Journal of Virology, February 2001, p. 1958-1967, Vol. 75, No. 4
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.4.1958-1967.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Haartman Institute, Department of Virology, University of Helsinki, FIN-00014 Helsinki,1 Department of Virology and MediCity Research Laboratories, University of Turku, FIN-20520 Turku,2 and Department of Biological and Environmental Science, University of Jyväskylä, FIN-40351 Jyväskylä,3 Finland
Received 18 July 2000/Accepted 14 November 2000
Human parechovirus 1 (HPEV-1) is a prototype member of
parechoviruses, a recently established picornavirus genus. Although there is preliminary evidence that HPEV-1 recognizes
V
integrins as cellular receptors, our understanding of early events
during HPEV-1 infection is still very limited. The aim of this study was to clarify the entry mechanisms of HPEV-1, including the attachment of the virus onto the host cell surface and subsequent internalization. In blocking experiments with monoclonal antibodies against different receptor candidates, antibodies against
V and
3 integrin subunits, in particular in combination,
appeared to be the most efficient ones in preventing the HPEV-1
infection. To find out whether HPEV-1 uses clathrin-coated vesicles or
other routes for the entry into the host cell, we carried out
double-labeling experiments of virus-infected cells with anti-HPEV-1
antibodies and antibodies against known markers of the clathrin and the
caveolin routes. At the early phase of infection (5 min postinfection
[p.i.]) HPEV-1 colocalized with EEA1 (early endosomes), and later,
after 30 min p.i., it colocalized with mannose-6-phosphate receptor
(late endosomes), whereas no colocalization with caveolin-1 was
observed. The data indicate that HPEV-1 utilizes the
clathrin-dependent endocytic pathway for entry into the host
cells. Interestingly, endocytosed HPEV-1 capsid proteins were observed
in the endoplasmic reticulum and cis-Golgi network 30 to 60 min p.i. Depolymerization of microtubules with nocodazole inhibited
translocation of the virus to the late endosomes but did not block
HPEV-1 replication, suggesting that the RNA genome may be released
early during the entry process.
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