Protection Against Marburg Virus Using a Recombinant VSV-Vaccine Depends on T and B Cell Activation.
Andrea Marzi, Andrea R Menicucci, Flora Engelmann, Julie Callison, Eva J Horne, Friederike Feldmann, Allen Jankeel, Heinz Feldmann, Ilhem Messaoudi
Author Information
Andrea Marzi: Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, United States.
Andrea R Menicucci: Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA, United States.
Flora Engelmann: Department of Cell Molecular Biology, Northwestern University, Evanston, IL, United States.
Julie Callison: Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, United States.
Eva J Horne: Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, United States.
Friederike Feldmann: Rocky Mountain Veterinary Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, United States.
Allen Jankeel: Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA, United States.
Heinz Feldmann: Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, United States.
Ilhem Messaoudi: Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA, United States.
Marburg virus (MARV) is the causative agent of hemorrhagic fever outbreaks with high case fatality rates. Closely related to Ebola virus, MARV is a filamentous virus with a negative-sense, single-stranded RNA genome. Although extensive studies on filovirus countermeasures have been conducted, there are no licensed treatments against MARV infections. An experimental vaccine based on the recombinant vesicular stomatitis virus (VSV) expressing the MARV-Musoke glycoprotein demonstrated complete protection when a single dose was administered 28 days and up to 14 months prior to MARV challenge. Here, we analyzed the protective efficacy of an updated vaccine expressing the MARV-Angola glycoprotein (VSV-MARV). A single dose of VSV-MARV given 5 weeks before challenge provided uniform protection with no detectable viremia. The vaccine induced B and T cell proliferation and, importantly, antigen-specific IgG production. Transcriptomic signatures confirm these findings and suggest innate immunity engendered by VSV-MARV may direct the development of protective humoral immunity.
