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Hosts and viruses are under a constant coevolution pressure. Schematically, a virus (as a population) requires a permanent supply of naive hosts to continue to exist, and survival of the host population relies on its ability to develop antiviral defenses. Severe acute respiratory syndrome coronavirus, Henipaviruses (Hendra and Nipah) and filoviruses (Ebola and Marburg) are apt examples. On the one hand, they benignly colonize bats to survive, and on the other hand, thanks to the use of highly conserved cellular receptors (1), they are deadly pathogens for several other mammals, including humans, in which they induce self-extinguishing local epidemics. The virus and host coevolution can narrow down to a virus reservoir limited to a single animal species as illustrated by measles virus (MeV), a human-only pathogen. In the absence of an animal reservoir, the survival of MeV relies on its access to human populations large enough to allow an unbroken chain of acute infections (2). Measles, a major childhood killer disease of the prevaccination era, is attributable to an acute infection by one of the most highly contagious human pathogens. Virus transmission is limited because of the short time window during which infected individuals are contagious and because of the lifelong sterilizing immunity that MeV induces. Since the identification of CD46/membrane cofactor protein (MCP) (1993) and CD150/signalling lymphocyte-activation molecule (SLAM) (2000) as receptors mediating MeV entry into human cells, several transgenic mouse models of measles disease have been developed. However, these poorly reproduce the human disease, with viral dissemination observed only in mouse neonates. The mouse interferon (IFN) system appears to be a major host-restriction parameter because only human receptor transgenic mice with a disabled IFN system show susceptibility to MeV infection (3). However, in PNAS, Iwasaki and Yanagi (4) present an original strategy to overcome IFN-mediated restriction in mouse …

Virus-driven conditional expression of an interferon antagonist as a tool to circumvent host restriction