Hantavirus mutagenesis is impacted by mutagens and host antiviral proteins
Hantaviruses are emerging zoonotic viruses that infect humans with high fatality rates. We currently have a poor understanding of the processes that contribute to hantavirus mutagenesis and therefore the potential for viral adaptation. To understand the drivers of mutations in hantaviruses, we calculated and compared mutational spectra across 14 divergent hantavirus species. We found that…
Hantaviruses, a group of emerging zoonotic viruses, are capable of infecting humans with high fatality rates. Despite their potential for viral adaptation, our understanding of the mechanisms behind hantavirus mutagenesis remains limited. In a recent study, researchers analyzed mutational spectra across 14 distinct hantavirus species and discovered that conserved mutagens from various host species play a significant role in shaping hantavirus mutagenesis, contributing to at least six out of the 12 possible mutation types.
The study also highlighted differences in mutational signatures among hantaviruses, which may be attributed to variations in host mutagen levels that influence somatic mutations. However, no evidence was found to suggest that distinct human diseases associated with specific hantaviruses exhibit differing mutational signatures. Furthermore, there were no indications of tissue tropism discrepancies between reservoir hosts.
To delve deeper into the factors influencing hantavirus mutagenesis, the researchers employed a novel method to quantify the impact of ZAP-mediated selection. Their findings revealed that ZAP significantly influences mutational patterns in transition mutation types across hantaviruses. Additionally, the researchers uncovered evidence suggesting that APOBEC family proteins are primarily responsible for mutagenesis in all hantaviruses, with the possible exception of Nova virus.
These results strongly indicate that both mutagens and host antiviral proteins are crucial drivers of hantavirus mutagenesis, ultimately contributing to the genetic diversity necessary for viral adaptation.
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