Journal of Virology, November 2008, p. 10963, Vol. 82, No. 22
0022-538X/08/$08.00+0 doi:10.1128/JVI.02006-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Mouse APOBEC3 Is a Friend Virus-Restricting FactorAPOBEC3 enzymes are potent inhibitors of retroviral replication, but lentiviruses have evolved mechanisms to evade host APOBEC3. Murine leukemia viruses exclude mouse APOBEC3 from virions and cleave virion-incorporated APOBEC3. Based on the previous mapping of a Friend virus resistance gene, Takeda et al. (p. 10998-11008) show that polymorphisms at the mouse APOBEC3 locus influence Friend virus replication both in cultured cells and in mice. Furthermore, mice lacking the resistant APOBEC3 allele display exacerbated disease development upon Friend virus infection. This work indicates that mouse APOBEC3 is a physiological restriction factor to mouse gammaretroviruses.
Tulane Calicivirus Reverse Genetics System
Tulane virus (TV) is a new calicivirus isolated from the stools of rhesus macaques. Unlike caliciviruses of humans, TV is capable of replicating in cultured cells. Wei et al. (p. 11429-11436) have successfully developed a reverse genetics system for TV by transfecting full-length viral RNA made in vitro in a permissive monkey cell line. This work provides a new tool for overcoming the difficulties of studying calicivirus pathogenesis and replication.
NK T Cells Play a Crucial Role in Determining the Outcome of Herpes Simplex Virus 1 Infection
The clinical outcome of an infection with herpes simplex virus 1 (HSV-1) can be considered a race between progression of infection and deployment of host defenses. Grubor-Bauk et al. (p. 11073-11083) show that both subsets of CD1d-dependent NK T cells participate in enhancing resistance to HSV-1 and appear to have an essential role in determining whether the virus is controlled rapidly or whether there is rapid amplification and escalation toward neuronal damage and lethal outcome.
Thogoto Virus Employs a Unique Strategy To Suppress the Interferon Response
The NS1 protein of influenza viruses counteracts the induction of type I interferons by inhibiting RIG-I. Thogoto virus, a tick-borne member of the Orthomyxoviridae family, does not express an NS1 protein but rather suppresses alpha/beta interferon induction by ML, a splice variant of the matrix protein. Vogt et al. (p. 11446-11453) demonstrate that ML interacts with the general transcription factor IIB. Surprisingly, this interaction specifically interferes with IRF3 and NF-
B-dependent gene expression but not cellular transcription in general. Thus, Thogoto virus has evolved a unique strategy to counteract the interferon system.
Revisting Rotavirus Reassortment
Rotaviruses (RVs) are thought to exist as a heterogeneous pool of reassortants, with each isolate displaying a unique constellation of the 11 viral double-stranded RNA (dsRNA) gene segments. However, whole-genome sequencing by Heiman et al. (p. 11106-11116) now indicates that human RVs are strongly biased in favor of maintaining certain gene constellations. This result differs from the previous notion that RVs randomly exchange dsRNAs and instead suggests that viral genes coevolve to create protein sets that operate best when kept together.
Parvovirus Populations inside Hosts Characterized by Complex Genetic Diversity
Canine parvovirus (CPV) is a recently emerged pathogen that evolves at a surprisingly high rate. Hoelzer et al. (p. 11096-11105) show that despite such rapid population-level evolution, the extent of intrahost genetic diversity is limited. Relatively little genetic variation is observed during natural infections with CPV and its ancestor, feline panleukopenia virus (FPV). This is true even when CPV was intentionally transferred back to the host species of FPV. However, despite this limited genetic variation, there is evidence for both gene rearrangements and mixed infections, which would facilitate recombination and possibly tissue-specific differentiation.
Journal of Virology, November 2008, p. 10963, Vol. 82, No. 22
0022-538X/08/$08.00+0 doi:10.1128/JVI.02006-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.
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