ArticleJournal of virology2013
Identification of virulence determinants within the L genomic segment of the pichinde arenavirus.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Identification of Factors Contributing to Pathogenic Variability Among Lassa Virus Strains Using the Guinea Pig Model and Reverse Genetics.The Journal of infectious diseases · 2025Article
- Characterization of bi-segmented and tri-segmented recombinant Pichinde virus particles.Journal of virology · 2024Article
- Unraveling factors responsible for pathogenic differences in Lassa virus strains.bioRxiv : the preprint server for biology · 2024Article
- Identifying the genetic basis of viral spillover using Lassa virus as a test case.Royal Society open science · 2023Article
- Combating Lassa Fever in West African Sub-Region: Progress, Challenges, and Future Perspectives.Viruses · 2023Review
- Virulent infection of outbred Hartley guinea pigs with recombinant Pichinde virus as a surrogate small animal model for human Lassa fever.Virulence · 2020Article
- Pichinde Virus Infection of Outbred Hartley Guinea Pigs as a Surrogate Animal Model for Human Lassa Fever: Histopathological and Immunohistochemical Analyses.Pathogens (Basel, Switzerland) · 2020Article
- Article
- Xapuri virus, a novel mammarenavirus: natural reassortment and increased diversity between New World viruses.Emerging microbes & infections · 2018Article
- Ancient Evolution of Mammarenaviruses: Adaptation via Changes in the L Protein and No Evidence for Host-Virus Codivergence.Genome biology and evolution · 2018Article
- The S Genome Segment Is Sufficient to Maintain Pathogenicity in Intra-Clade Lassa Virus Reassortants in a Guinea Pig Model.Frontiers in cellular and infection microbiology · 2018Article
- Characterization of the Glycoprotein Stable Signal Peptide in Mediating Pichinde Virus Replication and Virulence.Journal of virology · 2016Article
- A Novel Live Pichinde Virus-Based Vaccine Vector Induces Enhanced Humoral and Cellular Immunity after a Booster Dose.Journal of virology · 2015Article
- In vitro and in vivo characterizations of pichinde viral nucleoprotein exoribonuclease functions.Journal of virology · 2015Article
- Human hemorrhagic Fever causing arenaviruses: molecular mechanisms contributing to virus virulence and disease pathogenesis.Pathogens (Basel, Switzerland) · 2015Review
- The Z proteins of pathogenic but not nonpathogenic arenaviruses inhibit RIG-I-like receptor-dependent interferon production.Journal of virology · 2015Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Several arenaviruses are responsible for causing viral hemorrhagic fevers (VHF) in humans. Lassa virus (LASV), the causative agent of Lassa fever, is a biosafety level 4 (BSL4) pathogen that requires handling in BSL4 facilities. In contrast, the Pichinde arenavirus (PICV) is a BSL2 pathogen that can cause hemorrhagic fever-like symptoms in guinea pigs that resemble those observed in human Lassa fever. Comparative sequence analysis of the avirulent P2 strain of PICV and the virulent P18 strain shows a high degree of sequence homology in the bisegmented genome between the two strains despite the polarized clinical outcomes noted for the infected animals. Using reverse genetics systems that we have recently developed, we have mapped the sequence changes in the large (L) segment of the PICV genome that are responsible for the heightened virulence phenotype of the P18 strain. By monitoring the degree of disease severity and lethality caused by the different mutant viruses, we have identified specific residues located within the viral L polymerase gene encoded on the L segment essential for mediating disease pathogenesis. Through quantitative reverse transcription-PCR (RT-PCR) analysis, we have confirmed that the same set of residues is responsible for the increased viral replicative potential of the P18 strain and its heightened disease severity in vivo. Our laboratory findings serve to reinforce field observations that a high level of viremia often correlates with severe disease outcomes in LASV-infected patients.
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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.