Hepatitis C Virus entry: the early steps in the viral replication cycle

Sabahi, Ali

doi:10.1186/1743-422x-6-117

Cited by 34 publications

(25 citation statements)

References 130 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Kinetics of entry inhibition HCV entry into hepatocytes is a multi-step process that begins with virus binding to the cell followed by post-binding events involving several specific entry factors, including SR-BI, CD81, claudin 1 (CLDN1), and occludin (OCLN) for recent review [37]. Kinetic inhibition assays, utilizing entry factor inhibitors added at different times following virus binding, were used to determine at what stage of the entry process a factor is involved.…”

Section: Hcvcc Infection Of Hepatocyte Cell Linesmentioning

confidence: 99%

Small molecule scavenger receptor BI antagonists are potent HCV entry inhibitors

Syder

Lee

Zeisel

et al. 2011

Journal of Hepatology

129

108

View full text Add to dashboard Cite

Section: Hcvcc Infection Of Hepatocyte Cell Linesmentioning

confidence: 99%

Small molecule scavenger receptor BI antagonists are potent HCV entry inhibitors

Syder

Lee

Zeisel

et al. 2011

Journal of Hepatology

129

108

View full text Add to dashboard Cite

“…Interestingly, none of these is exclusively expressed on the surface of hepatocytes or other target cells (reviewed in Ref. 17).…”

Section: Lds and Virusesmentioning

confidence: 99%

Emerging Role of Lipid Droplets in Host/Pathogen Interactions

Herker¹,

Ott²

2012

Journal of Biological Chemistry

100

View full text Add to dashboard Cite

Lipid droplets (LDs) are highly dynamic cell organelles involved in energy homeostasis and membrane trafficking. Here, we review how select pathogens interact with LDs. Several RNA viruses use host LDs at different steps of their life cycle. Some intracellular bacteria and parasites usurp host LDs or encode their own lipid biosynthesis machinery, thus allowing production of LDs independently of their host. Although many mechanistic details of host/pathogen LD interactions are unknown, a picture emerges in which the unique cellular architecture and energy stored in LDs are important in the replication of diverse pathogens. Lipid Droplets: More than Just Fat StorageLipid droplets (LDs) 3 are cytoplasmic organelles composed of a hydrophobic core of neutral lipids (triglycerides and cholesterol esters) surrounded by a phospholipid monolayer and a growing list of associated proteins (reviewed in Ref. 1). All cells produce LDs, but the LDs vary significantly in size (i.e. Ͻ1-100 m in diameter), triglyceride/cholesterol ester ratio, and protein decoration depending on the cell type.Several proteins are involved in the generation, maturation, and degradation of LDs. Prominent among these are perilipin, adipocyte differentiation-related protein (ADRP), and TIP47 (tail-interacting protein 47), the founding members of the growing family of LD-associated PAT proteins (reviewed in Ref.2).The turnover of LDs is rapid (e.g. 24 h in cultured hepatoma cells), with droplets constantly being produced at the endoplasmic reticulum (ER), trafficked through the cytoplasm by kinesin and dynein motors (3), and degraded by the action of lipases such as adipocyte triglyceride lipase and hormone-sensitive lipase, as well as by macroautophagy (4,5). Mitochondria are often found in close proximity to LDs, and membrane bridges between the organelles have been described that might facilitate the efflux of fatty acids toward ␤-oxidation (6). The shielding of LDs through the PAT proteins tightly controls their turnover and the access of lipases (7,8).The prevailing model suggests that LDs originate at the ER, with triglycerides and cholesterol esters accumulating between the bilayer of the ER membrane and the cytosolic layer eventually engulfing the lipid content (1). Support for this model comes from the localization of the enzymes required for neutral lipid synthesis such as the diacylglycerol acyltransferases DGAT1 and DGAT2, which are localized mainly in the ER membrane (reviewed in Ref. 9). DGAT2, but not DGAT1, can also traffic onto LDs when cells are exposed to high levels of fatty acids (10). The detailed mechanisms by which proteins are targeted onto the surface of LDs are only emerging; depending on the protein, the process involves diverse mechanisms such as vesicle-mediated trafficking pathways via COPI (coat protein complex I), lateral diffusion within the ER membrane, or yet to be identified shuttling mechanisms. A mature droplet may bud off the membrane or stay attached to ER membranes that often tightly surround LDs (11). LD bi...

show abstract

“…It is increasingly appreciated that viruses can modulate lipid metabolism, composition, and signaling in the host to facilitate their entry [111][112][113], replication [109,114,115], and assembly [116][117][118][119].…”

Section: Lipoproteins As Double-edged Sword Of the Immune Systemmentioning

confidence: 99%

Plasma Lipoproteins as Crucial Components of Host Defence Against Infections

Bora¹,

Borah²

2017

Advances in Lipoprotein Research

View full text Add to dashboard Cite

Interactions between lipoproteins and infectious microorganisms are diverse and often multifaceted. There is a growing body of evidence which suggests that circulating plasma lipoproteins play an important role in warding off various infections.They are increasingly recognized as vital components of the host immune system. The purpose of this chapter is to provide the reader with an overview of this emerging domain. We review the anti-infective role of different lipoprotein particles and their components and further highlight the known molecular mechanisms involved therein. Instances where lipoproteins facilitate infections instead of protecting against them are also summarized. Finally, broad implications for the future in this active line of research are discussed.

show abstract

Hepatitis C Virus entry: the early steps in the viral replication cycle

Cited by 34 publications

References 130 publications

Small molecule scavenger receptor BI antagonists are potent HCV entry inhibitors

Small molecule scavenger receptor BI antagonists are potent HCV entry inhibitors

Emerging Role of Lipid Droplets in Host/Pathogen Interactions

Plasma Lipoproteins as Crucial Components of Host Defence Against Infections

Contact Info

Product

Resources

About