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Species-specific responses during Seoul orthohantavirus infection in human and rat lung microvascular endothelial cells

ABSTRACT: Species-specific responses during Seoul orthohantavirus infection in human and rat lung microvascular endothelial cells

PROVIDER: PRJNA1030382 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26452800.fastq.gz	Fastqsanger.gz
	SRR26452900.fastq.gz	Fastqsanger.gz
	SRR26453000.fastq.gz	Fastqsanger.gz
	SRR26452801.fastq.gz	Fastqsanger.gz
	SRR26452901.fastq.gz	Fastqsanger.gz

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Species-specific responses during Seoul orthohantavirus infection in human and rat lung microvascular endothelial cells

Project description:Orthohantaviruses are viruses generally carried by rodents in which they do not cause overt disease. Seoul orthohantavirus (SEOV) predominantly exists as a persistent infection in the omnipresent reservoir host, the Norway rat, Rattus norvegicus. Upon respiratory transmission via aerosolized infectious rodent excreta to humans, SEOV causes an acute disease named hemorrhagic fever with renal syndrome (HFRS). Lack of disease in rats is attributed to downregulation of pro-inflammatory and upregulation of regulatory host responses. As lung microvascular endothelial cells (LMECs) represent a primary target of infection in both human and rats, infections in these cells provide a unique opportunity to study the central role of LMECs in the dichotomy between pathogenicity in both species. In this study, host responses to SEOV infection in primary human and rat LMECs were directly compared on a transcriptional level. As infection of rat LMECs was more efficient than human LMECs, most anti-viral defense responses were also observed earlier in rat LMECs. Most prominently SEOV-induced processes in both species included responses to cytokine stimulus, negative regulation of innate immune responses, responses to type I and II interferons, regulation of pattern recognition receptor signaling and MHC-I signaling. However, over time, in the rat LMECs, responses shifted from an anti-viral towards a more immunotolerant state displayed by a PD-L1, B2M-, JAK2-focused interaction network aiding in negative regulation of cytotoxic CD8-positive T cell activation. This suggests a novel mechanism demonstrating how species-specific orthohantavirus-induced endothelium and T cell cross-talk might be crucial for development of acute disease in humans and persistence in rodents.

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Species-specific responses during Seoul orthohantavirus infection in human and rat lung microvascular endothelial cells.

Project description:Seoul orthohantavirus (SEOV) is a rat-borne zoonotic virus that is transmitted via inhalation of aerosolized infectious excreta, and can cause hemorrhagic fever with renal syndrome (HFRS) in humans worldwide. In rats, SEOV predominantly exists as a persistent infection in the absence of overt clinical signs. Lack of disease in rats is attributed to downregulation of pro-inflammatory and upregulation of regulatory host responses. As lung microvascular endothelial cells (LMECs) represent a primary target of infection in both human and rats, infections in these cells provide a unique opportunity to study the central role of LMECs in the dichotomy between pathogenicity in both species. In this study, host responses to SEOV infection in primary human and rat LMECs were directly compared on a transcriptional level. As infection of rat LMECs was more efficient than human LMECs, the majority of anti-viral defense responses were observed earlier in rat LMECs. Most prominently, SEOV-induced processes in both species included responses to cytokine stimulus, negative regulation of innate immune responses, responses to type I and II interferons, regulation of pattern recognition receptor signaling and MHC-I signaling. However, over time, in the rat LMECs, responses shifted from an anti-viral state towards a more immunotolerant state displayed by a PD-L1, B2M-, JAK2-focused interaction network aiding in negative regulation of cytotoxic CD8-positive T cell activation. This suggests a novel mechanism by which species-specific orthohantavirus-induced endothelium and T cell crosstalk may play a crucial role in the development of acute disease in humans and persistence in rodents.

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