ArticleVirus genes2012
Autographa californica multiple nucleopolyhedrovirus orf114 is not essential for virus replication in vitro, but its knockout reduces per os infectivity in vivo.
Article in Virus genes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Construction of a shortened autographa californica multiple nucleopolyhedrovirus genome as protein expression vector.Archives of virology · 2025Article
- Characterization of lamin B receptor of Sf9 cells and its fate during Autographa californica nucleopolyhedrovirus infection.Cytotechnology · 2020Article
- Functional Characterization of the Group I Alphabaculovirus Specific Gene ac73.Virologica Sinica · 2019Article
- Article
- Protein composition analysis of polyhedra matrix of Bombyx mori nucleopolyhedrovirus (BmNPV) showed powerful capacity of polyhedra to encapsulate foreign proteins.Scientific reports · 2017Article
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Authors and funding
4 authors.
Funding
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Abstract
Autographa californica multiple nucleopolyhedrovirus (AcMNPV) orf114 (ac114) is one of the highly conserved unique genes in the lepidopteran group I nucleopolyhedrovirus. So far, the biological function of ac114 is unknown. To study the function of ac114 in the virus life cycle, an ac114 knockout baculovirus shuttle vector (bacmid) was generated. Fluorescence and light microscopy showed that the ac114 knockout mutant was able to produce infectious budded viruses (BVs) and occlusion bodies (OBs). Titration assays demonstrated that the ac114 knockout virus had similar growth kinetics to the control virus during the infection phase. Electron microscopy indicated that ac114 did not affect the morphogenesis of BVs and occlusion-derived viruses (ODVs); however, the numbers of ODVs per OB of the ac114 knockout virus were significantly lower than those of the control virus. RT-PCR demonstrated that ac114 was a late stage expression gene and that its transcription initiated at an A residue, 16 nucleotides upstream of the ATG start codon. Intracellular localization analysis revealed that the Ac114-GFP fusion protein localized predominantly as punctate patches in the cytoplasm of infected Sf9 cells. Bioassays showed that the ac114 knockout did not change the killing speed of AcMNPV in Spodoptera exigua larvae, but reduced its viral infectivity significantly. Taken together, these data indicate that ac114 is an auxiliary gene that facilitates embedding of ODVs into OBs, thus affecting the per os infectivity of the virus.
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