ArticleNature communications2023
Two point mutations in protocadherin-1 disrupt hantavirus recognition and afford protection against lethal infection.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- Article
- Omics Approaches in Hantavirus Research: Current Advances, Challenges, and Future Perspectives.Biotech (Basel (Switzerland)) · 2026Review
- Potential Effects of Bee Products Against Hantavirus Infection: Potential Mechanisms of Action and Future Directions.Life (Basel, Switzerland) · 2026Review
- Differential tropisms of old and new world hantaviruses influence virulence and developing host-directed antiviral candidates.PLoS pathogens · 2025Article
- Decoding the blueprint of receptor binding by filoviruses through large-scale binding assays and machine learning.Cell host & microbe · 2025Article
- Viral entry as a low barrier to zoonosis.Nature microbiology · 2025Article
- Review
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Andes virus (ANDV) and Sin Nombre virus (SNV) are the etiologic agents of severe hantavirus cardiopulmonary syndrome (HCPS) in the Americas for which no FDA-approved countermeasures are available. Protocadherin-1 (PCDH1), a cadherin-superfamily protein recently identified as a critical host factor for ANDV and SNV, represents a new antiviral target; however, its precise role remains to be elucidated. Here, we use computational and experimental approaches to delineate the binding surface of the hantavirus glycoprotein complex on PCDH1's first extracellular cadherin repeat domain. Strikingly, a single amino acid residue in this PCDH1 surface influences the host species-specificity of SNV glycoprotein-PCDH1 interaction and cell entry. Mutation of this and a neighboring residue substantially protects Syrian hamsters from pulmonary disease and death caused by ANDV. We conclude that PCDH1 is a bona fide entry receptor for ANDV and SNV whose direct interaction with hantavirus glycoproteins could be targeted to develop new interventions against HCPS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.