MAb therapy controls CNS-resident lyssavirus infection via a CD4 T cell-dependent mechanism.

ABSTRACT: Infections with rabies virus (RABV) and related lyssaviruses are uniformly fatal once virus accesses the central nervous system (CNS) and causes disease signs. Current immunotherapies are thus focused on the early, pre-symptomatic stage of disease, with the goal of peripheral neutralization of virus to prevent CNS infection. Here, we evaluated the therapeutic efficacy of F11, an anti-lyssavirus human monoclonal antibody (mAb), on established lyssavirus infections. We show that a single dose of F11 limits viral load in the brain and reverses disease signs following infection with a lethal dose of lyssavirus, even when administered after initiation of robust virus replication in the CNS. Importantly, we found that F11-dependent neutralization is not sufficient to protect animals from mortali

SUBMITTER: Mastraccio KE 

PROVIDER: S-EPMC10565638 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature