期刊
JOURNAL OF VIROLOGY
卷 87, 期 10, 页码 5904-5915出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.03489-12
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资金
- Canadian Institutes of Health Research [93804]
- Natural Sciences and Engineering Council of Canada [418719]
- Canada Foundation for Innovation [16389]
- Violet E. Powell Research Fund
- Funding Program for Next Generation World-Leading Researchers from the Japan Society for the Promotion of Science (JSPS)
- Program of Japan Initiative for Global Research Network on Infectious Diseases from the Ministry of Education, Culture, Science, Sports and Technology (MEXT) of Japan
- National Science Foundation [DMR-1120296]
Herpes simplex virus 2 (HSV-2) is an important human pathogen that is the major cause of genital herpes infections and a significant contributor to the epidemic spread of human immunodeficiency virus infections. The UL21 gene is conserved throughout the Alphaherpesvirinae subfamily and encodes a tegument protein that is dispensable for HSV-1 and pseudorabies virus replication in cultured cells; however, its precise functions have not been determined. To investigate the role of UL21 in the HSV-2 replicative cycle, we constructed a UL21 deletion virus (HSV-2 Delta UL21) using an HSV-2 bacterial artificial chromosome, pYEbac373. HSV-2 Delta UL21 was unable to direct the production of infectious virus in noncomplementing cells, whereas the repaired HSV-2 Delta UL21 strain grew to wild-type (WT) titers, indicating that UL21 is essential for virus propagation. Cells infected with HSV-2 Delta UL21 demonstrated a 2-h delay in the kinetics of immediate early viral gene expression. However, this delay in gene expression was not responsible for the inability of cells infected with HSV-2 Delta UL21 to produce virus insofar as late viral gene products accumulated to WT levels by 24 h postinfection (hpi). Electron and fluorescence microscopy studies indicated that DNA-containing capsids formed in the nuclei of Delta UL21-infected cells, while significantly reduced numbers of capsids were located in the cytoplasm late in infection. Taken together, these data indicate that HSV-2 UL21 has an early function that facilitates viral gene expression as well as a late essential function that promotes the egress of capsids from the nucleus.
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