ArticleJournal of virology2019
Analysis of a Subacute Sclerosing Panencephalitis Genotype B3 Virus from the 2009-2010 South African Measles Epidemic Shows That Hyperfusogenic F Proteins Contribute to Measles Virus Infection in the Brain.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Structural and mechanistic basis for antibody neutralization of the measles fusion protein.Nature communications · 2026Article
- Stabilized Full-Length Measles Fusion Protein Elicits Potent Immunity and Protection In Vivo.bioRxiv : the preprint server for biology · 2025Article
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- Structural and Mechanistic Basis for Antibody Neutralization of the Measles Fusion Protein.bioRxiv : the preprint server for biology · 2025Article
- Amino acid changes accumulated in the fusion protein allow neuropathogenic measles viruses to use a broad repertoire of host factors for cell fusion triggering.Journal of virology · 2025Article
- The measles virus matrix F50S mutation from a lethal case of subacute sclerosing panencephalitis promotes receptor-independent neuronal spread.Journal of virology · 2025Article
- A neutralizing antibody prevents postfusion transition of measles virus fusion protein.Science (New York, N.Y.) · 2024Article
- Functional properties of measles virus proteins derived from a subacute sclerosing panencephalitis patient who received repeated remdesivir treatments.Journal of virology · 2024Article
- Antiviral activity of nitazoxanide againstJournal of virus eradication · 2023Article
- Brain tropism acquisition: The spatial dynamics and evolution of a measles virus collective infectious unit that drove lethal subacute sclerosing panencephalitis.PLoS pathogens · 2023Article
- Suppression of viral RNA polymerase activity is necessary for persistent infection during the transformation of measles virus into SSPE virus.PLoS pathogens · 2023Article
- Interaction of the Hemagglutinin Stalk Region with Cell Adhesion Molecule (CADM) 1 and CADM2 Mediates the Spread between Neurons and Neuropathogenicity of Measles Virus with a Hyperfusogenic Fusion Protein.Journal of virology · 2023Article
- Host-Pathogen Interactions Influencing Zoonotic Spillover Potential and Transmission in Humans.Viruses · 2023Review
- Collective fusion activity determines neurotropism of an en bloc transmitted enveloped virus.Science advances · 2023Article
- Article
- Viral-induced neuroinflammation: Different mechanisms converging to similar exacerbated glial responses.Frontiers in neuroscience · 2023Review
- Article
- Short-Stalk Isoforms of CADM1 and CADM2 Trigger Neuropathogenic Measles Virus-Mediated Membrane Fusion by Interacting with the Viral Hemagglutinin.Journal of virology · 2022Article
- Options in the Treatment of Subacute Sclerosing Panencephalitis: Implications for Low Resource Areas.Current treatment options in neurology · 2022Review
- Human parainfluenza virus evolution during lung infection of immunocompromised individuals promotes viral persistence.The Journal of clinical investigation · 2021Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 5 countries.
Funding
Abstract
During a measles virus (MeV) epidemic in 2009 in South Africa, measles inclusion body encephalitis (MIBE) was identified in several HIV-infected patients. Years later, children are presenting with subacute sclerosing panencephalitis (SSPE). To investigate the features of established MeV neuronal infections, viral sequences were analyzed from brain tissue samples of a single SSPE case and compared with MIBE sequences previously obtained from patients infected during the same epidemic. Both the SSPE and the MIBE viruses had amino acid substitutions in the ectodomain of the F protein that confer enhanced fusion properties. Functional analysis of the fusion complexes confirmed that both MIBE and SSPE F protein mutations promoted fusion with less dependence on interaction by the viral receptor-binding protein with known MeV receptors. While the SSPE F required the presence of a homotypic attachment protein, MeV H, in order to fuse, MIBE F did not. Both F proteins had decreased thermal stability compared to that of the corresponding wild-type F protein. Finally, recombinant viruses expressing MIBE or SSPE fusion complexes spread in the absence of known MeV receptors, with MIBE F-bearing viruses causing large syncytia in these cells. Our results suggest that alterations to the MeV fusion complex that promote fusion and cell-to-cell spread in the absence of known MeV receptors is a key property for infection of the brain.
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