Herpes Virus Infection of RPE and MDCK Cells: Polarity of Infection

Topp, Kimberly; Rothman, Alana; LaVail, Jennifer H.

doi:10.1006/exer.1996.0209

Cited by 22 publications

(27 citation statements)

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“…Previous studies have reported on HSV infection of epithelial cells by either the basolateral surface (25,38) or by both the apical and basolateral surfaces (16,17,25,39,46,47,55). HSV can apparently enter HaCaT keratinocytes from either the apical or the basolateral surfaces by endocytosis, although the basolateral domain seems to be preferred at low MOI ( Fig.…”

Section: Discussionmentioning

confidence: 85%

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Herpes Simplex Virus Type 1 Enters Human Epidermal Keratinocytes, but Not Neurons, via a pH-Dependent Endocytic Pathway

Nicola

Hou

Major

et al. 2005

J Virol

220

242

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Herpes simplex virus (HSV) enters some laboratory cell lines via a pH-dependent, endocytic mechanism. We investigated whether this entry pathway is used in human cell types relevant to pathogenesis. Three different classes of lysosomotropic agents, which raise endosomal pH, blocked HSV entry into primary and transformed human keratinocytes, but not into human neurons or neuroblastoma lines. In keratinocytes, incoming HSV particles colocalized with markers of endocytic uptake. Treatment with the isoflavone genistein, an inhibitor of protein tyrosine kinases, reduced the delivery of incoming viral particles to the nuclear periphery and virusinduced gene expression in keratinocytes but not neurons. Moreover, in keratinocyte monolayer islets, HSV infected both the inner and outer cells in a genistein-sensitive manner, suggesting viral endocytosis from both basolateral and apical plasma membrane surfaces. Together, the results indicate that HSV enters human epidermal keratinocytes, but not neurons, by a low-pH, endocytic pathway that is dependent on host tyrosine phosphorylation. Thus, HSV utilizes fundamentally different cellular entry pathways to infect important target cell populations.

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Section: Discussionmentioning

confidence: 85%

“…5 and 6). HSV infection of Madin-Darby canine kidney (MDCK) cells is facilitated by disruption of cell junctions, either by mechanical wounding (17,38) or by calcium depletion (17,25,46,55), suggesting that HSV also favors the basolateral surfaces of MDCK cells.…”

Section: Discussionmentioning

confidence: 99%

Herpes Simplex Virus Type 1 Enters Human Epidermal Keratinocytes, but Not Neurons, via a pH-Dependent Endocytic Pathway

Nicola

Hou

Major

et al. 2005

J Virol

220

242

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“…Since release of virus in a basal direction could result in direct transmission to fetal tissue, a more physiologic assessment of a productive HCMV infection of ST would be measurement of basal release. This approach requires culture of ST on semipermeable membranes that allow apical and basal virus diffusion.Semipermeable membrane cell culture models have been used to demonstrate polarized infection by herpes simplex virus type 1 of Madin-Darby canine kidney (MDCK) epithelial cells (21, 49, 50) but not retinal pigment epithelial cells (49,50). HCMV infections in semipermeable membrane cultures of retinal pigment epithelial cells (50) and a colon epithelial…”

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confidence: 99%

mentioning

confidence: 99%

“…Semipermeable membrane cell culture models have been used to demonstrate polarized infection by herpes simplex virus type 1 of Madin-Darby canine kidney (MDCK) epithelial cells (21,49,50) but not retinal pigment epithelial cells (49,50). HCMV infections in semipermeable membrane cultures of retinal pigment epithelial cells (50) and a colon epithelial cell line, Caco-2 (13,27), have been explored (13,27) to com-pare the susceptibilities of apical and basolateral membranes and to investigate directional release of progeny virus.…”

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Polarized Release of Human Cytomegalovirus from Placental Trophoblasts

