Initiation of Human Cytomegalovirus Infection Requires Initial Interaction with Cell Surface Heparan Sulfate

Compton, Teresa; Nowlin, Dawn M.; Cooper, Neil R.

doi:10.1006/viro.1993.1192

Cited by 377 publications

(328 citation statements)

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“…Both specific and nonspecific receptors are involved in CMV infection. Nonspecific receptors include heparan sulfate and annexin II with the viral glycoproteins gB and gH and the glycoprotein M and glycoprotein N (gN) complex (49). Some cell type-specific receptors have been described:…”

Section: Variability Of CMV Strainsmentioning

confidence: 99%

The Cell Biology of Cytomegalovirus: Implications for Transplantation

Kaminski

Fishman

2016

American Journal of Transplantation

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Interpretation of clinical data regarding the impact of cytomegalovirus (CMV) infection on allograft function is complicated by the diversity of viral strains and substantial variability of cellular receptors and viral gene expression in different tissues. Variation also exists in nonspecific (monocytes and dendritic cells) and specific (NK cells, antibodies) responses that augment T cell antiviral activities. Innate immune signaling pathways and expanded pools of memory NK cells and cd T cells also serve to amplify host responses to infection. The clinical impact of specific memory T cell anti-CMV responses that cross-react with graft antigens and alloantigens is uncertain but appears to contribute to graft injury and to the abrogation of allograft tolerance. These responses are modified by diverse immunosuppressive regimens and by underlying host immune deficits. The impact of CMV infection on the transplant recipient reflects cellular changes and corresponding host responses, the convergence of which has been termed the "indirect effects" of CMV infection. Future studies will clarify interactions between CMV infection and allograft injury and will guide interventions that may enhance clinical outcomes in transplantation.

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Section: Variability Of CMV Strainsmentioning

confidence: 99%

The Cell Biology of Cytomegalovirus: Implications for Transplantation

Kaminski

Fishman

2016

American Journal of Transplantation

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“…For example, the cell surface heparan GAGs are the site for the initial viral attachment of herpesvirus, pseudorabies virus, and cytomegalovirus onto the cell surface (40,42,43). Likewise, several sulfated polysaccharides are potent and selective inhibitors of infection due to various enveloped viruses, including vesicular stomatitis virus (VSV, a rhabdovirus) and human immunodeficiency virus (HIV, a lentivirus) (44).…”

Section: Figmentioning

confidence: 99%

Retroviral Gene Transfer Is Inhibited by Chondroitin Sulfate Proteoglycans/Glycosaminoglycans in Malignant Pleural Effusions

Batra

Olsen

Hoganson

et al. 1997

Journal of Biological Chemistry

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Gene therapy may be an important adjuvant for treating cancer in the pleural space. The initial results of retroviral gene transfer to cancer cells in malignant pleural effusions revealed that transduction was markedly inhibited, and studies to characterize the inhibitory factor(s) were performed. The inhibition was contained within the soluble, rather than cellular, components of the effusions and was demonstrated with amphotropic, gibbon ape leukemia virus, and vesicular stomatitis virus-glycoprotein pseudotyped retroviral vectors. After excluding complement proteins, a series of studies identified chondroitin sulfates (CSs) as the inhibitory substances. First, treatment of the effusions with mammmalian hyaluronidase or chondroitinases, but not Streptomyces hyaluronidase, abolished the inhibitory activity. Second, addition of exogenous CS glycosaminoglycans mimicked the inhibition observed with pleural effusions. Third, immunoassays and biochemical analyses of malignant pleural effusion specimens revealed CS in relevant concentrations within pleural fluid. Fourth, proteoglycans/glycosaminoglycans isolated from the effusions inhibited retroviral gene transfer. Analyses of the mechanism of inhibition indicate that the chondroitin sulfates interact with vector in solution rather than at the target cell surface. These results suggest that drainage of the malignant pleural effusion, and perhaps enzymatic pretreatment of the pleural cavity, will be necessary for efficient retroviral vector mediated gene delivery to pleural metastases.

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“…The initial interaction between human cytomegalovirus (HCMV) and host cells is mediated by cell surface heparan sulfate proteoglycans (HSPGs) (Compton et al, 1993 ;Neyts et al, 1992). After stable attachment to the cell surface, virions undergo a pH-independent fusion event with the host cell plasma membrane (Compton et al, 1992) whereby the viral nucleocapsid is deposited in the cell cytoplasm.…”

Section: Introductionmentioning

confidence: 99%

Interference with annexin II has no effect on entry of human cytomegalovirus into fibroblast cells.

Pietropaolo¹,

Compton

1999

Journal of General Virology

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Annexin II has been identified as a human cytomegalovirus (HCMV)-binding protein, shown to be a component of purified virions and proposed as a cellular receptor for the virus. In addition, annexin II is capable of associating with the major HCMV envelope glycoprotein, gB (gpUL55). As one approach to examine the role of annexin II in virus entry, a high-titre polyclonal annexin IIspecific antibody was produced and its effects in virus entry and cell-to-cell spread assays were tested. This anti-annexin II serum recognized virion and cell surface annexin II and annexin IIderived peptides. Recombinant annexin II, with characteristic calcium-and phospholipid-binding activities, was also examined. Pretreatment of cells, virions or both with polyclonal anti-annexin II serum, affinity-purified anti-annexin II antibodies or recombinant annexin II protein prior to infection was inconsequential to the entry of HCMV into fibroblasts. HCMV was also able to dosedependently penetrate annexin II-deficient 293 cells. Furthermore, the spread of HCMV from cell to cell was not inhibited in the presence of polyclonal anti-annexin II antibodies or exogenous annexin II protein. These experiments do not support a direct role of annexin II in virus entry or spread. Alternative roles for the gB-annexin II interaction are proposed.

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Initiation of Human Cytomegalovirus Infection Requires Initial Interaction with Cell Surface Heparan Sulfate

Cited by 377 publications

References 0 publications

The Cell Biology of Cytomegalovirus: Implications for Transplantation

The Cell Biology of Cytomegalovirus: Implications for Transplantation

Retroviral Gene Transfer Is Inhibited by Chondroitin Sulfate Proteoglycans/Glycosaminoglycans in Malignant Pleural Effusions

Interference with annexin II has no effect on entry of human cytomegalovirus into fibroblast cells.

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