Omsk hemorrhagic fever virus is a tick‐borne encephalitis virus adapted to muskrat through host‐jumping

• Published in: Journal of medical virology 2022-06, Vol.94 (6), p.2510-2518
• Main Authors: Kovalev, Sergey Y., Mazurina, Elena A.
• Format: Article
• Language: English
• Subjects: Amino acids; Aquatic mammals; clusteron approach; Disease transmission; E protein; Ecology; Encephalitis; Etiology; Fever; Genomes; Glycoproteins; Hemorrhage; host‐jump; Infectious diseases; Nucleotides; Omsk hemorrhagic fever; Omsk hemorrhagic fever virus; Ondatra zibethicus; Protein E; quantum evolution; roboviruses; Rodents; Tick-borne encephalitis; tick‐borne encephalitis virus; Virology; Viruses; Zoonoses
• ISSN: 0146-6615; 1096-9071
• DOI: 10.1002/jmv.27581

Omsk hemorrhagic fever was first described in the early 1940s and is a natural focal infection, spread exclusively in four regions of Western Siberia, and associated with muskrat (Ondatra zibethicus). The etiological agent of this disease is the Omsk hemorrhagic fever virus (OHFV) which is closely related to the tick‐borne encephalitis virus (TBEV), and its range entirely lies within the TBEV area. OHFV belongs to the mammalian tick‐borne flaviviruses and the ecological group of arboviruses. The problem concerning the origin of OHFV remains unresolved to date. This study analyzed all nucleotide sequences of the OHFV genome obtained in the present study and available in GenBank, including the E gene fragment and the amino acid sequences of the surface glycoprotein encoded by it. The conclusions, based on the clusteron approach, suggest that OHFV originated directly from the TBEV of the Far Eastern subtype due to the host‐jump phenomenon, that is, through a rapid change from an arthropod host, Ixodes persulcatus, to a rodent, O. zibethicus. The muskrat was introduced to Western Siberia in the second half of the 1930s. The peculiarities of the biology and ecology of the muskrat in the new habitat became the reason for the TBEV cross‐species transmission. Calculations show that host‐jumping occurred between 1931 and 1947 and accompanied a cascade of adaptive amino acid substitutions in protein E. As a result, the virus changed its transmission to contact, alimentary, and airborne routes. Based on the data obtained, OHFV would be more correctly attributed to zoonotic viruses transmitted by rodents and, accordingly, to the ecological group of roboviruses. Highlights The problem concerning the origin of OHFV remains unresolved to date. Our study found OHFV originated directly from the TBEV due to the host‐jump phenomenon. OHFV should be attributed to zoonotic viruses transmitted by rodents and, accordingly, to the ecological group of roboviruses.