Abstract
Virus infection has drawn extensive attention since it causes serious or even deadly diseases, consequently inducing a series of social and public health problems. Caveolin-1 is the most important structural protein of caveolae, a membrane invagination widely known for its role in endocytosis and subsequent cytoplasmic transportation. Caveolae/caveolin-1 is tightly associated with a wide range of biological processes, including cholesterol homeostasis, cell mechano-sensing, tumorigenesis, and signal transduction. Intriguingly, the versatile roles of caveolae/caveolin-1 in virus infections have increasingly been appreciated. Over the past few decades, more and more viruses have been identified to invade host cells via caveolae-mediated endocytosis, although other known pathways have been explored. The subsequent post-entry events, including trafficking, replication, assembly, and egress of a large number of viruses, are caveolae/caveolin-1-dependent. Deprivation of caveolae/caveolin-1 by drug application or gene editing leads to abnormalities in viral uptake, viral protein expression, or virion release, whereas the underlying mechanisms remain elusive and must be explored holistically to provide potential novel antiviral targets and strategies. This review recapitulates our current knowledge on how caveolae/caveolin-1 functions in every step of the viral infection cycle and various relevant signaling pathways, hoping to provide a new perspective for future viral cell biology research.
Highlights
Since 2009, the World Health Organization (WHO) has announced a total of six “public health emergencies of international concern”, all of which are related to virus infections [1], indicating the huge threat of virus infections to humankind
Another study has shown that Hepatitis B virus (HBV) infection in HepaRG cells is inhibited by 35% when the cholesterol level is reduced with nystatin (Ny) and MβCD treatment, but not with NH4Cl and bafilomycin A1 (Baf) which effectively block the vacuolar H+ ATPase pumps [24]
Canine respiratory coronavirus (CRCoV; causes an acute intestinal infectious disease characterized by vomiting, diarrhea, dehydration, and recurrence), which is a member of Coronaviridae family, has been reported to hijack caveolae endocytosis to enter HRT-18G cells by using chemical inhibitors of pathways involved in viral entry, small interfering RNA (siRNA), and confocal microscopy assays [39]
Summary
Yifan Xing 1,2,† , Zeyu Wen 1,2,† , Wei Gao 1,2 , Zhekai Lin 1,2 , Jin Zhong 2,3 and Yaming Jiu 1,2, *.
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