Mouse hepatitis virus strain A59 is released from opposite sides of different epithelial cell types.

Rossen, John W. A.; Strous, G J; Horzinek, Marian C.; Rottier, Peter J. M.

doi:10.1099/0022-1317-78-1-61

Cited by 15 publications

(18 citation statements)

References 37 publications

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“…In contrast, mouse hepatitis virus strain A59, a well-studied murine coronavirus, preferentially infects from the apical surface and buds from the basolateral surface of porcine kidney or human colon carcinoma cells expressing the recombinant MHV receptor and murine kidney epithelial cells. However, the same mouse virus almost exclusively infects and (23,24). We found that HCoV-229E efficiently infected differentiated airway epithelia from the apical surface and also preferentially exited through the same surface.…”

Section: Discussionmentioning

confidence: 77%

“…In polarized CaCo-2 intestinal epithelia, HCoV-229E also preferentially infects and exits via the apical surface (D. M. Blau and K. V. Holmes, unpublished data). The mechanism specifying directional release of virions that bud at intracellular membranes is unclear (23,24). Perhaps through evolution the respiratory and enteric coronaviruses adopted an optimal means to spread to neighboring epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

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Human Coronavirus 229E Infects Polarized Airway Epithelia from the Apical Surface

Wang

Deering

Macke

et al. 2000

J Virol

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Gene transfer to differentiated airway epithelia with existing viral vectors is very inefficient when they are applied to the apical surface. This largely reflects the polarized distribution of receptors on the basolateral surface. To identify new receptor-ligand interactions that might be used to redirect vectors to the apical surface, we investigated the process of infection of airway epithelial cells by human coronavirus 229E (HCoV-229E), a common cause of respiratory tract infections. Using immunohistochemistry, we found the receptor for HCoV-229E (CD13 or aminopeptidase N) localized mainly to the apical surface of airway epithelia. When HCoV-229E was applied to the apical or basolateral surface of well-differentiated primary cultures of human airway epithelia, infection primarily occurred from the apical side. Similar results were noted when the virus was applied to cultured human tracheal explants. Newly synthesized virions were released mainly to the apical side. Thus, HCoV-229E preferentially infects human airway epithelia from the apical surface. The spike glycoprotein that mediates HCoV-229E binding and fusion to CD13 is a candidate for pseudotyping retroviral envelopes or modifying other viral vectors.While gene transfer is considered the most direct means to treat or prevent the lung disease associated with cystic fibrosis, several barriers prevent the practical application of this approach (36). A problem that currently limits efficient gene transfer to airway epithelia is that the receptor in most cases is localized to the basolateral surface. This has been demonstrated for several retroviral envelopes (32, 33), adenovirus (19,31,34), and adeno-associated virus (7). Thus, the mere fact that a viral vector is derived from a respiratory pathogen does not imply that it will efficiently transduce airway epithelia via the apical surface.As a first step in identifying novel ligand-receptor interactions that might be exploited to direct vectors to the apical surface of airway epithelia, we studied the infection process of human coronavirus 229E (HCoV-229E) in well-differentiated airway epithelia. Human coronaviruses are enveloped, plusstranded RNA viruses represented by the two serologically unrelated strains, HCoV-229E and HCoV-OC43, that cause mainly upper respiratory tract infections (3, 16). Epidemiological data demonstrate that the HCoV infections are responsible for approximately one-third of common colds (17, 35). HCoV-229E contains a genomic RNA of 27,277 nucleotides, a nucleocapsid (N) protein and a lipid envelope with three major membrane proteins. The three membrane proteins are the membrane (M) glycoprotein, the envelope (E) protein, and the surface spike (S) glycoprotein (11).We selected HCoV-229E for our studies for several reasons. First, it is a common cause of respiratory infections in humans (16). Second, the viral proteins involved in cell binding and the host cell glycoprotein that serves as the receptor have been identified (20,38). Third, infection by HCoV-229E involves both binding ...