Hemmings

Guilbert

2002

J Virol

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Human cytomegalovirus (HCMV) is a ubiquitous infectious pathogen that, when transmitted to the fetus in utero, can result in numerous sequelae, including late-onset sensorineural damage. The villous trophoblast, the cellular barrier between maternal blood and fetal tissue in the human placenta, is infected by HCMV in vivo. Primary trophoblasts cultured on impermeable surfaces can be infected by HCMV, but release of progeny virus is delayed and minimal. It is not known whether these epithelial cells when fully polarized can release HCMV and, if so, if release is from the basal membrane surface toward the fetus. We therefore ask whether, and in which direction, progeny virus release occurs from HCMV-infected trophoblasts cultured on semipermeable (3.0-m-pore-size) membranes that allow functional polarization. We show that infectious HCMV readily diffuses across cell-free 3.0-m-pore-size membranes and that apical infection of confluent and multilayered trophoblasts cultured on these membranes reaches cells at the membrane surface. Using two different infection and culture protocols, we found that up to 20% of progeny virus is released but that <1% of released virus is detected in the basal culture chamber. These results suggest that very little, if any, HCMV is released from an infected villous trophoblast into the villous stroma where the virus could ultimately infect the fetus.Human cytomegalovirus (HCMV) is endemic, infecting 40 to 80% of urban populations in developed countries (10). The incidence of congenital HCMV infection is between 0.2 and 2.2% of all live-born infants. Such infections are one of the most common causes of mental retardation and nonhereditary sensorineural deafness in children (46,48). Only 40% of pregnant women with primary HCMV infections give birth to infected infants (47) suggesting an effective fetal barrier, either physical or immunological. How HCMV is transmitted to the fetus during pregnancy is unknown; however, congenital infections are associated with chronic villitis (38, 41) and infection of the placenta (1, 4, 16, 32, 36-39, 41, 44, 45), which may also act as a viral reservoir (19). Passage through the placenta (2, 3) could occur in two directions: through the cytotrophoblast (CT) columns in anchoring villi or across the villous syncytiotrophoblast (ST) in the intervillous space.Infection originating in the uterine wall could lead to infection of extravillous CT involved in either interstitial or endovascular invasion. Infection could then progress in a cell-to-cell manner through the CT columns of anchoring villi to the chorionic stroma and eventually infect the fetus (15). Although this route is possible during a reactivated uterine infection, endovascular CT comes into direct contact with maternal blood and therefore could also be exposed to a primary infection.The ST lines all chorionic villi within the intervillous space, thereby interfacing maternal blood and fetal tissues. The ST is thus positioned to either physically prevent or to actively participate in the dissemina...

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Characterization of a continuous feline mammary epithelial cell line susceptible to feline epitheliotropic viruses

Liu

Ossiboff

Stucker

et al. 2009

Journal of Virological Methods

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Mucosal epithelial cells are the primary targets for many common viral pathogens of cats. Viral infection of epithelia can damage or disrupt the epithelial barrier that protects underlying tissues. In vitro cell culture systems are an effective means to study how viruses infect and disrupt epithelial barriers, however no true continuous or immortalized feline epithelial cell culture lines are available. A continuous cell culture of feline mammary epithelial cells (FMEC UCD-04-2) that forms tight junctions with high transepithelial electrical resistance (>2000Omegacm(-1)) 3-4 days after reaching confluence was characterized. In addition, it was shown that FMECs are susceptible to infection with feline calicivirus (FCV), feline herpesvirus (FHV-1), feline coronavirus (FeCoV), and feline panleukopenia virus (FPV). These cells will be useful for studies of feline viral disease and for in vitro studies of feline epithelia.

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Herpes Virus Infection of RPE and MDCK Cells: Polarity of Infection

Cited by 22 publications

References 0 publications

Herpes Simplex Virus Type 1 Enters Human Epidermal Keratinocytes, but Not Neurons, via a pH-Dependent Endocytic Pathway

Herpes Simplex Virus Type 1 Enters Human Epidermal Keratinocytes, but Not Neurons, via a pH-Dependent Endocytic Pathway

Polarized Release of Human Cytomegalovirus from Placental Trophoblasts

Characterization of a continuous feline mammary epithelial cell line susceptible to feline epitheliotropic viruses

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