The Human Polyomavirus, JCV, Uses Serotonin Receptors to Infect Cells

@article{Elphick2004TheHP,
  title={The Human Polyomavirus, JCV, Uses Serotonin Receptors to Infect Cells},
  author={Gwendolyn F. Elphick and William Querbes and Joslynn A Jordan and Gretchen V Gee and Sylvia Eash and Kate Manley and Aisling S. Dugan and Megan L. Stanifer and Anushree Bhatnagar and Wesley K. Kroeze and Bryan L. Roth and Walter J. Atwood},
  journal={Science},
  year={2004},
  volume={306},
  pages={1380 - 1383}
}
The human polyomavirus, JCV, causes the fatal demyelinating disease progressive multifocal leukoencephalopathy in immunocompromised patients. We found that the serotonergic receptor 5HT2AR could act as the cellular receptor for JCV on human glial cells. The 5HT2A receptor antagonists inhibited JCV infection, and monoclonal antibodies directed at 5HT2A receptors blocked infection of glial cells by JCV, but not by SV40. Transfection of 5HT2A receptor–negative HeLa cells with a 5HT2A receptor… Expand
Inhibitory effect of serotonin antagonists on JC virus propagation in a carrier culture of human neuroblastoma cells
TLDR
It is indicated that 5HT2AR antagonists have an inhibitory effect on JCV infection and reproduction, and JCI cells are applicable to an experimental model for pharmacological evaluation of antiviral agents against JCV. Expand
5-HT2 Receptors Facilitate JC Polyomavirus Entry
TLDR
To define the roles of serotonin receptors in infection, HEK293A cells, which are poorly permissive to JCPyV, were transfected with 14 different isoforms of serotonin receptor and data confirm that the carbohydrate LSTc is the attachment receptor for JCPYV and that the type 2 serotonin receptors contribute to J CPyV infection by facilitating entry. Expand
Serotonin receptor 2A blocker (risperidone) has no effect on human polyomavirus JC infection of primary human fetal glial cells
TLDR
Data indicate that risperidone does not inhibit JCV(Mad1) attachment, internalisation, and replication in PHFG cells, and 5HT2AR blockers may not be effective in treating progressive multifocal leukoencephalopathy (PML). Expand
Polyomavirus JC infects human brain microvascular endothelial cells independent of serotonin receptor 2A.
TLDR
Data indicate that the productive in vitro infection of HBMVE cells by JCV is independent of 5HT(2A)R, which indicates that the mechanism by which JCV gains entry into the brain by infecting endothelial cells remains unclear. Expand
Interferon beta1-a and selective anti-5HT(2a) receptor antagonists inhibit infection of human glial cells by JC virus.
TLDR
IFNbeta1-a was found to be a potent inhibitor of both virus infection and viral early and late gene expression and several 5HT(2a) receptor antagonists inhibited initial infection of cells by JCV but were less effective at reducing viral loads in an already established infection. Expand
JC Polyomavirus Uses Extracellular Vesicles To Infect Target Cells
TLDR
This is the first demonstration of a polyomavirus using extracellular vesicles as a means of transmission and likely plays a critical role in the dissemination and spread of JCPyV both to and within the central nervous system. Expand
The biology of JC polyomavirus
TLDR
Significant progress has been made in understanding the biology of JCPyV and here an overview of the field is presented and some important questions that remain unanswered are discussed. Expand
The role of sialic acid in human polyomavirus infections
TLDR
This review focuses on what is known about the human polyomaviruses and the role that sialic acid plays in determining viral tropism and shows that viral entry of both JCV and BKV is dependent on the ability to interact with sIALic acid. Expand
Review on the role of the human Polyomavirus JC in the development of tumors
TLDR
The published literature is summarized and critically analyzed, in order to describe the current knowledge on the possible role of JCPyV in the development of human tumors. Expand
The human polyomaviruses
TLDR
The biological and physical characteristics and the lifecycle, namely receptor(s) interaction, mode of entry, intracellular trafficking, viral transcription and replication, and progeny assembly of these two human Polyomaviruses are examined. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 39 REFERENCES
JC Virus Enters Human Glial Cells by Clathrin-Dependent Receptor-Mediated Endocytosis
TLDR
It is demonstrated that JCV, unlike SV40, enters glial cells by receptor-mediated clathrin-dependent endocytosis, and is compared with that of the related polyomavirus, simian virus 40 (SV40). Expand
Infection of Glial Cells by the Human Polyomavirus JC Is Mediated by an N-Linked Glycoprotein Containing Terminal α(2-6)-Linked Sialic Acids
TLDR
It is found that JCV binds to a limited number of cell surface receptors on human glial cells that are not shared by the related polyomavirus simian virus 40, and these receptors play a fundamental role in mediating many virus-cell and cell-cell recognition processes. Expand
Differential distribution of the JC virus receptor-type sialic acid in normal human tissues.
TLDR
The data show a striking correlation between the expression of the JCV receptor-type sialic acid on cells and their susceptibility to infection by the virus, and support the hypothesis of JCV persistence in lymphoid tissue and B-cell-facilitated viral dissemination to the CNS. Expand
JC virus infection of hematopoietic progenitor cells, primary B lymphocytes, and tonsillar stromal cells: implications for viral latency
TLDR
Direct evidence is provided that JCV is not strictly neurotropic but can infect CD34+ hematopoietic progenitor cells and those cells which have differentiated into a lymphocytic, but not monocytical, lineage. Expand
JC virus binds to primary human glial cells, tonsillar stromal cells, and B-lymphocytes, but not to T lymphocytes.
TLDR
The binding of purified JCV virions to primary cultures of glial cells, tonsillar stromal cells, peripheral blood lymphocytes, and to several established cell lines demonstrates that JCV selectively interacts with cells in vivo that are known to be susceptible to infection and supports the hypothesis that B cells may be involved in trafficking of JCV to the CNS. Expand
Construction of a novel JCV/SV40 hybrid virus (JCSV) reveals a role for the JCV capsid in viral tropism.
TLDR
A JCV-SV40 chimeric viral genome is constructed that contains the regulatory region and the early genes of SV40 and the late structural genes of JCV, and the hybrid virus induced SV40-like cytopathic effect in human glial cells and hemagglutinated human type O red blood cells similar to JCV. Expand
Detection of JC Virus DNA in Human Tonsil Tissue: Evidence for Site of Initial Viral Infection
TLDR
The first evidence of the JCV genome in tonsil tissue is provided and it is suggested that tonsils may serve as an initial site of viral infection. Expand
Derivation and characterization of POJ cells, transformed human fetal glial cells that retain their permissivity for JC virus.
TLDR
Although normal glial cell cultures rapidly lose their permissivity for the virus after subculture, the transformed cells (designated POJ) had a greatly expanded life span and remained permissive for JC virus even after 30 passages in vitro. Expand
Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy.
TLDR
A papova-like virus has been cultivated from the brain of a case of progressive multifocal leucoencephalopathy complicating Hodgkin's disease, suggesting that it is a new papovavirus. Expand
Establishment of a line of human fetal glial cells that supports JC virus multiplication.
TLDR
The SVG cells represent a unique line of continuous rapidly growing human fetal astroglial cells that synthesizes a replication-proficient SV40 T protein, which obviates a host restriction barrier that limited JCV studies to primary cultures of human fetal brain and thus should allow for more detailed molecular studies of human brain cells and JCV that infects them. Expand
...
1
2
3
4
...