HIV-1 Is a Poor Inducer of Innate Immune Responses

ABSTRACT Effective host immune responses against viral infection rely on the detection of the virus, activation of downstream signaling pathways, and the secretion of interferons (IFNs) and other cytokines. Many viruses can potently stimulate these responses, whereas the immune response against huma...

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Autores principales:	Oya Cingöz, Stephen P. Goff
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2019
Materias:	HIV-1 innate immunity interferon-stimulated genes interferons Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/f20d19c90cc44177b60f48cfb5900951
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spelling	oai:doaj.org-article:f20d19c90cc44177b60f48cfb59009512021-11-15T15:55:14ZHIV-1 Is a Poor Inducer of Innate Immune Responses10.1128/mBio.02834-182150-7511https://doaj.org/article/f20d19c90cc44177b60f48cfb59009512019-02-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.02834-18https://doaj.org/toc/2150-7511ABSTRACT Effective host immune responses against viral infection rely on the detection of the virus, activation of downstream signaling pathways, and the secretion of interferons (IFNs) and other cytokines. Many viruses can potently stimulate these responses, whereas the immune response against human immunodeficiency virus type 1 (HIV-1) remains relatively less well characterized. Here we show that HIV-1 infection with reporter viruses does not activate sensing pathways in cell lines and primary cells that are otherwise responsive to foreign nucleic acids. After entry into cells, reverse transcription and reporter expression occur without the virus ever being detected by cellular sensors or stimulating an interferon response. Using multiple methods, including the use of reporter cell lines for type I IFN and NF-κB pathway activation, quantifying mRNA levels for IFN-stimulated genes (ISGs), and assaying for markers of innate immune activation, we show that single-round pseudotyped HIV-1-based reporter viruses fail to induce innate immune responses. IMPORTANCE Human immunodeficiency virus type 1 (HIV-1) continues to be a major burden to human health worldwide. How infected cells recognize and respond to HIV-1 infection is important in order to better understand the biology of the virus and the cellular pathways activated upon infection and to identify potential targets that interfere with viral replication. In this study, we investigated innate immune responses of different cell types following infection with single-cycle (replication-defective) HIV-1 reporter virus. We report that infection with a commonly used HIV-1 strain (lacking the env, nef, and vpr genes) does not measurably activate cellular defense mechanisms and that the virus is able to avoid recognition by cellular sensors.Oya CingözStephen P. GoffAmerican Society for MicrobiologyarticleHIV-1innate immunityinterferon-stimulated genesinterferonsMicrobiologyQR1-502ENmBio, Vol 10, Iss 1 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	HIV-1 innate immunity interferon-stimulated genes interferons Microbiology QR1-502
spellingShingle	HIV-1 innate immunity interferon-stimulated genes interferons Microbiology QR1-502 Oya Cingöz Stephen P. Goff HIV-1 Is a Poor Inducer of Innate Immune Responses
description	ABSTRACT Effective host immune responses against viral infection rely on the detection of the virus, activation of downstream signaling pathways, and the secretion of interferons (IFNs) and other cytokines. Many viruses can potently stimulate these responses, whereas the immune response against human immunodeficiency virus type 1 (HIV-1) remains relatively less well characterized. Here we show that HIV-1 infection with reporter viruses does not activate sensing pathways in cell lines and primary cells that are otherwise responsive to foreign nucleic acids. After entry into cells, reverse transcription and reporter expression occur without the virus ever being detected by cellular sensors or stimulating an interferon response. Using multiple methods, including the use of reporter cell lines for type I IFN and NF-κB pathway activation, quantifying mRNA levels for IFN-stimulated genes (ISGs), and assaying for markers of innate immune activation, we show that single-round pseudotyped HIV-1-based reporter viruses fail to induce innate immune responses. IMPORTANCE Human immunodeficiency virus type 1 (HIV-1) continues to be a major burden to human health worldwide. How infected cells recognize and respond to HIV-1 infection is important in order to better understand the biology of the virus and the cellular pathways activated upon infection and to identify potential targets that interfere with viral replication. In this study, we investigated innate immune responses of different cell types following infection with single-cycle (replication-defective) HIV-1 reporter virus. We report that infection with a commonly used HIV-1 strain (lacking the env, nef, and vpr genes) does not measurably activate cellular defense mechanisms and that the virus is able to avoid recognition by cellular sensors.
format	article
author	Oya Cingöz Stephen P. Goff
author_facet	Oya Cingöz Stephen P. Goff
author_sort	Oya Cingöz
title	HIV-1 Is a Poor Inducer of Innate Immune Responses
title_short	HIV-1 Is a Poor Inducer of Innate Immune Responses
title_full	HIV-1 Is a Poor Inducer of Innate Immune Responses
title_fullStr	HIV-1 Is a Poor Inducer of Innate Immune Responses
title_full_unstemmed	HIV-1 Is a Poor Inducer of Innate Immune Responses
title_sort	hiv-1 is a poor inducer of innate immune responses
publisher	American Society for Microbiology
publishDate	2019
url	https://doaj.org/article/f20d19c90cc44177b60f48cfb5900951
work_keys_str_mv	AT oyacingoz hiv1isapoorinducerofinnateimmuneresponses AT stephenpgoff hiv1isapoorinducerofinnateimmuneresponses
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HIV-1 Is a Poor Inducer of Innate Immune Responses

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