ORCID Profile
0000-0002-0707-5588
Current Organisation
Universidade Federal de Minas Gerais
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Publisher: Cold Spring Harbor Laboratory
Date: 13-04-2023
DOI: 10.1101/2023.04.12.536671
Abstract: Splicing is a highly conserved, intricate mechanism intimately linked to transcription elongation, serving as a pivotal regulator of gene expression. Alternative splicing may generate specific transcripts incapable of undergoing translation into proteins, designated as unproductive. A plethora of respiratory viruses, including Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), strategically manipulate the host’s splicing machinery to circumvent antiviral responses. During the infection, SARS-CoV-2 effectively suppresses interferon (IFN) expression, leading to B cell and CD8+ T cell leukopenia, while simultaneously increasing the presence of macrophages and neutrophils in patients with severe COVID-19. In this study, we integrated publicly available omics datasets to systematically analyze transcripts at the isoform level and delineate the nascent-peptide translatome landscapes of SARS-CoV-2-infected human cells. Our findings reveal a hitherto uncharacterized mechanism whereby SARS-CoV-2 infection induces the predominant expression of unproductive splicing isoforms in key IFN signaling genes, interferon-stimulated genes (ISGs), class I MHC genes, and splicing machinery genes, including IRF7, OAS3, HLA-B, and HNRNPH1. In stark contrast, cytokine and chemokine genes, such as IL6, CXCL8, and TNF, predominantly express productive (protein-coding) splicing isoforms in response to SARS-CoV-2 infection. We postulate that SARS-CoV-2 employs a previously unreported tactic of exploiting the host splicing machinery to bolster viral replication and subvert the immune response by selectively upregulating unproductive splicing isoforms from antigen presentation and antiviral response genes. Our study sheds new light on the molecular interplay between SARS-CoV-2 and the host immune system, offering a foundation for the development of novel therapeutic strategies to combat COVID-19.
Publisher: Portland Press Ltd.
Date: 10-2021
DOI: 10.1042/EBC20200072
Abstract: The immune system responds to infection or vaccination through a dynamic and complex process that involves several molecular and cellular factors. Among these factors, long non-coding RNAs (lncRNAs) have emerged as significant players in all areas of biology, particularly in immunology. Most of the mammalian genome is transcribed in a highly regulated manner, generating a ersity of lncRNAs that impact the differentiation and activation of immune cells and affect innate and adaptive immunity. Here, we have reviewed the range of functions and mechanisms of lncRNAs in response to infectious disease, including pathogen recognition, interferon (IFN) response, and inflammation. We describe ex les of lncRNAs exploited by pathogenic agents during infection, which indicate that lncRNAs are a fundamental part of the arms race between hosts and pathogens. We also discuss lncRNAs potentially implicated in vaccine-induced immunity and present ex les of lncRNAs associated with the antibody response of subjects receiving Influenza or Yellow Fever vaccines. Elucidating the widespread involvement of lncRNAs in the immune system will improve our understanding of the factors affecting immune response to different pathogenic agents, to better prevent and treat disease.
Location: Brazil
Location: Brazil
No related grants have been discovered for Izabela Mamede.