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Viral Infections and Vectors / Virology and Viral Diseases / Mosquito Borne Diseases and Control · Journal article
PLOS Neglected Tropical Diseases · August 3, 2026
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This is a descriptive genomic epidemiology study characterizing 58 years of Chandipura virus evolution across 23 genomes from India, Senegal, Kenya, and Nigeria. The analysis reveals region-specific lineage divergence, low overall genomic variability, purifying selection across most coding regions, and adaptive sites in structural proteins that overlap predicted B-cell epitopes, supporting the need for future surveillance and vaccine development. The work provides foundational genomic context but does not test clinical hypotheses or measure intervention efficacy.
Retrospective genomic epidemiology and phylogenetic analysis. Five human Chandipura virus isolates from India; 17 sandfly-derived isolates from Senegal and Kenya; one hedgehog-derived isolate from Nigeria, collected over 1966–2024.. n = 23. India (human encephalitis reports, sandfly distribution); Senegal and Kenya (sandfly-derived isolates); Nigeria (hedgehog-derived isolate)..
23 whole-genome sequences analysed over six decades (1966–2024): 5 human-derived from India, 17 sandfly-derived from Senegal and Kenya, 1 hedgehog-derived from Nigeria Phylogenetic reconstruction revealed clear lineage segregation between Indian and African strains despite low overall genomic variability Phosphoprotein exhibited relatively higher variability; human-derived sequences more conserved than vector-derived sequences
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This work establishes that CHPV shows regional genetic divergence and structural protein sites under adaptive selection that align with predicted immune epitopes, supporting the rationale for surveillance and vaccine development strategies. However, no clinical outcomes, treatment efficacy, or diagnostic performance data are provided; the findings inform future research directions rather than immediate clinical practice.
A descriptive genomic and phylogenetic analysis of 23 viral sequences over 58 years with no clinical outcomes, comparators, or interventional data; establishes epidemiological landscape and evolutionary patterns but does not test a hypothesis or measure clinical impact.
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This work establishes that CHPV shows regional genetic divergence and structural protein sites under adaptive selection that align with predicted immune epitopes, supporting the rationale for surveillance and vaccine development strategies. However, no clinical outcomes, treatment efficacy, or diagnostic performance data are provided; the findings inform future research directions rather than immediate clinical practice.
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Over six decades (1966-2024), 23 whole-genome sequences of Chandipura virus (CHPV), a neurotropic rhabdovirus associated with acute encephalitis primarily in India, have been analyzed. The virus is believed to be transmitted mainly by Sergentomyia and Phlebotomus sandflies. An epidemiological geographical map was developed showing global CHPV detection in sandflies, district-level human encephalitis reports in India, and sandfly species distribution across the country. This integrated landscape links viral occurrence with vector ecology and outbreak potential. To investigate evolutionary dynamics, we analyzed 23 complete genomes, comprising 5 human-derived isolates from India, 17 sandfly-derived isolates from Senegal and Kenya, and one hedgehog-derived isolate from Nigeria. Phylogenetic reconstruction revealed clear lineage segregation between Indian and African strains, indicating region-specific evolution. Despite this divergence, overall genomic variability remained low. Among all genes, the phosphoprotein exhibited relatively higher variability, while human-derived sequences were more conserved than vector-derived sequences, suggesting stronger evolutionary constraints in the human host. Selection pressure analyses indicated predominantly purifying selection across coding regions. Episodic diversification analysis detected adaptive events in structural proteins. In the glycoprotein, all diversification sites (P272H, L424W, K503R) overlapped with predicted B-cell epitopes. In the matrix protein, both sites (K20R, D97N) mapped to antigenic regions. In contrast, among the two diversification sites in the nucleoprotein (N35E, A187V), only A187V overlapped with an epitope, whereas N35E was outside predicted antigenic domains. Collectively, these findings provide a comprehensive evolutionary and epidemiological perspective on CHPV and highlight the urgent need for systematic genomic surveillance to inform future diagnostic, vaccine and public health intervention strategies.
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