Your browser doesn't support javascript.
loading
IL-1ß and IL-18 inhibition of HIV-1 replication in Jurkat cells and PBMCs.
Wang, Xue; Mbondji-Wonje, Christelle; Zhao, Jiangqin; Hewlett, Indira.
Afiliación
  • Wang X; Lab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA. Electronic address: xue.wang@fda.hhs.gov.
  • Mbondji-Wonje C; Lab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA.
  • Zhao J; Lab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA.
  • Hewlett I; Lab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA. Electronic address: indira.hewlett@fda.hhs.gov.
Biochem Biophys Res Commun ; 473(4): 926-930, 2016 05 13.
Article en En | MEDLINE | ID: mdl-27049306
HIV-1 infection-induced apoptosis is able to ensure viral replication. The death of some CD4+ T cells residing in lymphoid tissues can be induced by HIV-1 infection through caspase-1 driven pyroptosis with release of cytokine of IL-1ß and IL-18. It is not well known whether IL-1ß and IL-18 affect HIV-1 replication in lymphocytic cells. Using susceptible lymphocytic cell line, Jurkat cells, and primary peripheral blood mononuclear cells (PBMCs), we studied the effects of IL-1ß and IL-18 on HIV-1 replication. We found that treatment with exogenous IL-1ß protein (rIL-1ß) and IL-18 protein (rIL-18), or expression of IL-1ß and IL-18 significantly reduced HIV-1 replication. HIV-1 infection enhanced caspase-3 expression and its activation, and had no effects on caspase-1 activity. Treatment with rIL-1ß and rIL-18 dramatically lowered caspase-3 activity. IL-1ß and IL-18 also played roles in diminishing reactivation of viral replication from latency in J1.1 cells. These results indicate that IL-1ß and IL-18 are able to inhibit HIV-1 replication, and their effects may be due to signaling through apoptosis involved in inactivation of caspase-3 activity.
Asunto(s)
Palabras clave

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Replicación Viral / Leucocitos Mononucleares / VIH-1 / Interleucina-18 / Interleucina-1beta Límite: Humans Idioma: En Revista: Biochem Biophys Res Commun Año: 2016 Tipo del documento: Article

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Replicación Viral / Leucocitos Mononucleares / VIH-1 / Interleucina-18 / Interleucina-1beta Límite: Humans Idioma: En Revista: Biochem Biophys Res Commun Año: 2016 Tipo del documento: Article