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The viral host response is the process by which a host interacts with and responds to viruses that it encounters. It includes various mechanisms, such as immune mechanisms that are elicited in an attempt to eliminate the virus or halt its growth.
TRIM23 is identified as an essential regulator of virus-induced autophagy that mediates restriction to several RNA and DNA viruses. K27-mediated ubiquitylation activates TRIM23 GTPase activity, triggering its relocalization and selective autophagy.
During acute HIV type 1 infection, a subset of γδ T cells that express Δ42PD1 are shown to home to the gut, where they activate innate immunity and inflammation through direct interaction of Δ42PD1 with Toll-like receptor 4. Blockade of this pathway reduces mucosal damage.
Flaviviruses stimulate cross-reactive immune responses that may reduce or exacerbate manifestations of subsequent flavivirus infection. Recent work demonstrates that cross-reactive T cells protect against Zika in HLA transgenic mice, a key step in the development of safe and effective vaccines.
The quest to improve influenza vaccines is aided by research into the immune response that they generate. Two recent studies have focused their attention on the specificities of antibodies induced after vaccination with conventional inactivated influenza vaccines.