Genomic analysis of hyperparasitic viruses associated with entomopoxviruses-Reference-Cited by-同舟云学术

Genomic analysis of hyperparasitic viruses associated with entomopoxviruses

Published:2024 Issue:1 Volume:10 Page:
ISSN:2057-1577
Container-title:Virus Evolution
language:en
Short-container-title:

Author:

Barth Zachary K¹^ORCID,Hicklin Ian²,Thézé Julien³,Takatsuka Jun⁴^ORCID,Nakai Madoka⁵,Herniou Elisabeth A⁶^ORCID,Brown Anne M²⁷⁸,Aylward Frank O¹⁷^ORCID

Affiliation:

1. Department of Biological Sciences, Virginia Tech , 926 West Campus Drive, Blacksburg, VA 24061, USA

2. Department of Biochemistry, Virginia Tech , Blacksburg, VA 24061, USA

3. Université Clermont Auvergne, INRAE, VetAgro Sup, UMR EPIA , Saint-Genès-Champanelle, France

4. Forestry and Forest Products Research Institute , Matsunosato, Tsukuba, Ibaraki 305-8687, Japan

5. Institute of Agriculture, Tokyo University of Agriculture and Technology , Saiwai, Fuchu, Tokyo 183-8509, Japan

6. Institut de Recherche sur la Biologie de l’Insecte, UMR7261 CNRS-Université de Tours , 20 Avenue Monge, Parc de Grandmont, Tours 37200, France

7. Center for Emerging, Zoonotic, and Arthropod-Borne Pathogens, Virginia Tech , 1981 Kraft Dr, Blacksburg, VA 24061, USA

8. Research and Informatics, University Libraries, Virginia Tech , Blacksburg, VA 24061, USA

Abstract

Abstract Polinton-like viruses (PLVs) are a diverse group of small integrative dsDNA viruses that infect diverse eukaryotic hosts. Many PLVs are hypothesized to parasitize viruses in the phylum Nucleocytoviricota for their own propagation and spread. Here, we analyze the genomes of novel PLVs associated with the occlusion bodies of entomopoxvirus (EPV) infections of two separate lepidopteran hosts. The presence of these elements within EPV occlusion bodies suggests that they are the first known hyperparasites of poxviruses. We find that these PLVs belong to two distinct lineages that are highly diverged from known PLVs. These PLVs possess mosaic genomes, and some essential genes share homology with mobile genes within EPVs. Based on this homology and observed PLV mosaicism, we propose a mechanism to explain the turnover of PLV replication and integration genes.

Funder

National Institutes of Health

National Science Foundation

Publisher

Oxford University Press (OUP)

Link

https://academic.oup.com/ve/advance-article-pdf/doi/10.1093/ve/veae051/58517653/veae051.pdf

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