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Journal of Virology, March 2000, p. 2288-2292, Vol. 74, No. 5
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
JC Virus Enters Human Glial Cells by
Clathrin-Dependent Receptor-Mediated Endocytosis
M. T.
Pho,
A.
Ashok, and
Walter J.
Atwood*
Department of Molecular Microbiology and
Immunology, Brown University, Providence, Rhode Island 02912
Received 4 August 1999/Accepted 10 December 1999
The human polyomavirus JC virus (JCV) is the etiologic agent of a
fatal central nervous system (CNS) demyelinating disease known as
progressive multifocal leukoencephalopathy (PML). PML occurs
predominantly in immunosuppressed patients and has increased dramatically as a result of the AIDS pandemic. The major target cell of
JCV infection and lytic replication in the CNS is the oligodendrocyte.
The mechanisms by which JCV initiates and establishes infection of
these glial cells are not understood. The initial interaction between
JCV and glial cells involves virus binding to N-linked glycoproteins
containing terminal
(2-6)-linked sialic acids. The subsequent steps
of entry and targeting of the viral genome to the nucleus have not been
described. In this report, we compare the kinetics and mechanisms of
infectious entry of JCV into human glial cells with that of the related
polyomavirus, simian virus 40 (SV40). We demonstrate that JCV, unlike
SV40, enters glial cells by receptor-mediated clathrin-dependent endocytosis.
*
Corresponding author. Mailing address: Department of
Molecular Microbiology and Immunology, Brown University, Box G-B616, 117 Meeting St., Providence, RI 02912. Phone: (401) 863-3116. Fax:
(401) 863-1971. E-mail: Walter_Atwood{at}Brown.edu.
Journal of Virology, March 2000, p. 2288-2292, Vol. 74, No. 5
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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