Caveolae provide a specialized membrane environment for respiratory syncytial virus assembly

Ludwig, Alexander; Nguyen, Tra Huong; Leong, Daniel J.; Ravi, Laxmi Iyer; Tan, Boon Huan; Sandin, Sara; Sugrue, Richard J.

doi:10.1242/jcs.198853

Cited by 23 publications

(26 citation statements)

References 97 publications

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“…Similarly, it was demonstrated that ApoA1 could bind to the Dengue virus and increase its infectivity by promoting its entry into cells, also via SR-BI [98]. This HDL receptor may serve as a receptor for viruses (i.e., the hepatitis C virus) but also appears to be concentrated in cholesterol and sphingolipid-enriched plasma membrane microdomains (lipid rafts) [99], which may serve as a platform for virus entry [100].…”

Section: Hdl and Virusesmentioning

confidence: 99%

High-Density Lipoproteins Are Bug Scavengers

2020

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Lipoproteins were initially defined according to their composition (lipids and proteins) and classified according to their density (from very low- to high-density lipoproteins—HDLs). Whereas their capacity to transport hydrophobic lipids in a hydrophilic environment (plasma) is not questionable, their primitive function of cholesterol transporter could be challenged. All lipoproteins are reported to bind and potentially neutralize bacterial lipopolysaccharides (LPS); this is particularly true for HDL particles. In addition, HDL levels are drastically decreased under infectious conditions such as sepsis, suggesting a potential role in the clearance of bacterial material and, particularly, LPS. Moreover, "omics" technologies have unveiled significant changes in HDL composition in different inflammatory states, ranging from acute inflammation occurring during septic shock to low-grade inflammation associated with moderate endotoxemia such as periodontal disease or obesity. In this review, we will discuss HDL modifications associated with exposure to pathogens including bacteria, viruses and parasites, with a special focus on sepsis and the potential of HDL therapy in this context. Low-grade inflammation associated with atherosclerosis, periodontitis or metabolic syndrome may also highlight the protective role of HDLs in theses pathologies by other mechanisms than the reverse transport of cholesterol.

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Section: Hdl and Virusesmentioning

confidence: 99%

High-Density Lipoproteins Are Bug Scavengers

2020

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“…Caveolae are a special subset of lipid rafts (LR) with a distinctive omega shape ranging from 50 to 100 nm in diameter [43–46]. The principal component of caveolae is Caveolin 1 (Cav1) [45,47].…”

Section: Introductionmentioning

confidence: 99%

“…Caveolae have been identified as PM domains that recruit calcium regulatory components [44,46], even more it has been reported that in airway smooth muscle (ASM), the PM fraction enriched in caveolae contains several calcium regulatory proteins and that silencing Cav1 reduces SOCE [19,49]. Also, the interplay between Cav1 and SOCE during Xenopus egg meiosis has been reported [14,47].…”

Section: Introductionmentioning

confidence: 99%

Cholesterol modulates the cellular localization of Orai1 channels and its disposition among membrane domains

Bohórquez-Hernández

Gratton

Pacheco

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Store Operated Calcium Entry (SOCE) is one of the most important mechanisms for calcium mobilization in to the cell. Two main proteins sustain SOCE: STIM1 that acts as the calcium sensor in the endoplasmic reticulum (ER) and Orai1 responsible for calcium influx upon depletion of ER. There are many studies indicating that SOCE is modulated by the cholesterol content of the plasma membrane (PM). However, a myriad of questions remain unanswered concerning the precise molecular mechanism by which cholesterol modulates SOCE. In the present study we found that reducing PM cholesterol results in the internalization of Orai1 channels, which can be prevented by overexpressing caveolin 1 (Cav1). Furthermore, Cav1 and Orai1 associate upon SOCE activation as revealed by FRET and coimmunoprecipitation assays. The effects of reducing cholesterol were not limited to an increased rate of Orai1 internalization, but also, affects the lateral movement of Orai1, inducing movement in a linear pattern (unobstructed diffusion) opposite to basal cholesterol conditions were most of Orai1 channels moves in a confined space, as assessed by Fluorescence Correlation Spectroscopy, Cav1 overexpression inhibited these alterations maintaining Orai1 into a confined and partially confined movement. These results not only highlight the complex effect of cholesterol regulation on SOCE, but also indicate a direct regulatory effect on Orai1 localization and compartmentalization by this lipid.

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“…Additionally, RSV G interacts with both RSV M and F protein, which appears to be required for complete virion assembly 26 , 27 . During initial virus entry, RSV glycoproteins have been shown to internalize via clathrin-mediated endocytosis, whereas caveolin is heavily incorporated into the envelope of mature RSV filaments 28 – 31 . RSV G was also found to be cleaved in the Vero cell line during endosomal recycling, and has been implicated in the maturation and egress of RSV 3 , 5 , 29 , 32 .…”

Section: Introductionmentioning

confidence: 99%

RSV glycoprotein and genomic RNA dynamics reveal filament assembly prior to the plasma membrane

et al. 2017

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The human respiratory syncytial virus G protein plays an important role in the entry and assembly of filamentous virions. Here, we report the use of fluorescently labeled soybean agglutinin to selectively label the respiratory syncytial virus G protein in living cells without disrupting respiratory syncytial virus infectivity or filament formation and allowing for interrogations of respiratory syncytial virus virion assembly. Using this approach, we discovered that plasma membrane-bound respiratory syncytial virus G rapidly recycles from the membrane via clathrin-mediated endocytosis. This event is then followed by the dynamic formation of filamentous and branched respiratory syncytial virus particles, and assembly with genomic ribonucleoproteins and caveolae-associated vesicles prior to re-insertion into the plasma membrane. We demonstrate that these processes are halted by the disruption of microtubules and inhibition of molecular motors. Collectively, our results show that for respiratory syncytial virus assembly, viral filaments are produced and loaded with genomic RNA prior to insertion into the plasma membrane.

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Caveolae provide a specialized membrane environment for respiratory syncytial virus assembly

Cited by 23 publications

References 97 publications

High-Density Lipoproteins Are Bug Scavengers

High-Density Lipoproteins Are Bug Scavengers

Cholesterol modulates the cellular localization of Orai1 channels and its disposition among membrane domains

RSV glycoprotein and genomic RNA dynamics reveal filament assembly prior to the plasma membrane

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