The landscape of ifn/isg signaling in hiv-1-infected macrophages and its possible role in the hiv-1 latency

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dc.coverageDOI: 10.3390/cells10092378
dc.creatorRojas, Masyelly
dc.creatorLuz-Crawford, Patricia
dc.creatorSoto-Rifo, Ricardo
dc.creatorReyes-Cerpa, Sebastián
dc.creatorToro-Ascuy, Daniela
dc.date2021
dc.date.accessioned2025-11-18T19:54:15Z
dc.date.available2025-11-18T19:54:15Z
dc.description<p>A key characteristic of Human immunodeficiency virus type 1 (HIV-1) infection is the generation of latent viral reservoirs, which have been associated with chronic immune activation and sustained inflammation. Macrophages play a protagonist role in this context since they are persistently infected while being a major effector of the innate immune response through the generation of type-I interferons (type I IFN) and IFN-stimulated genes (ISGs). The balance in the IFN signaling and the ISG induction is critical to promote a successful HIV-1 infection. Classically, the IFNs response is fine-tuned by opposing promotive and suppressive signals. In this context, it was described that HIV-1-infected macrophages can also synthesize some antiviral effector ISGs and, positive and negative regulators of the IFN/ISG signaling. Recently, epitranscriptomic regulatory mechanisms were described, being the N6-methylation (m6A) modification on mRNAs one of the most relevant. The epitranscriptomic regulation can affect not only IFN/ISG signaling, but also type I IFN expression, and viral fitness through modifications to HIV-1 RNA. Thus, the establishment of replication-competent latent HIV-1 infected macrophages may be due to non-classical mechanisms of type I IFN that modulate the activation of the IFN/ISG signaling network.</p>eng
dc.descriptionA key characteristic of Human immunodeficiency virus type 1 (HIV-1) infection is the generation of latent viral reservoirs, which have been associated with chronic immune activation and sustained inflammation. Macrophages play a protagonist role in this context since they are persistently infected while being a major effector of the innate immune response through the generation of type-I interferons (type I IFN) and IFN-stimulated genes (ISGs). The balance in the IFN signaling and the ISG induction is critical to promote a successful HIV-1 infection. Classically, the IFNs response is fine-tuned by opposing promotive and suppressive signals. In this context, it was described that HIV-1-infected macrophages can also synthesize some antiviral effector ISGs and, positive and negative regulators of the IFN/ISG signaling. Recently, epitranscriptomic regulatory mechanisms were described, being the N6-methylation (m6A) modification on mRNAs one of the most relevant. The epitranscriptomic regulation can affect not only IFN/ISG signaling, but also type I IFN expression, and viral fitness through modifications to HIV-1 RNA. Thus, the establishment of replication-competent latent HIV-1 infected macrophages may be due to non-classical mechanisms of type I IFN that modulate the activation of the IFN/ISG signaling network.spa
dc.identifierhttps://investigadores.uandes.cl/en/publications/4899179f-8cd5-40a5-b25d-c6b2aacad855
dc.identifier.urihttps://repositorio.uandes.cl/handle/uandes/58669
dc.languageeng
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourcevol.10 (2021) date: 2021-09-09 nr.9 p.2378
dc.subjectEpitranscriptomic
dc.subjectIFN/ISG response
dc.subjectLatent HIV-1 reservoir
dc.subjectMacrophages
dc.subjectRegulation HIV
dc.subjectEpitranscriptomic
dc.subjectIFN/ISG response
dc.subjectLatent HIV-1 reservoir
dc.subjectMacrophages
dc.subjectRegulation HIV
dc.subjectSDG 3 - Good Health and Well-being
dc.titleThe landscape of ifn/isg signaling in hiv-1-infected macrophages and its possible role in the hiv-1 latencyeng
dc.typeArticleeng
dc.typeArtículospa
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