Role of cytokines in poxvirus host tropism and adaptation

Abstract

Poxviruses are a diverse family of double-stranded DNA viruses that cause mild-to-severe disease in selective hosts, including humans. Although most poxviruses are restricted to their hosts, some members can leap host species and cause zoonotic diseases and, therefore, are genuine threats to human and animal health. The recent global spread of monkeypox in humans suggests that zoonotic poxviruses can adapt to a new host, spread rapidly in the new host, and evolve to better evade host innate barriers. Unlike many other viruses, poxviruses express an extensive repertoire of self-defense proteins that play a vital role in the evasion of host innate and adaptive immune responses in their newest host species. The function of these viral immune modulators and host-specific cytokine responses can result in different host tropism and poxvirus disease progression. Here, we review the role of different cytokines that control poxvirus host tropism and adaptation.

Figure 1

Myxoma virus (MYXV) species leap from rabbits to hares. MYXV-Lau causes myxomatosis only in European rabbits (Oryctolagus cuniculus). However, during a recombination event, MYXV-Lau acquired a genomic cassette with a C7-like host range gene called M159 from an unknown poxvirus. This new MYXV isolate called MYXV-Tol can now cause myxomatosis-like disease in Iberian hares (Lepus granatensis) and European rabbits.