Abstract
• BmLV is originated from a plant virus. • BmLV can enter nontarget cells with transient propagation. • The Imd and RNAi pathways are activated by BmLV infection. • The transient propagation of BmLV is mediated by dysregulation of gene expression. Bombyx mori latent virus (BmLV), a novel positive-strand RNA virus was first identified in the B. mori cultured BmN cell line. Whether the infectivity of BmLV to silkworm larvae and non-silkworm cells is connected with dysregulation of gene expression are not well understood. A complete sequence of BmLV genomic RNA was identified and revealed that a fragment with 495 nt in length was deleted from the RNA-dependent RNA polymerase (RdRp) gene in some BmLV genomic RNAs. Studies on the infectivity of BmLV to nontarget cells showed that BmLV can infect silkworm larvae, Spodoptera frugiperda Sf-9 and H1299 lung cancer cells with transient propagation. The dysregulation of gene expression of Sf-9 cells followed by BmLV infection was analyzed. Out of 743 differentially expressed genes (DEGs), 300 were upregulated and 443 were downregulated. Gene Ontology (GO) analysis indicated the DEGs were enriched into oxidoreductase activity for CH-NH 2 group donors, glutamate biosynthetic process, response to stress and proteasome core complex. KEGG enrichment analysis showed that DEGs were mainly enriched into sulfur metabolism, RNA degradation, proteasome, pentose and glucuronate interconversions. Undesirable nutrients and temperature factors contributed to the propagation of BmLV in Sf-9 cells. Additionally, the Imd and RNAi pathways were activated by BmLV infection without stimulating Toll and JAK-STAT pathways. Therefore, it is suggested that BmLV is originated from plants, which can enter nontarget cells with transient propagation. The transient infection of BmLV may not only be regulated by Imd and RNAi immune pathways but also mediated by dysregulation of gene expression.
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