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      Infectious entry of equine herpesvirus-1 into host cells through different endocytic pathways

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          Abstract

          We investigated the mechanism by which equine herpesvirus-1 (EHV-1) enters primary cultured equine brain microvascular endothelial cells (EBMECs) and equine dermis (E. Derm) cells. EHV-1 colocalized with caveolin in EBMECs and the infection was greatly reduced by the expression of a dominant negative form of equine caveolin-1 (ecavY14F), suggesting that EHV-1 enters EBMECs via caveolar endocytosis. EHV-1 entry into E. Derm cells was significantly reduced by ATP depletion and treatments with lysosomotropic agents. Enveloped virions were detected from E. Derm cells by infectious virus recovery assay after viral internalization, suggesting that EHV-1 enters E. Derm cells via energy- and pH-dependent endocytosis. These results suggest that EHV-1 utilizes multiple endocytic pathways in different cell types to establish productive infection.

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          Infectious entry pathway of influenza virus in a canine kidney cell line

          K. Simons, A Helenius, KS Matlin (1981)
          The entry of fowl plague virus, and avian influenza A virus, into Madin- Darby canine kidney (MDCK) cells was examined both biochemically and morphologically. At low multiplicity and 0 degrees C, viruses bound to the cell surface but were not internalized. Binding was not greatly dependent on the pH of the medium and reached an equilibrium level in 60-90 min. Over 90% of the bound viruses were removed by neuraminidase but not by proteases. When cells with prebound virus were warmed to 37 degrees C, part of the virus became resistant to removal b neuraminidase, with a half-time of 10-15 min. After a brief lag period, degraded viral material was released into the medium. The neuraminidase- resistant virus was capable of infecting the cells and probably did so by an intracellular route, since ammonium chloride, a lysosomotropic agent, blocked both the infection and the degradation of viral protein. When the entry process was observed by electron microscopy, viruses were seen bound primarily to microvilli on the cell surface at 0 degrees C and, after warming at 37 degrees C, were endocytosed in coated pits, coated vesicles, and large smooth-surfaced vacuoles. Viruses were also present in smooth-surfaced invaginations and small smooth-surfaced vesicles at both temperatures. At physiological pH, no fusion of the virus with the plasma membrane was observed. When prebound virus was incubated at a pH of 5.5 or below for 1 min at 37 degrees C, fusion was, however, detected by ferritin immunolabeling. t low multiplicity, 90% of the prebound virus became neuraminidase- resistant and was presumably fused after only 30 s at low pH. These experiments suggest that fowl plague virus enters MDCK cells by endocytosis in coated pits and coated vesicles and is transported to the lysosome where the low pH initiates a fusion reaction ultimately resulting in the transfer of the genome into the cytoplasm. The entry pathway of fowl plague virus thus resembles tht earlier described for Semliki Forest virus.
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            THE FINE STRUCTURE OF THE GALL BLADDER EPITHELIUM OF THE MOUSE

            Eichi Yamada (1955)
            Sections of mouse gall bladder epithelium fixed by perfusion with buffered osmium tetroxide have been studied in the electron microscope as an example of simple columnar epithelium. The free surface presents many microvilli, each presenting a dense tip, the capitulum, and displaying a radiating corona of delicate filaments, the antennulae microvillares. Very small pit-like depressions, representing caveolae intracellulares, are encountered along the cell membrane of the microvilli. The free cell surface between microvilli shows larger cave-like depressions, likewise representing caveolae intracellulares, containing a dense material. The lateral cell borders are extensively folded into pleats, which do not interdigitate extensively with corresponding folds of the adjacent cell membrane. The terminal bars are shown to consist of thickened densities of the cell membrane itself in the region of insertion of the lateral cell wall with the free cell surface. This thickening is associated with an accumulation of dense cytoplasmic material in the immediate vicinity. The terminal bar is thus largely a cytoplasmic and cell membrane structure, rather than being primarily intercellular in nature. The basal cell membrane is relatively straight except for a conical eminence near the center of the cell, projecting slightly into the underlying tunica propria. The basal cell membrane itself is overlain by a delicate limiting membrane, which does not follow the lateral contours of the cell. Unmyelinated intercellular nerve terminals with synaptic vesicles have been encountered between the lateral walls of epithelial cells. A division of the gall bladder epithelial cell into five zones according to Ferner has been found to be convenient for this study. The following cytoplasmic components have been noted, and their distribution and appearance described: dense absorption granules, mitochondria, Golgi or agranular membranes, endoplasmic reticulum or ergastoplasm, ring figures, and irregular dense bodies, perhaps lipoid in nature. The nucleus of these cells is also described.
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              Human coronavirus 229E binds to CD13 in rafts and enters the cell through caveolae.

