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Hallmarks of primate lentiviral immunodeficiency infection recapitulate loss of innate lymphoid cells

ABSTRACT: Hallmarks of primate lentiviral immunodeficiency infection recapitulate loss of innate lymphoid cells

PROVIDER: PRJNA476787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7367600_1.fastq.gz	Fastqsanger.gz
	SRR7367600_2.fastq.gz	Fastqsanger.gz
	SRR7367591_1.fastq.gz	Fastqsanger.gz
	SRR7367591_2.fastq.gz	Fastqsanger.gz
	SRR7367601_1.fastq.gz	Fastqsanger.gz

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Hallmarks of primate lentiviral immunodeficiency infection recapitulate loss of innate lymphoid cells.

Project description:Innate lymphoid cells (ILCs) play critical roles in mucosal barrier defense and tissue homeostasis. While ILCs are depleted in HIV-1 infection, this phenomenon is not a generalized feature of all viral infections. Here we show in untreated SIV-infected rhesus macaques (RMs) that ILC3s are lost rapidly in mesenteric lymph nodes (MLNs), yet preserved in SIV+ RMs with pharmacologic or natural control of viremia. In healthy uninfected RMs, experimental depletion of CD4+ T cells in combination with dextran sodium sulfate (DSS) is sufficient to reduce ILC frequencies in the MLN. In this setting and in chronic SIV+ RMs, IL-7R? chain expression diminishes on ILC3s in contrast to the IL-18R? chain expression which remains stable. In HIV-uninfected patients with durable CD4+ T cell deficiency (deemed idiopathic CD4+ lymphopenia), similar ILC deficiencies in blood were observed, collectively identifying determinants of ILC homeostasis in primates and potential mechanisms underlying their depletion in HIV/SIV infection.

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Hallmarks of primate lentiviral immunodeficiency infection recapitulate loss of innate lymphoid cells

Project description:Innate lymphoid cells (ILCs) play critical roles in mucosal barrier defense and tissue homeostasis. While ILCs are depleted in HIV-1 infection, this phenomenon is not a generalized feature of all viral infections. Here we show in untreated SIV-infected rhesus macaques (RMs) that ILC3s are lost rapidly in mesenteric lymph nodes (MLN) yet preserved in SIV+ RMs with pharmacologic or natural control of viremia. In healthy uninfected RMs, experimental depletion of CD4+ T cells in combination with DSS is sufficient to reduce ILC frequencies in the MLN. In this setting and in chronic SIV+ RMs, IL-7R alpha chain expression diminishes on ILC3s in contrast to the IL-18R alpha chain expression which remains stable. In HIV-uninfected patients with durable CD4+ T cell deficiency, deemed idiopathic CD4+ lymphopenia, similar ILC deficiencies in blood were observed, collectively identifying determinants of ILC homeostasis in primates and potential mechanisms underlying their depletion in HIV/SIV infection.

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Project description:HIV accessory proteins manipulate host factors to evade cellular restriction and enhance viral replication. We used multiplex tandem mass tag (TMT)-based whole cell proteomics to gain a comprehensive, time-based overview of proteins and processes subverted during HIV infection. To make specific functional and mechanistic predictions and systematically identify candidate accessory protein targets, we categorized cellular proteins regulated by HIV according to their patterns of temporal expression. As well as depleting APOBEC family members, we found Vif to be necessary and sufficient for CUL5-dependent degradation of all members of the B56 family of regulatory subunits of the key cellular phosphatase PP2A. Quantitative phosphoproteomic analysis of HIV-infected cells confirmed Vif-dependent hyperphosphorylation of >200 cellular proteins, particularly substrates of the aurora kinases. The ability of Vif to target PP2A subunits spans primate and non-primate lentiviral lineages, and remodeling of the cellular phosphoproteome is therefore a second ancient and conserved Vif function.

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