期刊
JOURNAL OF VIROLOGY
卷 80, 期 24, 页码 12187-12196出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01275-06
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- NCI NIH HHS [R01 CA086839, R01CA86839] Funding Source: Medline
- NIDCR NIH HHS [R01 DE016680-02, R01 DE016680-04, R01 DE016680-03, R01 DE016680, R01 DE016680-01, R01 DE016680-05, R01DE016680] Funding Source: Medline
Open reading frame 45 (ORF45) of Kaposi's sarcoma-associated herpesvirus (KSHV) encodes an immediate-early protein. This protein is also present in virions as a tegument protein. ORF45 protein interacts with interferon regulatory factor 7 (IRF-7) and inhibits virus-induced type I interferon production by blocking activation of IRF-7. To define further the function of ORF45 and the mechanism underlying its action, we constructed an ORF45-null recombinant virus genome (BAC-stop45) by using a bacterial artificial chromosome (BAC) system. Stable 293T cells carrying the BAC36 (wild type) and BAC-stop45 genomes were generated. When monolayers of 293T BAC36 and 293T BAC-stop45 cells were induced with 12-O-tetradecanoylphorbol-13-acetate and sodium butyrate, no significant difference was found between them in overall viral gene expression and lytic DNA replication, but induced 293T BAC-stop45 cells released 10-fold fewer virions to the medium than did 293T BAC36 cells. When ORF45-null virus was used to infect cells, lower infectivity was observed than for wild-type BAC36. These results suggest that KSHV ORF45 plays roles in both early and late stages of viral infection, probably in viral ingress and egress.
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