ArticleJournal of biomedical science2024
Attenuation of neurovirulence of chikungunya virus by a single amino acid mutation in viral E2 envelope protein.
Article in Journal of biomedical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- The residue 86 of the Getah virus E2 glycoprotein mediates both glycosaminoglycan- and LDLR-dependent infection.PLoS pathogens · 2026Article
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- Eupatorium perfoliatum Counteracts TNF-α Mediated Pathogenesis in Chikungunya Virus Infection.Applied biochemistry and biotechnology · 2026Article
- Advances and perspectives for animal models of chikungunya virus infection.Biosafety and health · 2025Review
- The impact of variations in the chikungunya genome on the clinical manifestations and transmission of the disease.Journal of family medicine and primary care · 2025Review
- The Construction and Characterization of an Infectious Clone of the Asian Genotype Chikungunya Virus from Yunnan, China.Tropical medicine and infectious disease · 2025Article
- Global Transmission and Evolution of Chikungunya Virus: Origins, Adaptive Mutations, and Intercontinental Spread of the Three Genotypes.Transboundary and emerging diseases · 2025Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundChikungunya virus (CHIKV) has reemerged as a major public health concern, causing chikungunya fever with increasing cases and neurological complications.
methodsIn the present study, we investigated a low-passage human isolate of the East/ Central/South African (ECSA) lineage of CHIKV strain LK(EH)CH6708, which exhibited a mix of small and large viral plaques. The small and large plaque variants were isolated and designated as CHIKV-SP and CHIKV-BP, respectively. CHIKV-SP and CHIKV-BP were characterized in vitro and in vivo to compare their virus production and virulence. Additionally, whole viral genome analysis and reverse genetics were employed to identify genomic virulence factors.
resultsCHIKV-SP demonstrated lower virus production in mammalian cells and attenuated virulence in a murine model. On the other hand, CHIKV-BP induced higher pro-inflammatory cytokine levels, compromised the integrity of the blood-brain barrier, and led to astrocyte infection in mouse brains. Furthermore, the CHIKV-SP variant had limited transmission potential in Aedes albopictus mosquitoes, likely due to restricted dissemination. Whole viral genome analysis revealed multiple genetic mutations in the CHIKV-SP variant, including a Glycine (G) to Arginine (R) mutation at position 55 in the viral E2 glycoprotein. Reverse genetics experiments confirmed that the E2-G55R mutation alone was sufficient to reduce virus production in vitro and virulence in mice.
conclusionsThese findings highlight the attenuating effects of the E2-G55R mutation on CHIKV pathogenicity and neurovirulence and emphasize the importance of monitoring this mutation in natural infections.
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