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The Landscape of IFN/ISG Signaling in HIV-1-Infected Macrophages and Its Possible Role in the HIV-1 Latency.
Rojas, Masyelly; Luz-Crawford, Patricia; Soto-Rifo, Ricardo; Reyes-Cerpa, Sebastián; Toro-Ascuy, Daniela.
Afiliação
  • Rojas M; Facultad de Ciencias de la Salud, Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago 8910060, Chile.
  • Luz-Crawford P; Centro de Investigación e Innovación Biomédica, Facultad de Medicina, Universidad de los Andes, Santiago 7620001, Chile.
  • Soto-Rifo R; Centro de Investigación e Innovación Biomédica, Facultad de Medicina, Universidad de los Andes, Santiago 7620001, Chile.
  • Reyes-Cerpa S; Molecular and Cellular Virology Laboratory, Virology Program, Faculty of Medicine, Institute of Biomedical Sciences, Universidad of Chile, Santiago 8389100, Chile.
  • Toro-Ascuy D; Centro de Genómica y Bioinformática, Facultad de Ciencias, Universidad Mayor, Santiago 8580745, Chile.
Cells ; 10(9)2021 09 09.
Article em En | MEDLINE | ID: mdl-34572027
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interferon Tipo I / Infecções por HIV / Interferons / Latência Viral / Macrófagos Limite: Animals / Humans Idioma: En Revista: Cells Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Chile País de publicação: Suíça

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interferon Tipo I / Infecções por HIV / Interferons / Latência Viral / Macrófagos Limite: Animals / Humans Idioma: En Revista: Cells Ano de publicação: 2021 Tipo de documento: Article País de afiliação: Chile País de publicação: Suíça