Nature, Journal Year: 2015, Volume and Issue: 529(7584), P. 48 - 53
Published: Dec. 23, 2015
Language: Английский
Nature Reviews Molecular Cell Biology, Journal Year: 2017, Volume and Issue: 18(7), P. 407 - 422
Published: May 17, 2017
Language: Английский
Citations
1033
Nature Reviews Molecular Cell Biology, Journal Year: 2015, Volume and Issue: 16(3), P. 167 - 177
Published: Feb. 18, 2015
Language: Английский
Citations
810
Gut, Journal Year: 2015, Volume and Issue: 64(12), P. 1972 - 1984
Published: June 5, 2015
At least 250 million people worldwide are chronically infected with HBV, a small hepatotropic DNA virus that replicates through reverse transcription. Chronic infection greatly increases the risk for terminal liver disease. Current therapies rarely achieve cure due to refractory nature of an intracellular viral replication intermediate termed covalently closed circular (ccc) DNA. Upon infection, cccDNA is generated as plasmid-like episome in host cell nucleus from protein-linked relaxed (RC) genome incoming virions. Its fundamental role template all RNAs, and consequence new Biosynthesis RC-DNA by transcription pregenomic RNA now understood considerable detail, yet conversion still obscure, foremostly lack feasible, cccDNA-dependent assay systems. Conceptual recent experimental data link formation cellular repair, which increasingly appreciated critical interface between cells viruses. Together vitro HBV systems, based on identification bile acid transporter sodium taurocholate cotransporting polypeptide entry receptor, this offers novel opportunities decipher, eventually interfere with, persistence reservoir. After brief overview infectious cycle, review aims summarise current knowledge molecular biology, highlight restrictions have hitherto hampered faster progress discuss target new, potentially curative chronic hepatitis B.
Language: Английский
Citations
796
Nature Reviews Molecular Cell Biology, Journal Year: 2017, Volume and Issue: 18(3), P. 141 - 158
Published: Jan. 5, 2017
Language: Английский
Citations
484
Frontiers in Immunology, Journal Year: 2019, Volume and Issue: 10
Published: Oct. 30, 2019
Sepsis is a deadly inflammatory syndrome caused by an exaggerated immune response to infection. Much has been focused on host pathogens mediated through the interaction of pathogen-associated molecular patterns (PAMPs) and pattern recognition receptors (PRRs). PRRs are also activated nuclear, mitochondrial, cytosolic proteins, known as damage-associated (DAMPs) that released from cells during sepsis. Some well described members DAMP family extracellular cold-inducible RNA-binding protein (eCIRP), high mobility group box 1 (HMGB1), histones, adenosine triphosphate (ATP). DAMPs cell inflammasome activation or passively following death. Similarly, neutrophil traps (NETs) neutrophils inflammation. NETs webs DNA decorated with myeloperoxidase, elastase. Although contribute pathogen clearance, excessive NET formation promotes inflammation tissue damage in Here, we review their crosstalk sepsis respect sources, activation, release, function. A clear understating DAMPs, crucial for understanding pathophysiology development novel therapeutics.
Language: Английский
Citations
472
Nature Reviews Molecular Cell Biology, Journal Year: 2017, Volume and Issue: 18(9), P. 548 - 562
Published: May 24, 2017
Language: Английский
Citations
461
Nature Reviews Molecular Cell Biology, Journal Year: 2017, Volume and Issue: 18(4), P. 263 - 273
Published: March 1, 2017
Language: Английский
Citations
451
Nature Genetics, Journal Year: 2016, Volume and Issue: 48(10), P. 1273 - 1278
Published: Aug. 29, 2016
Language: Английский
Citations
368
Nature Reviews Molecular Cell Biology, Journal Year: 2018, Volume and Issue: 19(7), P. 436 - 450
Published: April 23, 2018
Language: Английский
Citations
367
Nature Reviews Molecular Cell Biology, Journal Year: 2018, Volume and Issue: 19(7), P. 464 - 478
Published: May 8, 2018
Language: Английский
Citations
365