Interferon consensus sequence binding protein: Not essential for interferon alpha-mediated antiviral response to vesicular-stomatitis virus infection in HL-60 cells.
- Author:
Byung Kiu PARK
1
Author Information
- Publication Type:Original Article
- Keywords: interferon consensus sequence binding protein; DNA binding domain; interferon alpha; vesicular stomatitis virus infection
- MeSH: Carrier Proteins*; Clone Cells; Consensus Sequence*; Consensus*; DNA; DNA, Complementary; HL-60 Cells*; Humans; Interferon-alpha; Interferons*; Leukemia; Plasmids; Vesicular Stomatitis
- From:Immune Network 2001;1(2):109-115
- CountryRepublic of Korea
- Language:Korean
- Abstract: BACKGROUND: The role of the interferon consensus sequence binding protein (ICSBP), a member of interferon regulatory factor family, in protecting against a vesicular stomatitis virus (VSV) infection has not been firmly elucidated. Thus, it was investigated utilizing the human promyelocytic leukemia HL-60 cells which do not express ICSBP. METHODS: HL-60 cells were stably transfected with plasmid containing cDNA for either ICSBP or DNA binding domain (DBD) and tested for their VSV-susceptibilities. The susceptibility of each transfectant group to a VSV infection was determined by a plaque assay at 1 h, 24 h, and 48 h post-infection in the presence (500 IU/ml) or absence of interferon alpha(IFN alpha). RESULTS: In the absence of IFN alpha, the three groups showed similar sensitivities to a VSV infection. However, when pre-treated with IFN, the viral titers in both the ICSBP and control clones steadily decreased over 48 h of incubation, indicating the existence of IFN alpha-mediated protection against VSV infection. The IFN alpha-treated ICSBP clones appeared to be more resistant to infection compared with the control clones, although the difference was not great . On the contrary, the viral titers in the IFN alpha-treated DBD clones increased at 24 h then decreased by 48 h. CONCLUSION: The expression of truncated ICSBP (DBD) does not appear to underlie the impaired protection against a VSV infection in the DBD clones, since even the control clones lacking ICSBP were protected from a VSV infection. This suggests that ICSBP does not play a critical role in the IFN alpha-mediated anti-VSV response of HL-60 cells, although it appears to confer some resistance to a VSV infection.
