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In addition, although the NS deletion mutants grew to wild- type rBRSV levels in cells lacking a functional IFN-a/b system, their replication as severely inhibited in IFNcompetent cells98 These results suggested that the NS proteins block induction of IFN-a/b gene expression Wild-type human respiratory syncytial virus (HRSV) is a poor inducer of a/b interferons (IFN-a/b) In accord with the results seen with BRSV, recombinant HRSV lacking the NS1 and NS2 genes was able to induce high levels of IFN-a and IFN-b in epithelial cells and macrophages99 The two proteins can function independently or coordinately Alphaviruses including Venezuelan (VEEV), eastern (EEEV), and western equine encephalitis viruses (WEEV) are potential agents of biological warfare and terrorism and important, naturally emerging zoonotic viruses A representative virus of this group is Sindbis virus, which possesses a nonstructural protein nsP2 that is a signi cant regulator of Sindbis virus host cell interactions.

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This protein not only is a component of the replicative enzyme complex required for replication and transcription of viral RNAs but also plays a role in suppressing the antiviral response in Sindbis virus-infected cells nsP2 may act by decreasing interferon (IFN) production100,101 In another study, White and co-workers102 found that a single change (G to A) at nucleotide 3 of the 50 untranslated region (UTR) of the Venezuelan equine encephalitis virus (VEEV) V3000 virulent strain genome resulted in a virus that was avirulent in mice This mutant showed no growth disadvantage compared to the wild-type virus in cells derived from IFN-a/bR( / )mice Induction of IFN-a/b was the same for avirulent and virulent viruses; however, the avirulent mutant virus was more sensitive than the virulent strain to the antiviral actions of IFN-a/b Thus, increased sensitivity to IFN-a/b must play a major role in the in vivo attenuation.

Virus zoonoses causing hemorrhagic fevers include the Bunyaviridae Thomas et al103 found that bunyaviruses activate PKR but are only marginally sensitive to its antiviral effect In addition, NSs appeared to be different from other IFN antagonists, since it inhibited dsRNA-dependent IFN induction but had no effect on the dsRNA-activated PKR and RNase L systems Bunyamwera virus, of the family Bunyaviridae, possesses a nonstructural protein NSs that is a virulence factor that inhibits IFN-b gene expression in the mammalian host In an unconventional mechanism of interferon antagonism, NSs targets the RNA polymerase II (RNAP II) complex103 106 Rift Valley fever virus (RVFV), a phlebovirus of the family Bunyaviridae, is a major public health threat in Egypt and sub-Saharan Africa Bouloy and coworkers107 could show that the ability of RVFV to inhibit IFN-a/b production correlated with viral virulence, thereby suggesting that the accessory protein NSs is an interferon antagonist.

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