expression and Rev–CRM1-dependent nuclear export of intron-containing HIV-1 RNA (icRNA) activates host sensing mechanisms and type I interferon (IFN-I)-dependent pro-inflammatory responses via MAVS in productively infected macrophages. Additionally, the ability of cells to distinguish intron-containing HIV-1 RNA from self mRNA is dependent on the localization of non-self HIV icRNA at peripheral membrane sites. Interestingly, HIV-1 infection-induced activation of macrophages, in turn, leads to upregulation of inhibitory receptor (IR) expression and reduced effector function of co-cultured autologous CD4+ and CD8+ T cells, and the phenotype is suppressed upon antagonism of IFN-I. These findings suggest that novel therapeutic strategies that suppress viral icRNA expression and IFN-I signaling cascades in tissue macrophages might have immunologic and therapeutic benefit in HIV-1 infected individuals on cART.
Перевести это во что-то понятное для масс нужно время, может как-то потом подумаю.