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Transcription from the long terminal repeats (LTRs) of complex retroviruses such as human T-lymphotropic virus type 1 is bidirectional. In studies of murine leukemia virus-induced tumors, Rasmussen et al. (p. 3780-3788) now describe chimeric RNA products consisting of proviral antisense and host cell gene sequences and show that the LTR alone is responsible for this activity. The results demonstrate a capacity for bidirectional transcription in the LTRs of simple retroviruses and suggest a new mechanism of insertional activation of protooncogenes.
The adenovirus E1A protein plays a major role in inducing cellular DNA synthesis in quiescent cells. However, the precise mechanisms underlying this process are unknown. Sha et al. (p. 4050-4059) provide intriguing new evidence that highlights a relationship between E1A and two transcriptional pathways of opposing action in epigenetically regulating E2F-dependent genes involved in controlling the onset of DNA replication. This work reveals how E1A functions to transition cells out of quiescence.
Herpesvirus envelopment at the inner nuclear membrane is mediated by a complex of two conserved viral proteins, pUL31 and pUL34. Roller et al. (p. 3921-3934) use extragenic suppressor analysis to show that these proteins make multiple interactions with distinct functions in envelopment, one of which mediates membrane curvature around the nucleocapsid. These findings identify new essential steps in herpesvirus replication that may serve as attractive targets for antiviral therapy.
Orf virus (ORFV) modulates immune responses in several animal species. However, the means by which ORFV alters host immunity are poorly understood. Diel et al. (p. 3962-3973) show that the novel ORFV protein, ORFV024, inhibits activation of the NF-κB signaling pathway by preventing activation of the IκB kinase complex. Deletion of the ORFV024-encoding gene does not affect ORFV pathogenesis in the natural host, suggesting that the protein contributes to another property in ORFV biology. This study represents the first description of an NF-κB inhibitor encoded by a parapoxvirus.
Influenza virus infection in mammalian hosts is resolved through a combination of immune clearance and depletion of available susceptible cells. Saenz et al. (p. 3974-3983) model these interactions using data gathered from studies of equine influenza and highlight a powerful role for innate immunity in controlling infection, with cell depletion serving a more limited function. The model also shows how variation in innate immunity induction and effectiveness can account for a range of different infection outcomes.