CLIC and membrane wound repair pathways enable pandemic norovirus entry and infection

Ayyar, B. Vijayalakshmi; Ettayebi, Khalil; Salmen, Wilhelm; Karandikar, Umesh C.; Neill, Frederick H.; Tenge, Victoria R.; Crawford, Sue E.; Bieberich, Erhard; Prasad, B. V. Venkataram; Atmar, Robert L.; Estes, Mary K.

doi:10.1038/s41467-023-36398-z

Cited by 26 publications

(24 citation statements)

References 78 publications

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“…3B) through an indirect mechanism not yet characterized. These results are consistent with previous studies that have shown effects of cholesterol on GII.3 as well as GII.4 replication (28,34). The average human bile pool only contains trace amounts of highly hydrophobic bile acids like TLCA due to their cytotoxicity at higher concentrations (36,50).…”

Section: Discussionsupporting

confidence: 93%

“…HuNoV (28,34,44,45). We found that addition of cholesterol largely increased VLP binding, but only in the presence of bile acids (Fig.…”

Section: Bile Acids Exert a Direct Effect On Hunov Vlp Binding To Cellsmentioning

confidence: 64%

“…Several such virus-receptor interactions are abolished when disrupting lipid raft formation, such as Vaccinia virus interaction with CD98 (52), and Human herpesvirus 6 interaction with CD46 (53). In a recent study, GII.4 replication in FUT2 expressing human intestinal enteroids was inhibited by MβCD treatment, despite the fact that no bile acids were present (28), suggesting that cholesterol might be important for multiple receptor interaction mechanisms. It is therefore tempting to speculate that receptor clustering by cholesterol mediated lipid raft formation might also be true for HuNoV interactions virus host interaction.…”

Section: Discussionmentioning

confidence: 99%

“…However, some studies have found that secretor-negative individuals can still be infected by HBGA-dependent norovirus genotypes (25)(26)(27). In a recent study it was demonstrated that the Shell (S) domain of VP1 binds to galectin 3 and apoptosis-linked gene 2-interacting protein X (ALIX) (28).…”

Section: Introductionmentioning

confidence: 99%

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Bile acids accumulate norovirus-like particles and enhance binding to and entry into human enteric epithelial cells

Palm

Danskog

Nord

et al. 2023

Preprint

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Human norovirus (HuNoV) is a leading cause of acute viral gastroenteritis, but despite high impact on public health and health care, the mechanisms of viral attachment to and entry into target cells are not yet fully understood. It is well known that body fluids such as blood can transmit unrelated viruses, but recent reports also indicate that saliva and bile contribute to transmission of HuNoV. For example, human bile acids increase cell surface ceramide levels in human enteroids, which improves norovirus entry into cells resulting in enhanced replication. Bile acids can also interact directly with the norovirus capsid, but it is not known whether bile or other gastrointestinal body fluids directly affect HuNoV attachment to host cells. In this study, we investigated the effects of patient-derived gastric juice, pancreatic juice, and bile on HuNoV GII.4 virus-like particle (VLP) attachment to and entry into a human duodenal cell line, HuTu-80. We show that while gastric juice and pancreatic juice do not affect viral attachment or entry, bile – in particular hydrophobic bile acids – significantly enhance cellular attachment and subsequent entry of GII.4 VLPs into cells. In addition, we show that hydrophobic bile acids induce accumulation of viral particles in the vicinity of cells. Our results suggest the presence of a new en masse infection mechanism, where bile acids aggregate virions, and allow direct and more efficient attachment to and entry into target cells.

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Section: Discussionsupporting

confidence: 93%

“…HuNoV (28,34,44,45). We found that addition of cholesterol largely increased VLP binding, but only in the presence of bile acids (Fig.…”

Section: Bile Acids Exert a Direct Effect On Hunov Vlp Binding To Cellsmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bile acids accumulate norovirus-like particles and enhance binding to and entry into human enteric epithelial cells

Palm

Danskog

Nord

et al. 2023

Preprint

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“…Excessive plasma membrane damage or defective plasma membrane repair is involved in many pathological conditions including muscular dystrophy, ischemia-reperfusion, heart failure, chronic inflammation, and neurodegenerative diseases [3]. Pathogens including parasites, bacteria, and viruses use diverse strategies to perforate the host cell plasma membrane and exploit the host cell repair responses to successfully infect their host [4][5][6][7][8][9]. In particular, the bacterial pathogen Listeria monocytogenes uses as a major virulence factor the pore-forming toxin listeriolysin O (LLO).…”

Section: Introductionmentioning

confidence: 99%

The Septin Cytoskeleton is Required for Plasma Membrane Repair

Prislusky,

Lam,

Contreras

et al. 2023

Preprint

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Mammalian cells are frequently exposed to mechanical and biochemical stresses resulting in plasma membrane injuries. Repair mechanisms rapidly reseal the plasma membrane to restore homeostasis and prevent cell death. In the present work, a silencing RNA (siRNA) screen was performed to uncover the plasma membrane repair mechanisms of cells injured by the bacterial pore-forming toxin listeriolysin O (LLO). The screen identified a novel role for the septin cytoskeleton in mediating plasma membrane repair. Upon cell injury, the septin cytoskeleton partially dissociates from actin stress fibers and remodels with cortical F-actin and myosin-II to form loop (and ring)-like domains that protrude from the cell surface. These domains strictly colocalize with the calcium-dependent phospholipid-binding protein, annexin A2 (ANXA2). Importantly, formation of the SEPT/F-actin/ANXA2 domains are dependent on SEPT7 expression and is functionally correlated with the plasma membrane repair efficiency. Our studies open new research avenues by identifying a novel role for the septin cytoskeleton in remodeling the plasma membrane for its repair.

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Membrane Tension Regulation is Required for Wound Repair

Raj,

Weiß,

Vos

et al. 2024

Advanced Science

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Disruptions of the eukaryotic plasma membrane due to chemical and mechanical challenges are frequent and detrimental and thus need to be repaired to maintain proper cell function and avoid cell death. However, the cellular mechanisms involved in wound resealing and restoration of homeostasis are diverse and contended. Here, it is shown that clathrin‐mediated endocytosis is induced at later stages of plasma membrane wound repair following the actual resealing of the wound. This compensatory endocytosis occurs near the wound, predominantly at sites of previous early endosome exocytosis which is required in the initial stage of membrane resealing, suggesting a spatio‐temporal co‐ordination of exo‐ and endocytosis during wound repair. Using cytoskeletal alterations and modulations of membrane tension and membrane area, membrane tension is identified as a major regulator of the wounding‐associated exo‐ and endocytic events that mediate efficient wound repair. Thus, membrane tension changes are a universal trigger for plasma membrane wound repair modulating the exocytosis of early endosomes required for resealing and subsequent clathrin‐mediated endocytosis acting at later stages to restore cell homeostasis and function.

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CLIC and membrane wound repair pathways enable pandemic norovirus entry and infection

Cited by 26 publications

References 78 publications

Bile acids accumulate norovirus-like particles and enhance binding to and entry into human enteric epithelial cells

Bile acids accumulate norovirus-like particles and enhance binding to and entry into human enteric epithelial cells

The Septin Cytoskeleton is Required for Plasma Membrane Repair

Membrane Tension Regulation is Required for Wound Repair

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