tailieunhanh - Báo cáo y học: "Chemokine control of HIV-1 infection: Beyond a binding competition"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: Chemokine control of HIV-1 infection: Beyond a binding competition. | Wu Retrovirology 2010 7 86 http content 7 1 86 RETR0VIR0L0GY VIEWPOINTS Open Access Chemokine control of HIV-1 infection Beyond a binding competition Yuntao Wu Abstract A recent paper by Cameron et al. demonstrated that certain chemokines such as CCL19 activate cofilin and actin dynamics promoting HIV nuclear localization and integration into resting CD4 T cells. Apparently these chomokines synergize with the viral envelope protein triggering cofilin and actin dynamics necessary for the establishment of viral latency. This study opens a new avenue for understanding chemokine interaction with HIV. Traditionally chemokine control of HIV infection focuses on competitive binding and down-modulation of the corecptors particularly CCR5. This new study suggests that a diverse group of chemokines may also affect HIV infection through synergistic or antagonistic interaction with the viral coreceptor signaling pathways. Introduction Despite the success of highly active antiretroviral therapy HAART in inhibiting HIV replication viral latency and low-level replication permit viral persistence 1 . HIV can be stably maintained in a variety of cells such as macrophages and resting CD4 T cells. In particular the long-lived resting memory CD4 T cells have been shown to be a major viral reservoir. Nevertheless little is known about the establishment of HIV latency in resting CD4 T cells in the body. Previous studies have suggested that HIV infection of resting CD4 T cells in vitro can lead to viral DNA synthesis although at a slower speed 2 3 . The virus is also capable of mediating nuclear migration with the help of the viral envelope protein that triggers signal transduction to promote cofilin and actin activities 4 5 viral DNA integration did not occur or was observed at an extremely low level. Because non-inte-grated viral DNA is not stable the establishment of a long-term reservoir in resting T cells requires stable integration that normally does not occur

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