MxA-independent inhibition of Hantaan virus replication induced by type I and type II interferon in vitro

• Published in: Virus research 2007-07, Vol.127 (1), p.100-105
• Main Authors: Oelschlegel, Robin, Krüger, Detlev H., Rang, Andreas
• Format: Article
• Language: English
• Subjects: A549; Animals; Antiviral state; Cercopithecus aethiops; GTP-Binding Proteins - metabolism; Hantaan virus; Hantavirus; Hantavirus - drug effects; Hantavirus - immunology; Hantavirus - pathogenicity; Hantavirus - physiology; Interferon Type I - blood; Interferon Type I - pharmacology; Interferon-alpha; Interferon-gamma; Interferon-gamma - blood; Interferon-gamma - pharmacology; Interferons - pharmacology; MxA; Myxovirus Resistance Proteins; RNA viruses; Vero; Vero Cells; Virus Replication - drug effects
• ISSN: 0168-1702; 1872-7492
• DOI: 10.1016/j.virusres.2007.03.027

Interferons (IFN) induce an antiviral state against Hantaan virus (HTNV) but the mechanisms responsible for inhibition are unclear. The IFN-inducible MxA is discussed to be important for control of infections with hantaviruses. To characterize the role of endogenous MxA, the inhibition of HTNV induced by type I and type II IFNs was compared in Vero and A549 cells. IFNα and IFNγ reduced production of infectious virions, viral RNA, and nucleocapsid protein with the same efficiency, although expression of MxA protein was detectable only in IFNα-treated A549 cells. Furthermore, knock down of MxA expression did not impair IFNα-induced inhibition. Thus, inhibition of HTNV induced by type I and type II IFNs did not dependent on expression of endogenous MxA. Taken together, these data suggest that MxA endogenously expressed in response to type I or type II IFNs does not play a pivotal role for the antiviral state against HTNV and that there is more than one mechanism by which cellular defences block hantavirus replication.