orthologue of mA3, A3G. We report that the virus containing A3G is only moderately susceptible to inhibition by the human factor. Whereas the vif-deficient HIV-1 vector produced in human epithelial cells expressing endogenous levels of A3G was efficiently inhibited, an MMTV vector remained fully infectious. Greater A3G expression levels were necessary to restrict infectivity of MMTV, but only when the factor retained its deaminase activity. Furthermore, the spreading kinetic of a replication competent MMTV was only moderately accelerated in cells with downmodulated A3G expression. These data suggest that MMTV has evolved a mechanism to neutralize antiviral activity of APOBEC3 proteins.
Insights
Mouse mammary tumor virus (MMTV) shows moderate resistance to human APOBEC3G (A3G) antiviral activity. MMTV appears to have evolved mechanisms to counteract A3G, unlike HIV-1.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Mouse mammary tumor virus (MMTV) infectivity is partially inhibited by mouse APOBEC3 (mA3).
- Understanding MMTV's interaction with APOBEC3 proteins is crucial for viral pathogenesis research.
Purpose of the Study:
- To investigate the sensitivity of MMTV to inhibition by human APOBEC3G (A3G).
- To compare MMTV's resistance to A3G with that of HIV-1.
Main Methods:
- Production of MMTV and HIV-1 vectors in cells expressing varying levels of A3G.
- Assessment of viral infectivity and replication kinetics.
- Evaluation of A3G's deaminase activity's role in inhibition.
Main Results:
- MMTV showed only moderate susceptibility to A3G inhibition, unlike vif-deficient HIV-1.
- Higher A3G expression levels were required to inhibit MMTV, dependent on deaminase activity.
- Downmodulation of A3G moderately accelerated MMTV replication, suggesting evolved resistance.
Conclusions:
- MMTV has developed mechanisms to neutralize the antiviral activity of APOBEC3 proteins.
- MMTV exhibits distinct resistance strategies compared to other retroviruses like HIV-1.
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