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Journal of Virology, January 2007, p. 19, Vol. 81, No. 1
0022-538X/07/$08.00+0 doi:10.1128/JVI.02401-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
| SPOTLIGHT |
The adenovirus E1B-55K protein plays a central role in the oncogenic transformation of primary mammalian cells, mainly by antagonizing p53-induced apoptosis and cell cycle arrest. Sieber and Dobner (p. 95-105) now report that the E1B-55K-related product, E1B-156R, can promote cell transformation without neutralizing p53 tumor suppressor activities. This work introduces a new function for E1B-156R and suggests that adenovirus E1B oncoproteins contribute to cell transformation through p53-dependent and -independent pathways.
Noncritical Role for Emerin Protein in Human Immunodeficiency Virus Type 1 Infection
Human immunodeficiency virus type 1 (HIV-1) replication proceeds through an integrated provirus. Recent results suggest that the inner nuclear membrane protein, emerin, plays a critical role in facilitating HIV-1 provirus integration. Shun et al. (p. 166-172) utilized expanded sets of small interfering RNA duplexes and mouse knockout cells to determine the requirement for emerin in HIV-1 infection. Knockout and wild-type littermate control cells supported indistinguishable levels of virus infectivity. Furthermore, expression of human emerin failed to enhance infectivity levels in mouse knockout cells. These results cast doubt on a universally important role for emerin protein in regulating HIV-1 infectivity.
Hepatitis B Virus Inhibition of Interferon Signaling
Treatment of chronic hepatitis B virus (HBV) infection with (pegylated) alpha interferon achieves a sustained response in only 30 to 40% of patients. The reasons for treatment failure in the majority of patients are not well understood. Christen et al. (p. 159-165) show that interferon signaling through the Jak-STAT pathway is inhibited in human hepatoma cell lines expressing HBV proteins and in liver biopsies of patients with chronic hepatitis B. Surprisingly, the molecular mechanisms of HBV interference with this pathway are very similar to those found in cells expressing hepatitis C virus proteins and in liver biopsies from patients with chronic hepatitis C.
A New Model for Studies of Cellular Immunity Elicited by Primate Lentiviruses
Studies of cellular immunity to simian immunodeficiency virus (SIV) in macaques are challenging because of extraordinary genetic heterogeneity within the major histocompatibility complex (MHC). Wiseman et al. (p. 349-361) show that feral cynomolgus macaques from the Indian Ocean island of Mauritius have remarkably simple MHC genetics, with six haplotypes accounting for nearly all MHC diversity. The potential value of these animals is illustrated by a pilot study examining SIV-specific cellular immunity in a pair of MHC-identical animals. The unusually simple MHC genetics of Mauritian macaques may enable studies of cellular immunity previously unimaginable in nonhuman primates.
Different B-Cell Responses after Inactivated and Live-Attenuated Influenza Virus Immunizations
Live-attenuated (LAIV) and inactivated (TIV) influenza virus vaccines are effective and immunogenic, but immune responses elicited by these two formulations have not been rigorously characterized. Sasaki et al. (p. 215-228) found significant differences in the B-cell (effector and memory) and antibody responses elicited after LAIV or TIV immunization in children and adults. These new data provide a more complete picture of the host response to these vaccines and suggest that different mechanisms are involved in generating protective immunity by live-attenuated and inactivated vaccines.
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