期刊
JOURNAL OF VIROLOGY
卷 87, 期 24, 页码 13386-13396出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02758-13
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资金
- Ecole Normale Superieure de Lyon
- InCa
- Croucher Foundation
- ARC
- InCa (Canceropole CLARA)
- La Ligue Contre le Cancer (Equipe Labelisee)
Type I interferon (IFN-I) inhibits the replication of different viruses. However, the effect of IFN-I on the human T-lymphotropic virus type 1 (HTLV-1) viral cycle is controversial. Here, we investigated the consequences of IFN-alpha addition for different steps of HTLV-1 and HTLV-2 infection. We first show that alpha interferon (IFN-alpha) efficiently impairs HTLV-1 and HTLV-2 de novo infection in a T cell line and in primary lymphocytes. Using pseudotyped viruses expressing HTLV-1 envelope, we then show that cell-free infection is insensitive to IFN-alpha, demonstrating that the cytokine does not affect the early stages of the viral cycle. In contrast, intracellular levels of Gag, Env, or Tax protein are affected by IFN-alpha treatment in T cells, primary lymphocytes, or 293T cells transfected with HTLV-1 or HTLV-2 molecular clones, demonstrating that IFN-alpha acts during the late stages of infection. We show that IFN-alpha does not affect Tax-mediated transcription and acts at a posttranscriptional level. Using either small interfering RNA (siRNA) directed against PKR or a PKR inhibitor, we demonstrate that PKR, whose expression is induced by interferon, plays a major role in IFN-alpha-induced HTLV-1/2 inhibition. These results indicate that IFN-alpha has a strong repressive effect on the HTLV-1 and HTLV-2 viral cycle during de novo infection of cells that are natural targets of the viruses.
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