Multidimensional mechanisms of SFTSV-host interactions: viral protein functions, m6A modification, tick saliva factors, and platelet regulation

Severe fever with thrombocytopenia syndrome virus (SFTSV), officially designated as Dabie bandavirus by the International Committee on Taxonomy of Viruses (ICTV), is an emerging zoonotic pathogen belonging to the order Bunyavirales and the family Phenuiviridae. First isolated and identified in 2010 from the serum of patients with severe fever with thrombocytopenia syndrome (SFTS) in China, SFTSV has since been reported in multiple provinces across China, as well as in South Korea, Japan, Vietnam, the United Arab Emirates (including Dubai), and Pakistan. With a case fatality rate of up to 30%, SFTSV poses a serious threat to public health and carries the potential for broader global spread. In nature, SFTSV is primarily transmitted through tick bites, although direct human-to-human or animal-to-human transmission can also occur through exposure to the blood, respiratory secretions, or other bodily fluids of infected individuals or animals. The pathogenic mechanisms of SFTSV are complex and multifaceted, involving the coordinated actions of multiple viral proteins, host epigenetic regulation, and virus–vector interactions. In this review, we take tick bites as the starting point to describe how SFTSV achieves cross-species transmission through ticks, summarize the viral life cycle, including internalization, replication, assembly, and egress, and discuss the antagonistic interplay between the viral life cycle and host defense responses, with the aim of providing a solid theoretical foundation for understanding the infection and pathogenesis of SFTSV.