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| The latent HIV-1 escapes host immune responses, and is insensitive to antiretroviral therapy, which is the major barrier for eradication of the virus from infected patients. One strategy to eradicate the reservoirs of HIV-1 is to reactivate the provirus. Reactivation of latent HIV-1 requires the stimulation of several signaling pathways, including ERK and NF-κB pathways which are also involved in DC-SIGN expression. DC-SIGN is important for the primary HIV-1 infection and the further dissemination. It is unclear whether DC-SIGN expression and latent HIV-1 reactivation interact with each other in DCs and how HIV-1 infection and latency will be effected by the interaction. We hypothesize that DC-SIGN expression and HIV-1 reactivation share the ERK and NF-κB signaling pathways in DCs. In line with this hypothesis, the signals stimulating DC-SIGN expression in DCs may be hijacked by latent HIV-1, promoting the virus replication and transmission. Meanwhile, when latent HIV-1 is reactivated, DC-SIGN expression will be also up regulated to help HIV-1 diffusing and escaping attack by HAART and immune response. The mutual benefit between DC-SIGN expression and HIV-1 reactivation may bring much trouble to clearance of latent HIV-1.????? |
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| Keywords:Internal medicine; DC-SIGN; latency; HIV-1; signaling pathways; dendritic cells |
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