Viral piracy of host RNA phosphatase DUSP11 by avipoxviruses DOI Open Access

Kayla H. Szymanik,

Dustin C. Hancks, Christopher S. Sullivan

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Авг. 6, 2024

Proper recognition of viral pathogens is an essential part the innate immune response. A common replicative intermediate and chemical signal that cells use to identify presence a triphosphorylated 5' end (5'ppp) RNA, which activates cytosolic RNA sensor RIG-I initiates downstream antiviral signaling. While 5'pppRNA generated by RNA-dependent polymerases (RdRps) can be potent activator response, endogenous polymerase III (RNAPIII) transcripts retain during transcription induce RIG-I-mediated We have previously shown host triphosphatase dual-specificity phosphatase 11 (DUSP11) act on both RNAs, altering their levels reducing ability activation. Our previous work explored how artificially altered DUSP11 impact activation, prompting further exploration into natural contexts DUSP11. Here, we identified homologs (vDUSP11s) present in some avipoxviruses. Consistent with known functions DUSP11, expression vDUSP11s: 1) reduces RNAPIII transcripts, 2) cell's sensitivity 5'pppRNA-mediated 3) restores virus infection defects seen absence results virus-relevant context where activity has been co-opted alter metabolism influence outcome infection.

Язык: Английский

Viral piracy of host RNA phosphatase DUSP11 by avipoxviruses DOI Creative Commons

Kayla H. Szymanik,

Emily A. Rex,

Vamshikrishna R Pothireddy

и другие.

PLoS Pathogens, Год журнала: 2025, Номер 21(4), С. e1013101 - e1013101

Опубликована: Апрель 21, 2025

Proper recognition of viral pathogens is an essential part the innate immune response. A common replicative intermediate and chemical signal that cells use to identify presence a triphosphorylated 5’ end (5’ppp) RNA, which activates cytosolic RNA sensor RIG-I initiates downstream antiviral signaling. While 5’pppRNA generated by RNA-dependent polymerases (RdRps) can be potent activator response, endogenous polymerase III (RNAPIII) transcripts retain 5’ppp during transcription induce RIG-I-mediated We have previously shown host triphosphatase dual-specificity phosphatase 11 (DUSP11) act on both RNAs, altering their levels reducing ability activation. Our previous work explored how experimentally altered DUSP11 activity impact activation, prompting further exploration into natural contexts activity. Here, we identified homologs (vDUSP11s) present in some avipoxviruses. Consistent with known functions DUSP11, expression vDUSP11s: 1) reduces RNAPIII transcripts, 2) cell’s sensitivity 5’pppRNA-mediated 3) restores virus infection defects seen absence DUSP11. results context where has been co-opted viruses alter metabolism influence outcome infection.

Язык: Английский

Процитировано

0
Innate Immune Recognition of EBV DOI

Jessica Stewart,

Blossom Damania

Current topics in microbiology and immunology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0
Inborn Errors of Nucleic Acid Sensing and Type I Interferon Signaling Determine Viral Susceptibility in Humans DOI
Leslie Naesens, Steven Callens, Tessa Kerre

и другие.

European Journal of Immunology, Год журнала: 2025, Номер 55(5)

Опубликована: Май 1, 2025

The innate immune system relies on nucleic acid (NA) sensors to detect viral infections and trigger type I interferon (IFN-I) responses, which are crucial for antiviral defense. NA pattern recognition receptors RNA or DNA within various cellular compartments, initiating signaling pathways. However, inherited deficiencies in these sensing mechanisms can result increased susceptibility severe infections. This review explores key genetic mutations affecting IFN-I pathways that predispose individuals life-threatening diseases, including herpesviruses, respiratory viruses, enteroviruses, arboviruses, vaccine-strain disseminated diseases. identification of monogenic defects afflicted by infections, along with the observed incomplete penetrance mutations, highlight intricate interplay host's intrinsic, innate, adaptive response invading pathogens. These insights into molecular basis immunity not only underscore clinical challenges associated but also offers opportunity personalized treatment strategies, screening, tailored vaccination protocols, targeted therapies.

Язык: Английский

Процитировано

0
Noncoding RNAs in skeletal development and disorders DOI Creative Commons
Qing Yao, Tailin He, Jian‐You Liao

и другие.

Biological Research, Год журнала: 2024, Номер 57(1)

Опубликована: Апрель 22, 2024

Protein-encoding genes only constitute less than 2% of total human genomic sequences, and 98% genetic information was previously referred to as "junk DNA". Meanwhile, non-coding RNAs (ncRNAs) consist approximately 60% the transcriptional output cells. Thousands ncRNAs have been identified in recent decades, their essential roles regulation gene expression diverse cellular pathways associated with fundamental cell processes, including proliferation, differentiation, apoptosis, metabolism, extensively investigated. Furthermore, networks they form modulate normal development under pathological conditions. In this review, we integrate current about classification, biogenesis, function how these support skeletal through critical signaling vivo. We also summarize updated knowledge involved common diseases disorders, but not limited osteoporosis, osteoarthritis, rheumatoid arthritis, scoliosis, intervertebral disc degeneration, by highlighting established from vivo, vitro, ex vivo studies.

Язык: Английский

Процитировано

2
The Innate Immune Viral Sensors and Their Functional Crosstalk DOI
Ji‐Seung Yoo

Microbiology and Biotechnology Letters, Год журнала: 2024, Номер 52(2), С. 105 - 113

Опубликована: Июнь 2, 2024

Язык: Английский

Процитировано

0
Deficiency of m6A RNA methylation promotes ZBP1-mediated cell death DOI
Shuang Li, Xiangyu Deng, Deepak Pathak

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июнь 30, 2024

Abstract m 6 A RNA methylation suppresses the immunostimulatory potential of endogenous RNA. Deficiency provokes inflammatory responses and cell death, but underlying mechanisms remain elusive. Here we showed that noncoding 7SK gains upon depletion subsequently activates RIG-I/MAVS axis to spark interferon (IFN) signaling cascades. Concomitant excess IFN deficiency synergistically facilitate formation G-quadruplexes (rG4) promote ZBP1-mediated necroptotic death. Collectively, our findings delineate a hitherto uncharacterized mechanism links dysregulation with ZBP1 activity in triggering

Язык: Английский

Процитировано

0
Viral piracy of host RNA phosphatase DUSP11 by avipoxviruses DOI Open Access

Kayla H. Szymanik,

Dustin C. Hancks, Christopher S. Sullivan

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Авг. 6, 2024

Proper recognition of viral pathogens is an essential part the innate immune response. A common replicative intermediate and chemical signal that cells use to identify presence a triphosphorylated 5' end (5'ppp) RNA, which activates cytosolic RNA sensor RIG-I initiates downstream antiviral signaling. While 5'pppRNA generated by RNA-dependent polymerases (RdRps) can be potent activator response, endogenous polymerase III (RNAPIII) transcripts retain during transcription induce RIG-I-mediated We have previously shown host triphosphatase dual-specificity phosphatase 11 (DUSP11) act on both RNAs, altering their levels reducing ability activation. Our previous work explored how artificially altered DUSP11 impact activation, prompting further exploration into natural contexts DUSP11. Here, we identified homologs (vDUSP11s) present in some avipoxviruses. Consistent with known functions DUSP11, expression vDUSP11s: 1) reduces RNAPIII transcripts, 2) cell's sensitivity 5'pppRNA-mediated 3) restores virus infection defects seen absence results virus-relevant context where activity has been co-opted alter metabolism influence outcome infection.

Язык: Английский

Процитировано

0