Virus entry into a polarized epithelial cell line (MDCK): similarities and dissimilarities between influenza C virus and bovine coronavirus

Schultze, Beate; Zimmer, Gert; Herrler, Georg

doi:10.1099/0022-1317-77-10-2507

Cited by 15 publications

(15 citation statements)

References 40 publications

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“…The entry of CCoV, FECV and FIPV occurs preferentially through the apical side of PKFA-2 cells. This is similar to the entry of other coronaviruses, i.e., bovine coronavirus [7,13], MHV [9] and TGEV [8]. Previously, we have shown that the porcine APN (pAPN) was mainly located on the apical surface of polarized LLC-PK1 cells [8], similar to the apical localization of the human APN in MDCK cells [16].…”

supporting

confidence: 66%

Feline and canine coronaviruses are released from the basolateral side of polarized epithelial LLC-PK1 cells expressing the recombinant feline aminopeptidase-N cDNA

et al. 2001

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In this study feline (FECV and FIPV) and canine (CCoV) coronavirus entry into and release from polarized porcine epithelial LLC-PK1 cells, stably expressing the recombinant feline aminopeptidase-N cDNA, were investigated. Virus entry appeared to occur preferentially through the apical membrane, similar to the entry of the related porcine coronavirus transmissible gastroenteritis virus (TGEV) into these cells. However, whereas TGEV is released apically, feline and canine coronaviruses were found to be released from the basolateral side of the epithelial cells. These observations indicate that local infections as caused by TGEV, FECV and CCoV do not strictly correlate with apical release, as suggested by earlier work.

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confidence: 66%

Feline and canine coronaviruses are released from the basolateral side of polarized epithelial LLC-PK1 cells expressing the recombinant feline aminopeptidase-N cDNA

et al. 2001

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“…Some viruses infect epithelia via the basolateral side (35,42,43), the apical side (44 -48), or both sides (49,50). The sidedness of infection may even vary with maturation of the epithelia.…”

Section: Discussionmentioning

confidence: 99%

Basolateral Localization of Fiber Receptors Limits Adenovirus Infection from the Apical Surface of Airway Epithelia

Walters

Grunst

Bergelson

et al. 1999

Journal of Biological Chemistry

333

304

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Recent identification of two receptors for the adenovirus fiber protein, coxsackie B and adenovirus type 2 and 5 receptor (CAR), and the major histocompatibility complex (MHC) Class I ␣-2 domain allows the molecular basis of adenoviral infection to be investigated. Earlier work has shown that human airway epithelia are resistant to infection by adenovirus. Therefore, we examined the expression and localization of CAR and MHC Class I in an in vitro model of well differentiated, ciliated human airway epithelia. We found that airway epithelia express CAR and MHC Class I. However, neither receptor was present in the apical membrane; instead, both were polarized to the basolateral membrane. These findings explain the relative resistance to adenovirus infection from the apical surface. In contrast, when the virus was applied to the basolateral surface, gene transfer was much more efficient because of an interaction of adenovirus fiber with its receptors. In addition, when the integrity of the tight junctions was transiently disrupted, apically applied adenovirus gained access to the basolateral surface and enhanced gene transfer. These data suggest that the receptors required for efficient infection are not available on the apical surface, and interventions that allow access to the basolateral space where fiber receptors are located increase gene transfer efficiency.The mechanism of infection by type 2 and type 5 adenovirus has been extensively studied. However, most of the knowledge on adenoviral infection has been obtained from studies done on immortalized cell lines. The first steps in adenovirus infection are thought to involve primarily two proteins in the capsid, fiber and penton base (1-3). The fiber protein is important for binding to a high affinity fiber receptor. In a human oral epidermoid carcinoma cell line (KB cells), A549 cells, and HeLa cells, this receptor is thought to be present in the range of 3,000 -10,000 receptors/cell (4 -6). NIH 3T3 cells, which are resistant to adenovirus infection, have less than 100 receptors/ cell (7). After binding to the fiber receptor, penton base interaction with ␣ V ␤ 3 and ␣ V ␤ 5 integrins facilitates internalization via receptor-mediated endocytosis (2,8,9). The acidic pH the virus encounters in the endosome may trigger a conformational change that releases the virus into the cytoplasm (10 -12) and allows the adenovirus capsid to travel to the nucleus (2, 13). Then viral proteins and DNA bind to the nuclear pore complex, capsid disassembly continues, and DNA enters the nucleus accompanied by DNA-associated protein 7 (1, 2, 14). These studies have concluded that a high affinity fiber receptor is required for binding and infection and that an ␣ V ␤ integrin acts as a co-receptor.We and others (15-22) have found infection of ciliated airway epithelia by adenovirus to be inefficient. In an in vitro model of human airway epithelia, we found that unlike infections of HeLa cells adenovirus infection of ciliated airway epithelia was quite limited and that which did occur w...

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“…The most studied human coronavirus, SARS-CoV, causes severe acute respiratory syndrome (SARS) and its original major outbreak is thought to have originated as a zoonosis from a bat coronavirus. Like most coronaviruses, SARS-CoV infects polarized epithelium specifically through the apical cell membrane [241][242][243]. The virus envelope protein (E) has a C-terminal PBM, through which it binds to the cellular PALS protein [244], a component of the Crumbs polarity complex that defines the apical domain, and controls the establishment of apicobasal polarity and the formation of TJs.…”

Section: Coronavirusesmentioning

confidence: 99%

Upsetting the Balance: When Viruses Manipulate Cell Polarity Control

Thomas

Banks

2018

Journal of Molecular Biology

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The central importance of cell polarity control is emphasized by the frequency with which it is targeted by many diverse viruses. It is clear that in targeting key polarity control proteins, viruses affect not only host cell polarity, but also influence many cellular processes, including transcription, replication, and innate and acquired immunity. Examination of the interactions of different virus proteins with the cell and its polarity controls during the virus life cycles, and in virally-induced cell transformation shows ever more clearly how intimately all cellular processes are linked to the control of cell polarity.

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Virus entry into a polarized epithelial cell line (MDCK): similarities and dissimilarities between influenza C virus and bovine coronavirus

Cited by 15 publications

References 40 publications

Feline and canine coronaviruses are released from the basolateral side of polarized epithelial LLC-PK1 cells expressing the recombinant feline aminopeptidase-N cDNA

Feline and canine coronaviruses are released from the basolateral side of polarized epithelial LLC-PK1 cells expressing the recombinant feline aminopeptidase-N cDNA

Basolateral Localization of Fiber Receptors Limits Adenovirus Infection from the Apical Surface of Airway Epithelia

Upsetting the Balance: When Viruses Manipulate Cell Polarity Control

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