              Kaoru Miyamoto, Ryuji Nomura, Takao Senda … (2004)
              CD13, a receptor for human coronavirus 229E (HCoV-229E), was identified as a major component of the Triton X-100-resistant membrane microdomain in human fibroblasts. The incubation of living fibroblasts with an anti-CD13 antibody on ice gave punctate labeling that was evenly distributed on the cell surface, but raising the temperature to 37 degrees C before fixation caused aggregation of the labeling. The aggregated labeling of CD13 colocalized with caveolin-1 in most cells. The HCoV-229E virus particle showed a binding and redistribution pattern that was similar to that caused by the anti-CD13 antibody: the virus bound to the cell evenly when incubated on ice but became colocalized with caveolin-1 at 37 degrees C; importantly, the virus also caused sequestration of CD13 to the caveolin-1-positive area. Electron microscopy confirmed that HCoV-229E was localized near or at the orifice of caveolae after incubation at 37 degrees C. The depletion of plasmalemmal cholesterol with methyl beta-cyclodextrin significantly reduced the HCoV-229E redistribution and subsequent infection. A caveolin-1 knockdown by RNA interference also reduced the HCoV-229E infection considerably. The results indicate that HCoV-229E first binds to CD13 in the Triton X-100-resistant microdomain, then clusters CD13 by cross-linking, and thereby reaches the caveolar region before entering cells.
              Article 0 comments Cited 102 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Rie Hasebe
                Michihito Sasaki
                Hirofumi Sawa
                Ryuichi Wada
                Takashi Umemura
                Takashi Kimura
                Journal
                Journal ID (nlm-ta): Virology
                Journal ID (iso-abbrev): Virology
                Title: Virology
                Publisher: Elsevier Inc.
                ISSN (Print): 0042-6822
                ISSN (Electronic): 1096-0341
                Publication date PMC-release: 31 August 2009
                Publication date (Print): 25 October 2009
                Publication date (Electronic): 31 August 2009
                Volume: 393
                Issue: 2
                Pages: 198-209
                Affiliations
                [a ]Laboratory of Prion Diseases, Graduate School of Veterinary Medicine, Hokkaido University, West 9 North 18, Kita-ku, Sapporo 060-0818, Japan
                [b ]Department of Molecular Pathobiology, Hokkaido University Research Center for Zoonosis Control, West 10 North 20, Kita-ku, Sapporo 001-0020, Japan
                [c ]Equine Research Institute, Japan Racing Association, 321-4 Togami-cho, Utsunomiya, Tochigi 320-0856, Japan
                [d ]Laboratory of Comparative Pathology, Graduate School of Veterinary Medicine, Hokkaido University, West 9 North 18, Kita-ku, Sapporo 060-0818, Japan
                [e ]21st Century COE Program for Zoonosis Control, Japan
                Author notes
                [* ]Corresponding author. Fax: +81 11 706 5185. kimura@ 123456czc.hokudai.ac.jp
                Article
                Publisher ID: S0042-6822(09)00470-X
                DOI: 10.1016/j.virol.2009.07.032
                PMC ID: 7111996
                PubMed ID: 19720389
                SO-VID: 37f2320c-ae11-4019-a2b1-60c0c4e1aa88
                Copyright statement: Copyright © 2009 Elsevier Inc. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 14 December 2008
                Date revision received : 21 July 2009
                Date accepted : 25 July 2009
                Categories
                Subject: Article

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: equine herpesvirus-1,equine brain microvascular endothelial cells,caveolar endocytosis
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: equine herpesvirus-1, equine brain microvascular endothelial cells, caveolar endocytosis

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