6 research outputs found
Serological evidence of zoonotic filovirus exposure among bushmeat hunters in Guinea
Human Ebola virus (EBOV) outbreaks caused by persistent EBOV infection raises questions on the role of zoonotic spillover in filovirus epidemiology. To characterise filovirus zoonotic exposure, we collected cross-sectional serum samples from bushmeat hunters (n = 498) in Macenta Prefecture Guinea, adjacent to the index site of the 2013 EBOV-Makona spillover event. We identified distinct immune signatures (20/498, 4.0%) to multiple EBOV antigens (GP, NP, VP40) using stepwise ELISA and Western blot analysis and, live EBOV neutralisation (5/20; 25%). Using comparative serological data from PCR-confirmed survivors of the 2013-2016 EBOV outbreak, we demonstrated that most signatures (15/20) were not plausibly explained by prior EBOV-Makona exposure. Subsequent data-driven modelling of EBOV immunological outcomes to remote-sensing environmental data also revealed consistent associations with intact closed canopy forest. Together our findings suggest exposure to other closely related filoviruses prior to the 2013-2016 West Africa epidemic and highlight future surveillance priorities
mAb therapy controls CNS-resident lyssavirus infection via a CD4 T cell-dependent mechanism
DATA AVAILABILITY : This study includes no data deposited in external repositories.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 antilyssavirus
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 FcRc-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.https://www.embopress.org/journal/17574684am2024Medical VirologySDG-03:Good heatlh and well-bein
The lncRNA lincNMR regulates nucleotide metabolism via a YBX1 - RRM2 axis in cancer
Despite some well-characterized functions in cancer, the impact of most long non-coding RNAs remains unknown. Here, the authors discover the lncRNA lincNMR which is upregulated in cancer and drives cell proliferation by interacting with YBX1 and controlling nucleotide metabolism
Evaluating SARS-CoV-2 Saliva and Dried Blood Spot Surveillance Strategies in a Congregate Population
The optimal approach to COVID-19 surveillance in congregate populations remains unclear. Our study at the US Naval Academy in Annapolis, Maryland, USA, assessed the concordance of antibody prevalence in longitudinally collected dried blood spots and saliva in a setting of frequent PCR-based testing. Our findings highlight the utility of salivary-based surveillance
Serological evidence of zoonotic filovirus exposure among bushmeat hunters in Guinea
Human Ebola virus (EBOV) outbreaks caused by persistent EBOV infection raises questions on the role of zoonotic spillover in filovirus epidemiology. To characterise filovirus zoonotic exposure, we collected cross-sectional serum samples from bushmeat hunters (n = 498) in Macenta Prefecture Guinea, adjacent to the index site of the 2013 EBOV-Makona spillover event. We identified distinct immune signatures (20/498, 4.0%) to multiple EBOV antigens (GP, NP, VP40) using stepwise ELISA and Western blot analysis and, live EBOV neutralisation (5/20; 25%). Using comparative serological data from PCR-confirmed survivors of the 2013-2016 EBOV outbreak, we demonstrated that most signatures (15/20) were not plausibly explained by prior EBOV-Makona exposure. Subsequent data-driven modelling of EBOV immunological outcomes to remote-sensing environmental data also revealed consistent associations with intact closed canopy forest. Together our findings suggest exposure to other closely related filoviruses prior to the 2013-2016 West Africa epidemic and highlight future surveillance priorities