Skip to content
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
mAb therapy controls CNS-resident lyssavirus infection via a CD4 T cell-dependent mechanism
EMBO Molecular Medicine, Volume 15, No. 10, Article e16394, Year 2023
Notification
URL copied to clipboard!
Description
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 mortality, and a CD4 T cell-dependent adaptive immune response is required for successful control of infection. F11 significantly changes the spectrum of leukocyte populations in the brain, and the FcRγ-binding function of F11 contributes to therapeutic efficacy. Thus, mAb therapy can drive potent neutralization-independent T cell-mediated effects, even against an established CNS infection by a lethal neurotropic virus. © 2023 Commonwealth of Australia and The Authors. Published under the terms of the CC BY 4.0 license. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.
Authors & Co-Authors
Coggins, Si'Ana Ana A.
United States, Bethesda
Uniformed Services University of the Health Sciences
United States, Rockville
Hjf
Yan, Lianying
United States, Bethesda
Uniformed Services University of the Health Sciences
Ahmed, Anwar E.
United States, Bethesda
Uniformed Services University of the Health Sciences
Vu, Bang K.
United States, Bethesda
Uniformed Services University of the Health Sciences
Smith, Ina L.
Australia, Canberra
Commonwealth Scientific and Industrial Research Organisation
Markotter, Wanda
South Africa, Pretoria
University of Pretoria
South Africa, Johannesburg
National Health Laboratory Service
Weir, Dawn L.
United States, Bethesda
Uniformed Services University of the Health Sciences
Laing, Eric D.
United States, Bethesda
Uniformed Services University of the Health Sciences
Broder, Christopher C.
United States, Bethesda
Uniformed Services University of the Health Sciences
Schaefer, Brian C.
United States, Bethesda
Uniformed Services University of the Health Sciences
Statistics
Citations: 2
Authors: 10
Affiliations: 5
Identifiers
Doi:
10.15252/emmm.202216394
ISSN:
17574676