HIV-1 infection does not induce tumor necrosis factor-alpha or interferon-beta gene transcription.
An early host defense against infection by RNA or DNA viruses is the induction, within infected cells, of tumor necrosis factor-alpha (TNF-alpha) gene transcription. The protein product of the TNF-alpha gene alone, or together with different types of interferons, inhibits viral propagation in diverse cell types. In this study, the effect of acute and chronic human immunodeficiency virus type 1 (HIV-1) infection on the transcription of the TNF-alpha and interferon-beta (IFN-beta) genes was examined in susceptible monocyte and T-cell lines as well as in primary human mononuclear phagocytes. Although Sendai virus, a prototypic inducer of TNF-alpha and IFN-beta mRNA, induced the transcription of both genes in the monocyte cell lines and TNF-alpha in the T-cell line and in primary mononuclear phagocytes, transcription of these genes was not inducible by HIV-1. Therefore, HIV-1 was able to infect these cells without triggering the transcription of genes encoding proteins important in immediate antiviral cellular defenses. These results may explain in part how HIV-1 is able to establish persistent intracellular infections and escape acute host responses that have evolved to combat viral infection.
Goldfeld
A E
AE
Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts.
Birch-Limberger
K
K
Schooley
R T
RT
Walker
B D
BD
D002460:Cell Line; D002478:Cells, Cultured; D015967:Gene Expression Regulation, Viral; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D007370:Interferon Type I / Q000235:genetics*; D009000:Monocytes / Q000382:microbiology; D010222:Parainfluenza Virus 1, Human / Q000502:physiology; D010586:Phagocytes / Q000382:microbiology; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*; D014779:Virus Replication
D007370:Interferon Type I; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha