ArticleViruses2020
Pathogenetic Potential Relating to Metabolic Activity in a Mouse Model of Infection with the Chikungunya Virus East/Central/South African Genotype.
Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Advances and perspectives for animal models of chikungunya virus infection.Biosafety and health · 2025Review
- Heterozygous interferon signaling deficient mice as animal models for Chikungunya virus infection in the heart.Scientific reports · 2025Article
- RT-RPA as a dual tool for detection and phylogenetic analysis of epidemic arthritogenic alphaviruses.Scientific reports · 2024Article
- Article
- Review
- Cardiomyopathy and Death Following Chikungunya Infection: An Increasingly Common Outcome.Tropical medicine and infectious disease · 2021Review
- Phylogenetic Characterization of Arboviruses in Patients Suffering from Acute Fever in Rondônia, Brazil.Viruses · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemics of the Chikungunya virus (CHIKV) from 2004 onwards were caused by the East/Central/South African (ECSA) genotype. However, the pathogenesis of the genotype infection has not been fully explained. In this study, we examined the pathogenic potential of CHIKV ECSA genotype M-30 (M-30) by comparing it with that of African genotype S-27 (S-27) in mice. Following low titer infections in type-I IFN receptor KO (A129) mice, we found that the M-30 infection caused high and acute fatality compared with the S-27 infection. M-30-infected A129 mice showed higher viral loads in their central nervous systems and peripheral organs, and increased levels of IFN-γ responses in their brains. Interestingly, M-30-infected mice did not show the hypophagia and reductions in weight which were observed in S-27-infected mice. Our observations provide a novel explanation of the pathogenic mechanisms attributed to virus proliferation, anti-type-II IFN response and metabolic activity in the CHIKV ECSA virus in mice.
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Registered trials
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