ArticleJournal of virology2011
Junin virus infects mouse cells and induces innate immune responses.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 50 citations in OpenAlex.
- Going wild: prioritizing experimental models of rodent-borne viruses to decode zoonotic spillover and pandemic risk.Journal of virology · 2026Review
- Article
- A dsRNA-binding mutant reveals only a minor role of exonuclease activity in interferon antagonism by the arenavirus nucleoprotein.PLoS pathogens · 2023Article
- Review
- Signal-regulatory protein alpha is an anti-viral entry factor targeting viruses using endocytic pathways.PLoS pathogens · 2021Article
- The board is set, the pieces are moving: Modulation of New World arenavirus entry by host proteins.PLoS pathogens · 2021Review
- Review
- Glycoprotein N-linked glycans play a critical role in arenavirus pathogenicity.PLoS pathogens · 2021Article
- RIG-I and MDA5 Protect Mice From Pichinde Virus Infection by Controlling Viral Replication and Regulating Immune Responses to the Infection.Frontiers in immunology · 2021Article
- CACNA1S haploinsufficiency confers resistance to New World arenavirus infection.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Distinct Molecular Mechanisms of Host Immune Response Modulation by Arenavirus NP and Z Proteins.Viruses · 2020Review
- Brothers in Arms: Structure, Assembly and Function ofViruses · 2020Review
- Lassa Virus, but Not Highly Pathogenic New World Arenaviruses, Restricts Immunostimulatory Double-Stranded RNA Accumulation during Infection.Journal of virology · 2020Article
- Guinea Pig Transferrin Receptor 1 Mediates Cellular Entry of Junín Virus and Other Pathogenic New World Arenaviruses.Journal of virology · 2020Article
- Comparison of the Innate Immune Responses to Pathogenic and Nonpathogenic Clade B New World Arenaviruses.Journal of virology · 2019Article
- Junín Virus Promotes Autophagy To Facilitate the Virus Life Cycle.Journal of virology · 2019Article
- TRIM2, a novel member of the antiviral family, limits New World arenavirus entry.PLoS biology · 2019Article
- Integrated Functional Analysis of the Nuclear Proteome of Classically and Alternatively Activated Macrophages.Mediators of inflammation · 2019Article
- Hemorrhagic Fever-Causing Arenaviruses: Lethal Pathogens and Potent Immune Suppressors.Frontiers in immunology · 2019Review
- Involvement of Pro-Inflammatory Macrophages in Liver Pathology of Pirital Virus-Infected Syrian Hamsters.Viruses · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Junín virus is the causative agent for Argentine hemorrhagic fever, and its natural host is the New World rodent Calomys musculinus. The virus is transmitted to humans by aerosolization, and it is believed that many of the clinical symptoms are caused by cytokines produced by sentinel cells of the immune system. Here we used the Junín virus vaccine strain Candid 1 to determine whether mouse cells could be used to study virus entry and antiviral innate immune responses. We show that Candid 1 can infect and propagate in different mouse-derived cell lines through a low-pH-dependent, transferrin receptor 1-independent mechanism, suggesting that there is a second entry receptor. In addition, Candid 1 induced expression of the antiviral cytokines tumor necrosis factor alpha and beta interferon in macrophages, and this induction was independent of viral replication. Using Candid 1, as well as virus-like particles bearing the viral glycoprotein, to infect different primary cells and established macrophage cell lines with deletions in the Toll-like receptor (TLR) pathway, we show that TLR2 is a cellular sensor of both the Parodi and Candid 1 viral glycoproteins. Because Junín virus is highly lethal in humans, the use of an experimentally tractable model system, such as the mouse, could provide a better understanding of the antiviral innate cellular responses to Junín virus and the role of these responses in pathogenesis.
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.