Selected article for: "cell surface and receptor cycle"

Author: Dai, Xiaofeng; Hakizimana, Olivier; Zhang, Xuanhao; Kaushik, Aman Chandra; Zhang, Jianying
Title: Orchestrated efforts on host network hijacking: Processes governing virus replication
  • Document date: 2020_2_12
  • ID: 1dc46btc_36
    Snippet: Viral entry is an early step of the virus life cycle, where lipids can serve as the attachment factor, internalization receptor, or transportation shuttle ( Figure 5 ). The ionic interactions between the virion and cell surface glycosphingolipids aid a number of enveloped and non-enveloped viruses in their entry, as the adhesion of virions to cell membrane permits them to be recognized by the specific internalization receptors [115] . For instanc.....
    Document: Viral entry is an early step of the virus life cycle, where lipids can serve as the attachment factor, internalization receptor, or transportation shuttle ( Figure 5 ). The ionic interactions between the virion and cell surface glycosphingolipids aid a number of enveloped and non-enveloped viruses in their entry, as the adhesion of virions to cell membrane permits them to be recognized by the specific internalization receptors [115] . For instance, the infection of subgroup D viruses of adenoviruses occurs after binding to α (2-3)-linked sialic acid (SA), a common carbohydrate component of glycolipids [116] , and uses a positive feedback loop between virus uncoating and lipid signaling for efficient membrane penetration [117] . Many RNA viruses and some DNA viruses use lipids such as low-density lipoprotein receptors (LDLR), phospholipids, and gangliosides for entry [118] . For example, glycosphingolipids are indispensable during the entry of parvovirus [119] , gangliosides are required for the entry of SV40 [120] , LDLR are used by several positive sense RNA viruses including HCV during infection [121] . In addition, viruses such as the double DNA simian virus 40 (SV40) and positive sense RNA echovirus type 1 (EV1) invade cells via caveolinmediated endocytosis [122] . As caveolins directly bind and concentrate cholesterols and glycol-sphingolipids as well as lipid-modified signaling molecules such as Src-like kinases, eNOS, H-Ras, and heterotrimeric G proteins [123] , caveolin-mediated endocytosis during viral invasion considerably enlarges the pool of viruses employing lipids for infection.

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