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Dev Comp Immunol. 2019 Jul;96:51-57. doi: 10.1016/j.dci.2019.02.017. Epub 2019 Feb 26.

Bombyx mori cypovirus encoded small peptide inhibits viral multiplication.

Author information

1
School of Biology & Basic Medical Science, Soochow University, Suzhou, 215123, China; National Engineering Laboratory for Modern Silk, Soochow University, Suzhou, China.
2
School of Biology & Basic Medical Science, Soochow University, Suzhou, 215123, China; Agricultural Biotechnology Research Institute, Agricultural Biotechnology and Ecological Research Institute, Soochow University, Suzhou, 215123, China.
3
School of Biology & Basic Medical Science, Soochow University, Suzhou, 215123, China.
4
School of Biology & Basic Medical Science, Soochow University, Suzhou, 215123, China; National Engineering Laboratory for Modern Silk, Soochow University, Suzhou, China. Electronic address: guanglicao@163.com.
5
School of Biology & Basic Medical Science, Soochow University, Suzhou, 215123, China; National Engineering Laboratory for Modern Silk, Soochow University, Suzhou, China; Agricultural Biotechnology Research Institute, Agricultural Biotechnology and Ecological Research Institute, Soochow University, Suzhou, 215123, China. Electronic address: gongcl@suda.edu.cn.

Abstract

Bombyx mori cypovirus (BmCPV) is one of the most infectious pathogen in sericulture and a member of the family Reoviridae. It specifically infects the midgut of silkworm. The BmCPV genome consists of 10 dsRNAs segments (S1-S10), which have generally been assumed to be monocistronic. In this study, a small open reading frame encoding the peptide S5-sORF, containing 27 amino acid residues, was predicted in a region of the negative (-) strand of BmCPV segment S5. An immunofluorescence assay detected S5-sORF in the cytoplasm and nuclei of BmCPV-infected cells, and it was also detected in the virion with western blotting, suggesting that S5-sORF may be assembled into the BmCPV virion. Viral gene expression was inhibited by overexpressed S5-sORF, and viral multiplication was dose-dependently suppressed by the S5-sORF peptide. A viable recombinant virus, BmCPV-S5-sORFmut, in which the start codon (ATG) of S5-sORF was mutated to a stop codon (TGA), was generated with reverse genetics. The proliferation of BmCPV was increased by the abolition of S5-sORF expression. Furthermore, the RNA transcript of S5-sORF and small peptide of S5-sORF were involved in BmCPV replication. The expression of genes related to the innate immune pathways and apoptosis in the silkworm were not significantly affected by S5-sORF overexpression. Our results suggest that a viral nucleotide sequence is utilized by the host to generate an antiviral peptide, which may be a novel strategy protecting the host from viral infection.

KEYWORDS:

BmCPV; Small antiviral peptide; Viral proliferation; sORF

PMID:
30822453
DOI:
10.1016/j.dci.2019.02.017

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