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ICP27 is a multifunctional phosphoprotein that plays critical roles during herpes simplex virus 1 (HSV-1) infection. Rojas et al. (p. 2200-2211) and Corbin-Lickfett et al. (p. 2212-2222) show that key viral replication events are curtailed during infection with ICP27 phosphorylation site mutants, including a crucial interaction between ICP27 and the mRNA export receptor, TAP/NXF1. ICP27 has a flexible N terminus that is even more disordered in phosphorylation site mutants, rendering ICP27 incapable of interacting with some partners. Thus, phosphorylation affects local structure, which in turn controls ICP27's interactions.
Early attempts to genetically map various vaccinia virus phenotypes using classical genetic crosses were confounded by experimental noise and a low frequency of recombinants. Lin and Evans (p. 2432-2443) devised a new method for tracking the intracellular movement of coinfecting vaccinia viruses expressing a green fluorescent protein fused to phage λ Cro DNA-binding protein (GFP-Cro). Images of living cells, combined with fluorescence in situ hybridization, indicate that the cytoplasm limits the mixing of coinfecting virosomes and thus reduces opportunities for recombination. These findings show why classical genetic maps of vaccinia virus proved so difficult to assemble 25 years ago.
Plants react to many types of viral infections by deploying defensive resources, including RNA silencing via production of small interfering RNAs (siRNAs) derived from the invading nucleic acid. Viroids are small plant pathogenic RNAs that, in contrast to viruses, lack protein-coding capacity. Although RNA silencing is a well-established antiviral response, its role in containing viroid infection is unclear. Di Serio et al. (p. 2477-2489) now report that RNA-dependent RNA polymerase 6, which catalyzes an amplification circuit for producing secondary siRNAs, restricts viroid accumulation and prevents invasion of the meristems where the stem cells reside. This work expands the plant antiviral response to include viroid RNA targets.
Increased compartmentalization of blood and cerebrospinal fluid (CSF) human immunodeficiency virus type 1 (HIV-1) populations has been associated with HIV-1-associated dementia. However, it is not known when this compartmentalization arises during the course of infection. Schnell et al. (p. 2395-2407) show that compartmentalization and clonal amplification of HIV-1 populations can occur in the CSF of some subjects early after HIV-1 transmission, in part through persistence of the putative transmitted variant or via independent evolution in the CNS environment. These results demonstrate that HIV-1 replication can occur in the CNS shortly after infection.
Inbred mouse strains demonstrate differences in susceptibility to respiratory syncytial virus (RSV) infection. Stark et al. (p. 2257-2269) analyzed RSV infection in recombinant offspring derived from susceptible (AKR/J) and resistant (C57BL/6J) mice and identified a region on proximal chromosome 6 significantly associated with differential RSV susceptibility. Gene expression analysis comparing lung transcripts obtained from parent strains at selected times following RSV exposure identified several candidate genes that map to this region. These studies support a significant genetic contribution to RSV susceptibility in mice.