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Autographa californica multiple nucleopolyhedrovirus

ABSTRACT: Autographa californica MNPV overview

PROVIDER: PRJNA69553 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1119940_1.fastq.gz	Fastqsanger.gz
	SRR1119940_2.fastq.gz	Fastqsanger.gz
	SRR1118212_1.fastq.gz	Fastqsanger.gz
	SRR1118212_2.fastq.gz	Fastqsanger.gz
	SRR1119903_1.fastq.gz	Fastqsanger.gz

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Autographa californica multiple nucleopolyhedrovirus

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Comprehensive analysis of host gene expression in Autographa californica nucleopolyhedrovirus-infected Spodoptera frugiperda cells

Project description:Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) is the best-studied baculovirus and most commonly used virus vector for baculovirus expression vector systems. The effect of AcMNPV infection on host cells is incompletely understood. A microarray based on Spodoptera frugiperda ESTs was used to investigate the impact of AcMNPV on host gene expression in cultured S. frugiperda, Sf21 cells. Most host genes were down-regulated over the time course of infection, although a small number were up-regulated. The most highly up-regulated genes encoded heat shock protein 70s and several poorly characterized proteins. Regulated genes with the highest score identified by functional annotation clustering included primarily products required for protein expression and trafficking in the ER and golgi. All were significantly down-regulated by approximately 12h post-infection. Microarray data were validated by qRT-PCR. This study provides the first comprehensive host transcriptome overview of Sf21 cells during AcMNPV infection.

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Autographa californica multiple nucleopolyhedrovirus strain:E2 bacmid

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Spodoptera frugiperda and Autographa californica Multiple Nucleopolyhedrovirus

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Selection and characterization of Autographa californica multiple nucleopolyhedrovirus DNA polymerase mutations.

Project description:Autographa californica multiple nucleopolyhedrovirus (AcMNPV) DNA polymerase (DNApol) is essential for viral DNA replication. AcMNPV mutants resistant to aphidicolin, a selective inhibitor of viral DNA replication, and abacavir, an efficacious nucleoside analogue with inhibitory activity against reverse transcriptase, were selected by the serial passage of the parental AcMNPV in the presence of increasing concentrations of aphidicolin or abacavir. These drug-resistant mutants had either a single (C543R) (aphidicolin) or a double (C543R and S611T) (abacavir) point mutation within conserved regions II and III. To confirm the role of these point mutations in AcMNPV DNA polymerase, a dnapol knockout virus was first generated, and several repair viruses were constructed by transposing the dnapol wild-type gene or ones containing a single or double point mutation into the polyhedrin locus of the dnapol knockout bacmid. The single C543R or double C543R/S611T mutation showed increased resistance to both aphidicolin and abacavir and, even in the absence of drug, decreased levels of virus and viral DNA replication compared to the wild-type repair virus. Surprisingly, the dnapol mutant repair viruses led to the generation of occlusion-derived viruses with mostly single and only a few multiple nucleocapsids in the ring zone and within polyhedra. Thus, these point mutations in AcMNPV DNA polymerase increased drug resistance, slightly compromised virus and viral DNA replication, and influenced the viral morphogenesis of occlusion-derived virus.

| S-EPMC3503129 | biostudies-literature

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