Abstract

Coronaviruses have caused three major epidemics since 2003, including the ongoing SARS-CoV-2 pandemic. In each case, the emergence of coronavirus in our species has been associated with zoonotic transmissions from animal reservoirs1,2, underscoring how prone such pathogens are to spill over and adapt to new species. Among the four recognized genera of the family Coronaviridae, human infections reported so far have been limited to alphacoronaviruses and betacoronaviruses3–5. Here we identify porcine deltacoronavirus strains in plasma samples of three Haitian children with acute undifferentiated febrile illness. Genomic and evolutionary analyses reveal that human infections were the result of at least two independent zoonoses of distinct viral lineages that acquired the same mutational signature in the genes encoding Nsp15 and the spike glycoprotein. In particular, structural analysis predicts that one of the changes in the spike S1 subunit, which contains the receptor-binding domain, may affect the flexibility of the protein and its binding to the host cell receptor. Our findings highlight the potential for evolutionary change and adaptation leading to human infections by coronaviruses outside of the previously recognized human-associated coronavirus groups, particularly in settings where there may be close human–animal contact.

Highlights

  • Viruses that belong to the family Coronaviridae

  • B.1.1.7 have been observed (A570D, D614G and S982A)[36,37], V550A may represent a common mechanism that enhances dynamic movements, accelerating membrane fusion events and transmission of the virus. This is the first report of Porcine deltacoronavirus (PDCoV) infection in humans, consistent with viraemia and systemic dissemination

  • The recent divergence of human strains detected in Haiti from their closest pig strains detected in China and the USA in the phylogeny highlights how little we know about the spreading of PDCoV and its introduction in Haiti

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Summary

Part of CN and part of SEA P A

B.1.1.7 have been observed (A570D, D614G and S982A)[36,37], V550A may represent a common mechanism that enhances dynamic movements, accelerating membrane fusion events and transmission of the virus

Conclusions
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