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The molecular programs underpinning ‘tolerance’ and ‘resistance’ in health and viral infection

ABSTRACT: The molecular programs underpinning ‘tolerance’ and ‘resistance’ in health and viral infection

PROVIDER: PRJNA763877 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15914000_1.fastq.gz	Fastqsanger.gz
	SRR15914000_2.fastq.gz	Fastqsanger.gz
	SRR15914001_1.fastq.gz	Fastqsanger.gz
	SRR15914001_2.fastq.gz	Fastqsanger.gz
	SRR15914002_1.fastq.gz	Fastqsanger.gz

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The molecular programs underpinning 'tolerance' and 'resistance' in health and viral infection

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Project description:The immune protection against invading pathogens is governed by pathogen elimination (‘resistance’) and by limitation of tissue damage that results from host-pathogen interactions (‘tolerance’). However, distinct molecular states of resistance and tolerance remain obscure. Here, we collected longitudinal lung transcriptomes and clinical phenotypes of disease severity during influenza A virus (IAV) infection across 39 genetically-distinct mouse strains (32 strains of time series data and additional 7 strains with selected time points). Using transcriptional diversity in this data, we uncovered two key programs that together describe the cellular states for resistance and tolerance. The identified programs offer an unprecedented comprehensive view on shared and distinct roles of resistance and tolerance for the regulation of immune defense – for instance, we identified an antagonistic regulation of resistance and tolerance on protein production. Importantly, the framework reveals that both inflammatory states and the healthy steady state are remarkably diverse in resistance and tolerance levels, with implications on disease severity: a baseline state (before infection) of high tolerance and low resistance results in increased severity of IAV infection. Overall, our work provides a framework for the study of resistance and tolerance that could aid in clinical diagnosis and disease management.

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Project description:Bats harbor highly virulent viruses that can infect other mammals, including humans, posing questions about their immune tolerance mechanisms. Bat cells employ multiple strategies to limit virus replication and virus-induced immunopathology, but the coexistence of bats and fatal viruses remains poorly understood. Here, we investigated the antiviral RNA interference (RNAi) pathway in bat cells and discovered that they have an enhanced antiviral RNAi response, producing canonical viral small interfering RNAs (vsiRNAs) upon Sindbis virus (SINV) infection that were missing in human cells. Disruption of Dicer function resulted in increased viral load for three different RNA viruses in bat cells, indicating an interferon-independent antiviral pathway. Furthermore, our findings reveal the simultaneous engagement of Dicer and pattern-recognition receptors (PRRs), such as retinoic acid-inducible gene I (RIG-I), with double-stranded RNA, suggesting that Dicer attenuates the interferon response initiation in bat cells. These insights advance our comprehension of the distinctive strategies bats employ to coexist with viruses.

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