10.3390/polym8030084

Vollständiger Abstract

Worum geht es in dieser Arbeit?

The geographic range and outbreak intensity of vector-borne viral infections are increasing as climate, land use, urbanization, and human mobility reshape vector ecology and human exposure. Despite their growing importance to public health, effective antiviral and preventive options remain limited for many emerging and reemerging vector-borne viruses due to viral genetic diversity, rapid evolutionary capacity, sporadic outbreak patterns, and economic constraints. While these viruses differ in taxonomy, genome organization, vector specificity, tissue tropism, and clinical manifestations, they exploit a shared vulnerability in host antiviral defense, particularly the timing of innate antiviral immunity to support viral replication, immune evasion, inflammatory dysregulation, and disease progression. Rather than simply suppressing antiviral defense, vector-borne viruses can delay early viral nucleic acid sensing, attenuate interferon induction or responsiveness, and extend the initial phase for viral replication. As viral burden increases and infected tissues undergo stress or damage, delayed immune activation can shift toward excessive inflammatory amplification, contributing to disease-specific pathology. In this study, we examine this temporal rewiring of innate antiviral immunity in representative vector-borne viruses such as dengue virus, chikungunya virus, and severe fever with thrombocytopenia syndrome virus and propose that understanding these conserved host dependencies may lead to broader, stage-specific, adaptable antiviral strategies that complement conventional virus-directed approaches.

Abstract: PubMed · Datensatz