Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human Parainfluenza Virus Fusion Complex Glycoproteins Imaged In Action On Authentic Viral Surfaces

ABSTRACT:

SUBMITTER: Tara Charlie Marcink

PROVIDER: EMPIAR-10476 | biostudies-other |

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Publications

Human parainfluenza virus fusion complex glycoproteins imaged in action on authentic viral surfaces.

Marcink Tara C TC Wang Tong T des Georges Amedee A Porotto Matteo M Moscona Anne A

PLoS pathogens 20200921 9

Infection by human parainfluenza viruses (HPIVs) causes widespread lower respiratory diseases, including croup, bronchiolitis, and pneumonia, and there are no vaccines or effective treatments for these viruses. HPIV3 is a member of the Respirovirus species of the Paramyxoviridae family. These viruses are pleomorphic, enveloped viruses with genomes composed of single-stranded negative-sense RNA. During viral entry, the first step of infection, the viral fusion complex, comprised of the receptor-b ...[more]

PMID: 32956394

Similar Datasets

Human parainfluenza virus fusion complex glycoproteins imaged in action on authentic viral surfaces.

Project description: Not available

| S-EPMC7529294 | biostudies-literature

Molecular features of the measles virus viral fusion complex that favor infection and spread in the brain [human]

Project description:A measles virus (MeV) isolate bearing a single amino acid change in the fusion protein (F) -- L454W -- was identified in two patients who died of MeV central nervous system (CNS) infection. We analyzed whether this mutation confers an advantage over wild type virus in the CNS, thereby contributing to disease in these patients. Using murine ex vivo organotypic brain cultures and human induced pluripotent stem cell-derived brain organoids, we show that specific CNS adaptive mutations in F result in augmented spread of virus ex vivo and that this is associated with an enhanced innate immune response. The spread of virus in brain organoids is blocked by an inhibitory peptide that targets F, confirming that dissemination in the brain tissue is attributable to F. A single mutation in MeV F thus alters the fusion complex to render the virus more neuropathogenic, allowing it to propagate in the face of the innate immune response.

2020-08-08 | GSE155884 | GEO

Subnanometer structure of an enveloped virus fusion complex on viral surface reveals new entry mechanisms.

Project description: Not available

| S-EPMC9917000 | biostudies-literature

Hijacking the Fusion Complex of Human Parainfluenza Virus as an Antiviral Strategy.

Project description: Not available

| S-EPMC7018645 | biostudies-literature

Molecular Features of the Measles Virus Viral Fusion Complex That Favor Infection and Spread in the Brain.

Project description: Not available

| S-EPMC8263006 | biostudies-literature

Rubella virus: first calcium-requiring viral fusion protein.

Project description: Not available