Recognition of HIV-1 capsid by PQBP1 licenses an innate immune sensing of nascent HIV-1 DNA

Yoh, Sunnie M.; Mamede, João I.; Lau, Derrick; Ahn, Narae; Sánchez-Aparicio, María Teresa; Temple, Joshua; Tuckwell, Andrew; Fuchs, Nina V.; Cianci, Gianguido C.; Riva, Laura; Curry, Heather M.; Yin, Xin; Gambut, Stéphanie; Simons, Lacy M.; Hultquist, Judd F.; König, Renate; Xiong, Yong; García‐Sastre, Adolfo; Böcking, Till; Hope, Thomas J.; Chanda, Sumit K.

doi:10.1016/j.molcel.2022.06.010

Cited by 29 publications

(30 citation statements)

References 66 publications

(123 reference statements)

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“…PAMPs are relatively conserved molecules in the evolution of pathogens. The main PAMPs are the nucleic acids of pathogens, including DNA (unmethylated CpG sequences), double-stranded RNA, single-stranded RNA, 5-triphosphate RNA (5’-ppp RNA), as well as lipoproteins, cell surface glycoproteins, membrane components, and viral capsids ( Tang et al., 2012 ; Yoh et al., 2022 ). DNA is one of the vital genetic materials of the virus, which can release its DNA into the cytoplasm once it has infected the host cell.…”

Section: Introductionmentioning

confidence: 99%

Regulation of cGAS/STING signaling and corresponding immune escape strategies of viruses

Ding

2022

Front. Cell. Infect. Microbiol.

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Innate immunity is the first line of defense against invading external pathogens, and pattern recognition receptors (PRRs) are the key receptors that mediate the innate immune response. Nowadays, there are various PRRs in cells that can activate the innate immune response by recognizing pathogen-related molecular patterns (PAMPs). The DNA sensor cGAS, which belongs to the PRRs, plays a crucial role in innate immunity. cGAS detects both foreign and host DNA and generates a second-messenger cGAMP to mediate stimulator of interferon gene (STING)-dependent antiviral responses, thereby exerting an antiviral immune response. However, the process of cGAS/STING signaling is regulated by a wide range of factors. Multiple studies have shown that viruses directly target signal transduction proteins in the cGAS/STING signaling through viral surface proteins to impede innate immunity. It is noteworthy that the virus utilizes these cGAS/STING signaling regulators to evade immune surveillance. Thus, this paper mainly summarized the regulatory mechanism of the cGAS/STING signaling pathway and the immune escape mechanism of the corresponding virus, intending to provide targeted immunotherapy ideas for dealing with specific viral infections in the future.

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Section: Introductionmentioning

confidence: 99%

Regulation of cGAS/STING signaling and corresponding immune escape strategies of viruses

Ding

2022

Front. Cell. Infect. Microbiol.

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“…In HIV infection, cGAS is the best-studied receptor in host innate immune responses ( Gao et al, 2013 ; Herzner et al, 2015 ; Sumner et al, 2020 ). At first, cGAS protein is recruited to the CA in a polyglutamine-binding protein-1 (PQBP1) or Non-POU (Pit-Oct-Unc) domain-containing octamer-binding protein (NONO)-dependent manner in the cytosol and nucleus respectively, enabling cGAS molecules to recognize the reverse transcriptional product of HIV ( Yoh et al, 2015 , 2022 ; Lahaye et al, 2018 ). Subsequently, cGAS binds to viral dsDNA and produces a second messenger 2′3′cGAMP.…”

Section: Human Immunodeficiency Virus Capsidmentioning

confidence: 99%

Human immunodeficiency virus-1 core: The Trojan horse in virus–host interaction

Wang

Zhang

et al. 2022

Front. Microbiol.

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Human immunodeficiency virus-1 (HIV-1) is the major cause of acquired immunodeficiency syndrome (AIDs) worldwide. In HIV-1 infection, innate immunity is the first defensive line for immune recognition and viral clearance to ensure the normal biological function of the host cell and body health. Under the strong selected pressure generated by the human body over thousands of years, HIV has evolved strategies to counteract and deceive the innate immune system into completing its lifecycle. Recently, several studies have demonstrated that HIV capsid core which is thought to be a protector of the cone structure of genomic RNA, also plays an essential role in escaping innate immunity surveillance. This mini-review summarizes the function of capsid in viral immune evasion, and the comprehensive elucidation of capsid-host cell innate immunity interaction could promote our understanding of HIV-1’s pathogenic mechanism and provide insights for HIV-1 treatment in clinical therapy.

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“…Yoh et al 82 have shown that PQBP1 directly binds to immunogenic reverse‐transcribed HIV‐1 DNA and interacts with cGAS, initiating downstream cascades. Furthermore, Yoh et al 83 have discovered a two‐step authentication immune‐activation system in the host to fight retroviral infection: After HIV‐1 infection occurs, PQBP1 recognizes the HIV‐1 capsid before replication begins. PQBP1 then wraps around and decorates the viral core, serving as an alarm signal to summon cGAS.…”

Section: Hiv‐mediated Cgas–sting Activation and Viral Suppressionmentioning

confidence: 99%

SARS‐CoV‐2, HIV, and HPV: Convergent evolution of selective regulation of cGAS–STING signaling

Shen

Rui

Wang

et al. 2022

Journal of Medical Virology

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Recognizing aberrant cytoplasmic double‐stranded DNA and stimulating innate immunity is essential for the host's defense against viruses and tumors. Cyclic GMP–AMP (cGAMP) synthase (cGAS) is a cytosolic DNA sensor that synthesizes the second messenger 2′3′‐cGAMP and subsequently activates stimulator of interferon genes (STING)‐mediated activation of TANK‐binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3) and the production of type I interferon (IFN‐I). Both the cGAS–STING‐mediated IFN‐I antiviral defense and the countermeasures developed by diverse viruses have been extensively studied. However, recent studies have revealed a convergent evolutionary feature of severe acute respiratory syndrome coronavirus 2 and human immunodeficiency virus (HIV) viral proteins in terms of the selective regulation of cGAS–STING‐mediated nuclear factor‐κB (NF‐κB) signaling without any effect on cGAS–STING‐mediated TBK1/IRF3 activation and IFN production. The potential beneficial effect of this cGAS–STING‐mediated, NF‐κB‐dependent antiviral effect, and the possible detrimental effect of IFN‐I in the pathogenesis of coronavirus disease 2019 and HIV infection deserve more attention and future investigation.

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Recognition of HIV-1 capsid by PQBP1 licenses an innate immune sensing of nascent HIV-1 DNA

Cited by 29 publications

References 66 publications

Regulation of cGAS/STING signaling and corresponding immune escape strategies of viruses

Regulation of cGAS/STING signaling and corresponding immune escape strategies of viruses

Human immunodeficiency virus-1 core: The Trojan horse in virus–host interaction

SARS‐CoV‐2, HIV, and HPV: Convergent evolution of selective regulation of cGAS–STING signaling

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