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ABSTRACT: Highly Pathogenic Avian Influenza A virus subtype H5N1 (clade 2.3.4.4b) Isolated from a natural protected area in Peru

PROVIDER: PRJNA1092710 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28478279.fastq.gz	Fastqsanger.gz
	SRR28478280.fastq.gz	Fastqsanger.gz
	SRR28478281.fastq.gz	Fastqsanger.gz
	SRR28478282.fastq.gz	Fastqsanger.gz
	SRR28478283.fastq.gz	Fastqsanger.gz

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Lethal Disease Following H5N1 Avian Influenza Virus Clade 2.3.4.4b Infection in Macaques

Project description:The H5N1 avian influenza virus clade 2.3.4.4b outbreak represents a major pandemic threat for humans. Although most human cases to date have been mild, several severe cases of respiratory illness have been reported. A key unanswered question is the pathogenesis of H5N1 infection in primates following respiratory infection. In this study, we observed severe clinical disease in cynomolgus and rhesus macaques following respiratory infection with the H5N1 isolate A/Texas/37/2024 (hu-TX37-H5N1). Cynomolgus macaques inoculated with a high dose of hu-TX37-H5N1 developed severe consolidative necrotizing pneumonia with extrapulmonary spread. Clinical disease was rapidly progressive and lethal in 100% (9 of 9) of macaques by day 5-9 following challenge. Rhesus macaques inoculated with varying doses of hu-TX37-H5N1 demonstrated dose-dependent mortality, and surviving animals showed robust natural protective immunity against high dose re-challenge. H5N1 infection in both cynomolgus and rhesus macaques was characterized by upregulation of proinflammatory cytokine, innate immune cell, complement and coagulation, apoptosis, and immune exhaustion pathways and downregulation of NK, T, and B cell activation and differentiation pathways. Taken together, our data demonstrate severe respiratory disease with H5N1 clade 2.3.4.4b in nonhuman primates and suggest that acute inflammation and immune dysregulation are key contributors to disease pathogenesis.

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