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Human Coronavirus 229E Infects Polarized Airway Epithelia from the Apical Surface

Wang

Deering

Macke

et al. 2000

J Virol

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“…A similar situation is found with Coronaviridae and Togaviridae. Infection of different epithelial cells with the mouse hepatitis virus resulted in budding from different membrane compartments (32). Also, infection of two different epithelial cell types with Semliki Forest virus or Sindbis virus gave rise to virus release from either the apical or basolateral membrane, depending on the cell type (55).…”

Section: Discussionmentioning

confidence: 99%

Sorting of Marburg Virus Surface Protein and Virus Release Take Place at Opposite Surfaces of Infected Polarized Epithelial Cells

Sänger

Mühlberger

Ryabchikova

et al. 2001

J Virol

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Marburg virus, a filovirus, causes severe hemorrhagic fever with hitherto poorly understood molecular pathogenesis. We have investigated here the vectorial transport of the surface protein GP of Marburg virus in polarized epithelial cells. To this end, we established an MDCKII cell line that was able to express GP permanently (MDCK-GP). The functional integrity of GP expressed in these cells was analyzed using vesicular stomatitis virus pseudotypes. Further experiments revealed that GP is transported in MDCK-GP cells mainly to the apical membrane and is released exclusively into the culture medium facing the apical membrane. When MDCKII cells were infected with Marburg virus, the majority of GP was also transported to the apical membrane, suggesting that the protein contains an autonomous apical transport signal. Release of infectious progeny virions, however, took place exclusively at the basolateral membrane of the cells. Thus, vectorial budding of Marburg virus is presumably determined by factors other than the surface protein.

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“…Cells of human, primate and rodent origin are described to be susceptible for hantavirus infection [11,34,35]. Viruses also show differences in the mechanism and site of entry/release in different epithelial cells [36-39]. MDCK cells are a well established cell culture model to study trafficking and viral pathogenesis in epithelial cells [19,40,41].…”

Section: Discussionmentioning

confidence: 99%

Polar release of pathogenic Old World hantaviruses from renal tubular epithelial cells

Krautkrämer

Lehmann

Bollinger

et al. 2012

Virol J

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BackgroundEpithelio- and endotheliotropic viruses often exert polarized entry and release that may be responsible for viral spread and dissemination. Hantaviruses, mostly rodent-borne members of the Bunyaviridae family infect epithelial and endothelial cells of different organs leading to organ dysfunction or even failure. Endothelial and renal epithelial cells belong to the target cells of Old World hantavirus. Therefore, we examined the release of hantaviruses in several renal epithelial cell culture models. We used Vero cells that are commonly used in hantavirus studies and primary human renal epithelial cells (HREpC). In addition, we analyzed MDCKII cells, an epithelial cell line of a dog kidney, which represents a widely accepted in vitro model of polarized monolayers for their permissiveness for hantavirus infection.ResultsVero C1008 and primary HREpCs were grown on porous-support filter inserts for polarization. Monolayers were infected with hantavirus Hantaan (HTNV) and Puumala (PUUV) virus. Supernatants from the apical and basolateral chamber of infected cells were analyzed for the presence of infectious particles by re-infection of Vero cells. Viral antigen and infectious particles of HTNV and PUUV were exclusively detected in supernatants collected from the apical chamber of infected Vero C1008 cells and HREpCs. MDCKII cells were permissive for hantavirus infection and polarized MDCKII cells released infectious hantaviral particles from the apical surface corresponding to the results of Vero and primary human epithelial cells.ConclusionsPathogenic Old World hantaviruses are released from the apical surface of different polarized renal epithelial cells. We characterized MDCKII cells as a suitable polarized cell culture model for hantavirus infection studies.

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Mouse hepatitis virus strain A59 is released from opposite sides of different epithelial cell types.

Cited by 15 publications

References 37 publications

Human Coronavirus 229E Infects Polarized Airway Epithelia from the Apical Surface

Human Coronavirus 229E Infects Polarized Airway Epithelia from the Apical Surface

Sorting of Marburg Virus Surface Protein and Virus Release Take Place at Opposite Surfaces of Infected Polarized Epithelial Cells

Polar release of pathogenic Old World hantaviruses from renal tubular epithelial cells

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