Viral genomes in any invertebrate samples
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ABSTRACT:
PROVIDER: PRJNA629998 | ENA |
REPOSITORIES: ENA
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Project description:Viral infections are associated with extensive remodeling of the cellular proteome. Viruses encode gene products that manipulate host proteins to redirect cellular processes or subvert antiviral immune responses. One way in which host antiviral proteins antagonize viral infection is by associating with viral genomes and inhibiting essential viral processes. Adenovirus (AdV) encodes gene products from the early E4 region which are necessary for productive infection. Some cellular antiviral proteins are known to be targeted by AdV E4 gene products, resulting in their degradation or mislocalization. However, the full repertoire of host proteins manipulated by viral E4 proteins has not been defined. To identify cellular proteins and processes manipulated by viral products, we developed a global, un-biased proteomics approach to analyze changes to the host proteome during infection with Adenovirus serotype 5 (Ad5) virus. We combined quantification of total protein abundance in the proteome together with an analysis of proteins associated with viral genomes using isolation of Proteins on Nascent DNA (iPOND). By Integrating these proteomics datasets, we identified cellular factors that are degraded in an E4-dependent manner or are associated with the viral genome in the absence of E4 proteins. We further show that some identified proteins exert inhibitory effects on Ad5 infection. Our systems-level analysis reveals cellular processes that are manipulated during Ad5 infection and points to host factors counteracted by early viral proteins as they remodel the host proteome to promote efficient infection. Importance Viral infections stimulate myriad changes to the host cell proteome. As viruses harness cellular processes and counteract host defenses, they impact abundance, modifications, or localization of cellular proteins. Elucidating the dynamic changes to the cellular proteome during viral replication is integral to understanding how virus-host interactions influence the outcome of infection. Adenovirus serotype 5 (Ad5) encodes early gene products from the E4 genomic region that are known to alter host response pathways and promote replication, but the full extent of proteome modifications they mediate is not known. We use an integrated proteomics approach to quantitate protein abundance and protein associations with viral DNA during virus infection. Systems-level analysis identifies cellular proteins and processes impacted in an E4-dependent manner that could overcome potentially inhibitory host defenses. This study provides a global view of Adenovirus-mediated proteome remodeling which can serve as a model to investigate virus-host interactions of DNA viruses.
2021-08-11 | PXD025339 | Pride
Project description:Epstein-Barr virus (EBV) is a human gamma-herpesvirus that is causally associated with various lymphomas and carcinomas. Although EBV is not typically associated with multiple myeloma (MM), it can be found in some B-cell lines derived from multiple myeloma patients. Here, we analyzed two EBV+ MM-patient derived cell lines IM9 and ARH77 and found defective viral genomes and atypical viral gene expression patterns. We performed RNA-seq transcriptomics to characterize the viral and cellular properties of the two EBV+ cell lines compared to canonical MM cell line 8226. Principal component analyses indicated that IM9 and ARH77 clustered together and distinct from 8226. ImmGen analysis designate these cells as stem-cell and bone marrow derived. IM9 and ARH77 displayed atypical viral gene expression, including a leaky lytic cycle gene expression with absence of lytic DNA amplification. Genome sequencing revealed that EBV genomes in ARH77 contain large deletions, while IM9 has copy number losses in multiple EBV loci. Both IM9 and ARH77 have numerous EBV genome heterogeneity suggestive of cell harboring multiple and variant viral genomes. Among the lytic genes, we identified atypical high-level expression of BLRF2 and BLRF1. BRLF2 encodes a tegument protein previously shown to bind BNRF1 and to also interact with cGAS, similar to KSHV ORF52, also known as the inhibitor of cGAS (KicGAS). We demonstrate the shRNA depletion of BLRF2 alters viral and host gene expression, including a reduction in lytic gene activation and DNA amplification. These findings demonstrate that aberrant viral genomes and lytic gene expression persist in rare B-cells derived from MM tumors, and suggest that EBV may contribute to etiology of MM.
2021-04-07 | GSE165195 | GEO
Project description:Epstein-Barr virus (EBV) is a human gamma-herpesvirus that is causally associated with various lymphomas and carcinomas. Although EBV is not typically associated with multiple myeloma (MM), it can be found in some B-cell lines derived from multiple myeloma patients. Here, we analyzed two EBV+ MM-patient derived cell lines IM9 and ARH77 and found defective viral genomes and atypical viral gene expression patterns. We performed RNA-seq transcriptomics to characterize the viral and cellular properties of the two EBV+ cell lines compared to canonical MM cell line 8226. Principal component analyses indicated that IM9 and ARH77 clustered together and distinct from 8226. ImmGen analysis designate these cells as stem-cell and bone marrow derived. IM9 and ARH77 displayed atypical viral gene expression, including a leaky lytic cycle gene expression with absence of lytic DNA amplification. Genome sequencing revealed that EBV genomes in ARH77 contain large deletions, while IM9 has copy number losses in multiple EBV loci. Both IM9 and ARH77 have numerous EBV genome heterogeneity suggestive of cell harboring multiple and variant viral genomes. Among the lytic genes, we identified atypical high-level expression of BLRF2 and BLRF1. BRLF2 encodes a tegument protein previously shown to bind BNRF1 and to also interact with cGAS, similar to KSHV ORF52, also known as the inhibitor of cGAS (KicGAS). We demonstrate the shRNA depletion of BLRF2 alters viral and host gene expression, including a reduction in lytic gene activation and DNA amplification. These findings demonstrate that aberrant viral genomes and lytic gene expression persist in rare B-cells derived from MM tumors, and suggest that EBV may contribute to etiology of MM.
2021-04-07 | GSE165194 | GEO