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Published on: January 9, 2019
Measles Virus Fusion Protein: Structure, Function and Inhibition
Philippe Plattet1, Lisa Alves2, Michael Herren3,4
1Division of Experimental and Clinical Research, , Vetsuisse Faculty, University of Bern, Bremgartenstrasse 109a, Bern 3001, Switzerland. philippe.plattet@vetsuisse.unibe.ch.
Measles virus (MeV) causes deadly measles outbreaks. Antiviral drugs targeting viral fusion offer a promising strategy to complement vaccines and prevent MeV infections.
Area of Science:
- Virology
- Immunology
- Drug Discovery
Background:
- Measles virus (MeV), a Paramyxoviridae family member, causes measles and approximately 120,000 deaths annually.
- Vaccination prevents MeV and canine distemper virus (CDV) diseases, but suboptimal delivery leads to outbreaks.
- Antiviral post-exposure prophylaxis is a novel strategy to address herd immunity gaps.
Purpose of the Study:
- To explore antiviral strategies against measles virus (MeV).
- To investigate the role of morbillivirus glycoproteins in viral entry and infection.
- To identify potential therapeutic targets for controlling MeV-induced membrane fusion.
Main Methods:
- Review of current research on morbillivirus-associated membrane fusion.
- Analysis of molecular mechanisms of viral entry and infection.
- Evaluation of existing anti-membrane fusion drug development approaches and drug resistance.
Main Results:
- Morbillivirus glycoprotein-induced membrane fusion is critical for viral entry, cell pathology, and disease outcome.
- Molecular understanding of morbillivirus fusion has advanced, enabling potential control through inhibitory molecules.
- Combined therapies are likely necessary due to drug resistance mechanisms.
Conclusions:
- Targeting morbillivirus membrane fusion with inhibitory molecules presents a feasible therapeutic strategy.
- Discovery of small-molecule compounds inhibiting fusion and/or attachment proteins is crucial.
- These discoveries may lead to realistic therapeutic options for measles and related diseases.
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