Journal of Virology, April 2007, p. 3675-3676, Vol. 81, No. 8
0022-538X/07/$08.00+0 doi:10.1128/JVI.00376-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
Articles of Significant Interest Selected from This Issue by the Editors
Human Papillomavirus E6 Isoforms Target PATJHigh-risk human papillomaviruses (HPV) encode two oncogenes. The E6 oncogene is associated with degradation of p53 and interacts with many PDZ-containing proteins to affect their stability and disrupt their localization. Storrs and Silverstein (p. 4080-4090) identify PATJ as a novel member of the membrane-associated family of PDZ proteins that binds and is degraded by both HPV 18 E6 and HPV 18 E6*. HPV 18 E6-mediated degradation of PATJ is not inhibited in cells in which E6AP was silenced by short hairpin RNA, suggesting that the E6-E6AP complex is not required for the degradation of this protein target.
The G1 Cytoplasmic Tail of Pathogenic Hantaviruses Encodes a Degron
The hantavirus G1 protein contains a 142-amino-acid cytoplasmic tail which, in NY-1 hantavirus, is ubiquitinated and proteasomally degraded. Sen et al. (p. 4323-4330) report that the G1 cytoplasmic tails of pathogenic, but not nonpathogenic, hantaviruses are degraded by the proteasome. An autonomous C-terminal degradation signal or "degron" unique to pathogenic hantaviruses was identified by homologous amino acid replacement using pathogenic and nonpathogenic G1 tails. Since pathogenic hantavirus G1 tails regulate the interferon pathway, the degron may represent a novel hantavirus virulence determinant.
Poliovirus-Induced Cleavage of the Sensor MDA-5
Infections with RNA viruses are detected by the innate immune system through membrane-bound Toll-like receptors or the cytoplasmic RNA helicases RIG-I and MDA-5. It is postulated that MDA-5 is crucial for sensing infections by picornaviruses, but there have been no studies on the role of this protein during infection with poliovirus, the prototypic picornavirus. Barral et al. (p. 3677-3684) show that MDA-5 is degraded in poliovirus-infected cells in a proteasome- and caspase-dependent manner. Poliovirus-induced cleavage of MDA-5 may be a mechanism to antagonize production of type I interferon in response to viral infection.
Respiratory Syncytial Virus Inhibits Na+ Channels in Airways
Respiratory syncytial virus (RSV) infections are associated with fluid accumulation in the respiratory tract and illnesses that range in severity from rhinitis and sinusitis to bronchiolitis and pneumonia. Kunzelmann et al. (p. 3714-3720) show that within minutes after RSV contacts the apical membrane of the mouse trachea, amiloride-sensitive Na+ transport by the epithelium is inhibited. This effect is mediated by protein kinase C and is not accompanied by any other alteration in epithelial transport. Thus, direct inhibition of epithelial Na+ channels by RSV may contribute to the fluid accumulation observed during RSV infections.
Control of Early Ectromelia Virus Infection Requires NK Cells
NK cells serve an essential function in the innate immune response to several viruses, including murine cytomegalovirus. However, the role of NK cells during ectromelia virus (ECTV) infection is less clear. Parker et al. (p. 4070-4079) show that the lack of NK cells during early ECTV infection results in increased virus replication and mortality, while the lack of NKT cells, 
T cells, and CD4 or CD8 T cells has no effect on control of early virus replication. In addition, the NK cell population expands and becomes activated during the early stages of ECTV infection. These data demonstrate a crucial role for NK cells in the recovery from ECTV infection.
In Vivo Cytomegalovirus Gene Expression is Tissue Specific
Cytomegalovirus (CMV) has a large genome that encodes many proteins involved in virus replication and immune evasion. While characterization of CMV gene expression in infected tissue-culture cells has been extensive, little is known about viral expression patterns that occur in an infected animal. Streblow et al. (p. 3816-3826) use microarray technology to globally characterize in vivo and in vitro rat CMV gene expression. This work demonstrates that in vivo rat CMV gene expression is tissue specific and cannot be predicted by the profiles observed in commonly used tissue culture cell systems.
Journal of Virology, April 2007, p. 3675-3676, Vol. 81, No. 8
0022-538X/07/$08.00+0 doi:10.1128/JVI.00376-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
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