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Existence of human-virus chimeric proteins generated during infection

ABSTRACT: Existence of human-virus chimeric proteins generated during infection

PROVIDER: PRJNA527980 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8750210_1.fastq.gz	Fastqsanger.gz
	SRR8750210_2.fastq.gz	Fastqsanger.gz
	SRR8750220_1.fastq.gz	Fastqsanger.gz
	SRR8750220_2.fastq.gz	Fastqsanger.gz
	SRR8750211_1.fastq.gz	Fastqsanger.gz

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Existence of human-virus chimeric proteins generated during infection

Project description:Influenza A virus (IAV) is a threat to mankind because it generates yearly epidemics and poorly predictable sporadic pandemics with catastrophic potential. Influenza has a small RNA genome (~14 Kb) composed of 8 mini-chromosomes (segments). Segments encode both structural proteins and proteins expressed only during infection. Segments are constituted by a 5’UTR followed by a coding region and a 3’UTR. Transcription of IAV RNA into mRNA depends on host RNA Polymerase II, as the viral polymerase cleaves 5’ capped cellular nascent transcripts to be used as primers to initiate mRNA synthesis. We hypothesized that host nascent transcripts bearing AUG could generate upstream ORFs in the viral segments, a phenomenon that would depend on the translatability of the viral 5’UTRs. Using orthogonal datasets we report the existence of this mechanism, which generate host-virus chimeric proteins. We show that most segments encode proteins in this manner, expanding the proteome diversity of IAV in infected cells. Host-virus chimeric proteins are conserved across IAV strains, pointing to an evolutionary conservation of function achieved by sampling of the evolutionary space before gene fixation. Thus, we discover a mechanism that generate human-virus chimeric proteins during infection.

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HUMAN-VIRUS CHIMERIC PROTEINS GENERATED DURING INFECTION

Project description:HUMAN-VIRUS CHIMERIC PROTEINS GENERATED DURING INFECTION

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HUMAN-VIRUS CHIMERIC PROTEINS GENERATED DURING INFECTION

Project description:RNA viruses are a major threat to global human health. The life cycles of many highly pathogenic RNA viruses like influenza A virus (IAV) and Lassa virus depends on host mRNA, as viral polymerases cleave 5′m7G-capped host transcripts to prime viral mRNA synthesis (‘cap-snatching’). We hypothesized that start codons within cap-snatched host transcripts could drive the expression of chimeric human-viral coding sequences. Here, we report the existence of this mechanism of gene origination (‘start-snatching’), which creates, depending on the translatability of the viral UTRs, human-virus protein chimeras either as N-terminally extended viral proteins or entirely novel polypeptides by genetic overprinting. We show that both types of chimeric proteins are made in IAV-infected cells, can generate T cell responses and contribute to virulence. Our results indicate that IAV, and likely a multitude of other human-, animal- and plant-viruses, use this host-dependent mechanism to expand their proteome diversity during infection.

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human.

Project description:Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human.

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Hybrid Gene Origination Creates Human-Virus Chimeric Proteins during Infection.

Project description:RNA viruses are a major human health threat. The life cycles of many highly pathogenic RNA viruses like influenza A virus (IAV) and Lassa virus depends on host mRNA, because viral polymerases cleave 5'-m7G-capped host transcripts to prime viral mRNA synthesis ("cap-snatching"). We hypothesized that start codons within cap-snatched host transcripts could generate chimeric human-viral mRNAs with coding potential. We report the existence of this mechanism of gene origination, which we named "start-snatching." Depending on the reading frame, start-snatching allows the translation of host and viral "untranslated regions" (UTRs) to create N-terminally extended viral proteins or entirely novel polypeptides by genetic overprinting. We show that both types of chimeric proteins are made in IAV-infected cells, generate T cell responses, and contribute to virulence. Our results indicate that during infection with IAV, and likely a multitude of other human, animal and plant viruses, a host-dependent mechanism allows the genesis of hybrid genes.

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human[ChIP-seq]

Project description:Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human[ChIP-seq]

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human [RNA-seq]

Project description:Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human [RNA-seq]

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