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IL-15 Enhances HIV-1 infection by Promoting Differentiation and Survival of CCR5+CD4+ T cells

ABSTRACT: IL-15 Enhances HIV-1 infection by Promoting Differentiation and Survival of CCR5+CD4+ T cells

PROVIDER: PRJNA821253 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18530546_1.fastq.gz	Fastqsanger.gz
	SRR18530546_2.fastq.gz	Fastqsanger.gz
	SRR18530547_1.fastq.gz	Fastqsanger.gz
	SRR18530547_2.fastq.gz	Fastqsanger.gz
	SRR18530548_1.fastq.gz	Fastqsanger.gz

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IL-15 Enhances HIV-1 infection by Promoting Differentiation and Survival of CCR5+CD4+ T cells

Project description:HIV-1 usually utilize CCR5 as the co-receptor and rarely switches to CXCR4-tropic until late stage of infection. CCR5+CD4+ T cells are the major virus-producing cells in patients as well as SIV-infected non-human primates. The differentiation of CCR5+CD4+ T cells is associated with the availability of IL-15, which increases during acute HIV-1 infection. Here, we report that CCR5 is expressed by CD4+ T cells exhibiting effector or effector memory phenotype with high expression levels of the IL-2/IL-15 receptor common beta and gamma chains. IL-15 but not IL-7 improves the survival of CCR5+CD4+ T cells, drives their expansion, and facilitates HIV-1 infection in vitro and in humanized mice. Our study suggests that IL-15 plays confounding roles in HIV-1 infection, and future studies on the IL-15-based boosting of anti-HIV-1 immunity should carefully exam the potential effects on the expansion of HIV-1 reservoirs in CCR5+CD4+ T cells.

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IL-15 enhances HIV-1 infection by promoting survival and proliferation of CCR5+CD4+ T cells.

Project description:HIV-1 usually utilizes CCR5 as its coreceptor and rarely switches to a CXCR4-tropic virus until the late stage of infection. CCR5+CD4+ T cells are the major virus-producing cells in viremic individuals as well as SIV-infected nonhuman primates. The differentiation of CCR5+CD4+ T cells is associated with the availability of IL-15, which increases during acute HIV-1 infection. Here, we report that CCR5 was expressed by CD4+ T cells exhibiting effector or effector memory phenotypes with high expression levels of the IL-2/IL-15 receptor common β and γ chains. IL-15, but not IL-7, improved the survival of CCR5+CD4+ T cells, drove their expansion, and facilitated HIV-1 infection in vitro and in humanized mice. Our study suggests that IL-15 plays confounding roles in HIV-1 infection, and future studies on the IL-15-based boosting of anti-HIV-1 immunity should carefully examine the potential effects on the expansion of HIV-1 reservoirs in CCR5+CD4+ T cells.

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