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      The regulation of lncRNAs and miRNAs in SARS-CoV-2 infection

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          Abstract

          The coronavirus disease 2019 (COVID-19) was a global endemic that continues to cause a large number of severe illnesses and fatalities. There is increasing evidence that non-coding RNAs (ncRNAs) are crucial regulators of viral infection and antiviral immune response and the role of non-coding RNAs in SARS-CoV-2 infection has now become the focus of scholarly inquiry. After SARS-CoV-2 infection, some ncRNAs’ expression levels are regulated to indirectly control the expression of antiviral genes and viral gene replication. However, some other ncRNAs are hijacked by SARS-CoV-2 in order to help the virus evade the immune system by suppressing the expression of type I interferon (IFN-1) and controlling cytokine levels. In this review, we summarize the recent findings of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) among non-coding RNAs in SARS-CoV-2 infection and antiviral response, discuss the potential mechanisms of actions, and prospects for the detection, treatment, prevention and future directions of SARS-CoV-2 infection research.

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          Most cited references137

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          SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor

          Summary The recent emergence of the novel, pathogenic SARS-coronavirus 2 (SARS-CoV-2) in China and its rapid national and international spread pose a global health emergency. Cell entry of coronaviruses depends on binding of the viral spike (S) proteins to cellular receptors and on S protein priming by host cell proteases. Unravelling which cellular factors are used by SARS-CoV-2 for entry might provide insights into viral transmission and reveal therapeutic targets. Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. A TMPRSS2 inhibitor approved for clinical use blocked entry and might constitute a treatment option. Finally, we show that the sera from convalescent SARS patients cross-neutralized SARS-2-S-driven entry. Our results reveal important commonalities between SARS-CoV-2 and SARS-CoV infection and identify a potential target for antiviral intervention.
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            Landscape of transcription in human cells

            Summary Eukaryotic cells make many types of primary and processed RNAs that are found either in specific sub-cellular compartments or throughout the cells. A complete catalogue of these RNAs is not yet available and their characteristic sub-cellular localizations are also poorly understood. Since RNA represents the direct output of the genetic information encoded by genomes and a significant proportion of a cell’s regulatory capabilities are focused on its synthesis, processing, transport, modifications and translation, the generation of such a catalogue is crucial for understanding genome function. Here we report evidence that three quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations taken together prompt to a redefinition of the concept of a gene.
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              Immunology of COVID-19: current state of the science

              The coronavirus disease 2019 (COVID-19) pandemic, caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has affected millions of people worldwide, igniting an unprecedented effort from the scientific community to understand the biological underpinning of COVID19 pathophysiology. In this review, we summarize the current state of knowledge of innate and adaptive immune responses elicited by SARS-CoV-2 infection and the immunological pathways that likely contribute to disease severity and death. We also discuss the rationale and clinical outcome of current therapeutic strategies as well as prospective clinical trials to prevent or treat SARS-CoV-2 infection.
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                Author and article information

                Contributors
                Journal
                Front Cell Dev Biol
                Front Cell Dev Biol
                Front. Cell Dev. Biol.
                Frontiers in Cell and Developmental Biology
                Frontiers Media S.A.
                2296-634X
                27 July 2023
                2023
                27 July 2023
                : 11
                : 1229393
                Affiliations
                BSL-3 Laboratory (Guangdong) , Guangdong Provincial Key Laboratory of Tropical Disease Research , School of Public Health , Department of Laboratory Medicine , Zhujiang Hospital , Southern Medical University , Guangzhou, China
                Author notes

                Edited by: Shoulong Deng, Chinese Academy of Medical Sciences and Peking Union Medical College, China

                Reviewed by: Qingbing Zheng, Xiamen University, China

                Yang Yang, Shenzhen Third People’s Hospital, China

                *Correspondence: Chenguang Shen, a124965468@ 123456smu.edu.cn ; Wei Zhao, zhaowei@ 123456smu.edu.cn
                [ † ]

                These authors have contributed equally to this work

                Article
                1229393
                10.3389/fcell.2023.1229393
                10416254
                85deea01-dd30-4028-b07f-e623729b02c6
                Copyright © 2023 Lin, Sun, Zhang, Zhao and Shen.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 26 May 2023
                : 20 July 2023
                Funding
                This work was supported by grants from National Natural Science Foundation of China (Grant number 32170939 and 82111530302). Guangdong Basic and Applied Basic Research Foundation (Grant number 2022B1515020075). Shenzhen Science and Technology Innovation Commission for Research and Development Project (Grant number JCYJ20190809183205622). Guangdong Science and Technology Program key projects (No. 2021B1212030014). The Basic Research Project of Key Laboratory of Guangzhou (No. 202102100001).
                Categories
                Cell and Developmental Biology
                Review
                Custom metadata
                Molecular and Cellular Pathology

                sars-cov-2,covid-19,non-coding rna,mirna,lncrna,mechanism
                sars-cov-2, covid-19, non-coding rna, mirna, lncrna, mechanism

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