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Snakehead vesiculovirus (SHVV), a strain of negative-stranded RNA viruses extracted from sick snakehead fish (Ophicephalus striatus), may pose a threat to the health of snakehead fish. Previous research has proved that the replication of SHVV can be significantly inhibited by glutamine starvation. To study how glutamine starvation inhibits SHVV replication, channel catfish ovary (CCO) cells with SHVV cultivated in the glutamine-free medium or the complete medium were used to investigate the differentially expressed proteins (DEPs). The results showed that 124 up-regulated and 246 down-regulated proteins were involved in many viral replication physiological processes, such as autophagy, post-translational modifications machinery, and functional pathways, including the PI3K-Akt signaling pathway and mTOR signaling pathway. Furthermore, a few proteins, such as Akt and Hsp90, which have been confirmed to be involved in the replication of RNA viruses, were also significantly differentially expressed. Taken together, our study demonstrated that glutamine starvation affects various functional pathways and the expression of some key proteins related to RNA viral replication, which will benefit future studies on the replication mechanisms of SHVV and the prevention of SHVV infection. [ABSTRACT FROM AUTHOR]

The Bm111 of Bombyx mori nucleopolyhedrovirus (BmNPV) encodes a small polypeptide (70 amino acids) of which the function remains unknown. To characterize its function, multiple sequence alignments were performed, and the predicted protein was found to share amazingly high (98 %) sequence identity with the Bombyx mandarina nucleopolyhedrovirus ORF110 (Boma110) but negligible with proteins of other insect viruses, indicating the close relationship between these two NPVs with silkworm larvae. The transcription of Bm111 was detected as early as 3 hpi in BmNPV-infected BmN cells, suggesting it is an early gene. To investigate the role of Bm111 in baculovirus life cycle, a Bm111-knockout virus was constructed by bacmid recombination in Escherichia coli. The results showed that knockout of the Bm111 did not affect the replication of virus DNA, but significantly extended the death time of infected silkworm larvae compared to the wild-type or rescued viruses. We also successfully expressed the recombinant protein Bm111 in E. coli to provide sufficient material for subsequent studies. Taken together, our data indicate that Bm111 only affects the virulence of BmNPV, but not its replication. [ABSTRACT FROM AUTHOR]

Bombyx mori bidensovirus ( BmBDV), which had been assigned to Densovirinae in Parvoviridae previously, replicates mainly in silkworm midgut olumnar cells and causes the fatal flacheric disease. In contrast to parvovirus, this virus possesses two single-stranded DNA genome segments and encodes a putative protein-primed DNA polymerase. The accumulating evidence suggests that it has unique characteristics different to parvovirus and adopts its own mechanisms for replication. So far, little is known about the replication mechanisms of BmBDV. In this review, we focus on the pathology associated with this virus and the viral biology such as viral genome structure, viral genes, and viral replication and expression strategies. [ABSTRACT FROM AUTHOR]

Bombyx mori bidensovirus ( BmBDV), which had been assigned to Densovirinae in Parvoviridae previously, replicates mainly in silkworm midgut olumnar cells and causes the fatal flacheric disease. In contrast to parvovirus, this virus possesses two single-stranded DNA genome segments and encodes a putative protein-primed DNA polymerase. The accumulating evidence suggests that it has unique characteristics different to parvovirus and adopts its own mechanisms for replication. So far, little is known about the replication mechanisms of BmBDV. In this review, we focus on the pathology associated with this virus and the viral biology such as viral genome structure, viral genes, and viral replication and expression strategies. [ABSTRACT FROM AUTHOR]

Open reading frame 17 ( Bm17) of Bombyx mori nucleopolyhedrovirus is a highly conserved gene in lepidopteran nucleopolyhedroviruses, suggesting that it performs an important role in the virus life cycle whose function is unknown. In this report, we describe the characterization of Bm17. Reversed transcriptive-PCR (RT-PCR) and Western blot analysis demonstrated that Bm17 was expressed as a late gen. Immunofluorescence analysis by confocal microscopy showed that BM17 protein was localized on cytoplasm and nucleus of infected cells. These results show that BM17 was a late protein localized in cytoplasm and nucleus. [ABSTRACT FROM AUTHOR]

It is unclear how, or to what extent, baculovirus DNA that has been damaged by ultraviolet (UV) light is repaired during infection and replication. In our previous study, expression of Bombyx mori nucleopolyhedrovirus (BmNPV) ORF Bm65, a homolog of Autographa californica multiple nucleopolyhedrovirus (AcMNPV) ac79, correlated with decreased inactivation of virus by UV irradiation. In the current study, we accumulated more evidence pointing to a role for Bm65 in repair of UV-induced DNA damage. The localization of Bm65 was studied using enhanced green fluorescent protein (EGFP) fusion constructs expressed in BmN cells transfected with a Bm65 expression plasmid. The results indicate that Bm65-EGFP accumulates in the nucleus. A host cell reactivation assay showed that Bm65 significantly increased the expression of UV-damaged mCherry reporter gene. An assay measuring cyclobutane pyrimidine dimers (CPDs) in UV-irradiated BmN cells found that CPD quantity was decreased in cells transfected with a Bm65 expression plasmid. We also showed that after UVC treatment, the viability of Bm65-transfected cells was higher than that of egfp-transfected cells. These results suggest that Bm65 may be involved in the repair of baculovirus DNA that has been damaged by UV light. [ABSTRACT FROM AUTHOR]

[Display omitted] • Trends of metabolite levels in silkworm hemolymph upon BmNPV treatment were revealed. • BmNPV reprogrammed metabolic pathways involving trehalose, glutamine, and tryptophan. • Tryptophan inhibited BmNPV replication while glutamine promoted it. • Trehalose and riboflavin affected BmNPV replication in a complex manner. Elucidating the mechanism of infection of Bombyx mori nuclear polyhedrosis virus (BmNPV) and host antiviral response remains a major scientific task in sericulture. Virus invasion causes a series of antiviral immune responses in the host, and successful infection leads to massive changes in the host's physiological and biochemical state. Current research mainly focuses on silkworm genes and proteins associated with viral infection and resistance, but little is known regarding the host metabolic pathways that the virus utilizes for optimal replication. In this work, key metabolites involved in viral infection were identified, including trehalose, riboflavin, tryptophan, tyrosine, and phenylalanine. The genes associated with metabolite biosynthesis and catabolism were analyzed, and their expression levels were found to be largely consistent with their respective metabolite levels before and after viral treatment in both strains. The screened metabolites were further investigated for their roles in viral replication using exogenous metabolite addition into the culture medium. The results showed that tryptophan effectively inhibited BmNPV replication, while glutamine promoted viral replication in a dose-dependent manner. Trehalose and riboflavin exhibited a complex effect on BmNPV replication. This study outlines the critical metabolites and metabolic pathways required for BmNPV to proliferate and infect the host, indicting the potential of metabolite-based treatment for viral inhibition. [ABSTRACT FROM AUTHOR]

Bombyx mori bidensovirus ( BmBDV), which had been assigned to Densovirinae in Parvoviridae previously, replicates mainly in silkworm midgut olumnar cells and causes the fatal flacheric disease. In contrast to parvovirus, this virus possesses two single-stranded DNA genome segments and encodes a putative protein-primed DNA polymerase. The accumulating evidence suggests that it has unique characteristics different to parvovirus and adopts its own mechanisms for replication. So far, little is known about the replication mechanisms of BmBDV. In this review, we focus on the pathology associated with this virus and the viral biology such as viral genome structure, viral genes, and viral replication and expression strategies. [ABSTRACT FROM AUTHOR]