TLR7 Controls VSV Replication in CD169⁺ SCS Macrophages and Associated Viral Neuroinvasion.

ABSTRACT: Vesicular stomatitis virus (VSV) is an insect-transmitted rhabdovirus that is neurovirulent in mice. Upon peripheral VSV infection, CD169⁺ subcapsular sinus (SCS) macrophages capture VSV in the lymph, support viral replication, and prevent CNS neuroinvasion. To date, the precise mechanisms controlling VSV infection in SCS macrophages remain incompletely understood. Here, we show that Toll-like receptor-7 (TLR7), the main sensing receptor for VSV, is central in controlling lymph-borne VSV infection. Following VSV skin infection, TLR7^-/- mice display significantly less VSV titers in the draining lymph nodes (dLN) and viral replication is attenuated in SCS macrophages. In contrast to effects of TLR7 in impeding VSV replication in the dLN, TLR7^-/- mice present

SUBMITTER: Solmaz G 

PROVIDER: S-EPMC6428728 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature