Abstract
MxA protein is expressed in response to type I and type III Interferon and constitute an important antiviral factor with broad antiviral activity to diverse RNA viruses. In addition, some studies expand the range of MxA antiviral activity to include particular DNA viruses like Monkeypox virus (MPXV) and African Swine Fever virus (ASFV). However, a broad profile of activity of MxA to large DNA viruses has not been established to date. Here, we investigated if some well characterized DNA viruses belonging to the Poxviridae family are sensitive to human MxA. A cell line inducibly expressing MxA to inhibitory levels showed no anti-Vaccinia virus (VACV) virus activity, indicating either lack of susceptibility of the virus, or the existence of viral factors capable of counteracting MxA inhibition. To determine if VACV resistance to MxA was due to a virus-encoded anti-MxA activity, we performed coinfections of VACV and the MxA-sensitive Vesicular Stomatitis virus (VSV), and show that VACV does not protect VSV from MxA inhibition in trans. Those results were extended to several VACV strains and two CPXV strains, thus confirming that those Orthopoxviruses do not block MxA action. Overall, these results point to a lack of susceptibility of the Poxviridae to MxA antiviral activity.
Highlights
Mx proteins are induced as part of the antiviral response triggered by type I and type III interferons
Upon Tet induction, MxA protein was expressed by these cells and showed the characteristic intracellular distribution previously described for MxA as revealed by staining with specific antibodies (Fig 1)
The MxA-sensitive Vesicular Stomatitis Virus suffered a 2.5 log reduction in progeny virus titer and a 20 fold inhibition in gene expression, in agreement with previous reports [24, 26]. Those results indicate that MxA protein expressed by MxA-293T cells was functional, and that Vaccinia virus (VACV) growth was not sensitive to the antiviral activity of MxA
Summary
Mx proteins are induced as part of the antiviral response triggered by type I and type III interferons. They belong to a family of large GTPases that includes dynamin, but despite this similarity, their detailed molecular mechanism of action is currently not known [1]. In the best studied example, mouse Mx1 inhibits influenza virus infection by blocking viral transcription and replication [2]. The antiviral range of activity of different Mx proteins seems to depend largely on the subcellular localization of the protein. Nuclear forms (like mouse Mx1) protect against viruses that replicate in the cell nucleus, while cytoplasmic forms (like mouse Mx2) inhibit replication of VSV and some other viruses that replicate in the cytoplasm
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