Differential innate immune activation by wild-type and NSs-deficient RVFV strains in human blood monocytes.

ABSTRACT: Rift Valley fever virus (RVFV) is a Phlebovirus causing febrile and haemorrhagic illness in ruminants and humans. The viral protein NSs is a major virulence factor that suppresses the IFN-β response in various hosts. Hence, RVFV variants lacking functional NSs, such as Clone 13, are highly attenuated. It is speculated that from the sites of infection, the virus disseminates to the target organs via the bloodstream. We hypothesized that primary infection of circulating immune cells and their response to infection are critical factors determining systemic RVFV spread and pathogenesis. Human PBMC from healthy blood donors were exposed to both wild-type (WT) RVFV and Clone 13 strains. Flow cytometric analysis revealed that monocytes expressing LRP1, a known RVFV receptor, are target cel

SUBMITTER: Nair N 

PROVIDER: S-EPMC12805856 | biostudies-literature | 2026 Dec

REPOSITORIES: biostudies-literature