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Entry of human parechovirus 1
P Joki-Korpela1, V Marjomäki, C Krogerus
1Haartman Institute, Department of Virology, University of Helsinki, FIN-00014 Helsinki, Finland. paivi.joki-korpela@helsinki.fi
Journal of Virology
|February 13, 2001
Summary
Human parechovirus 1 (HPEV-1) uses alpha(V) integrins for cell attachment and enters cells via clathrin-dependent endocytosis. Microtubules are involved in its transport, but viral RNA release may occur early during entry.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Human parechovirus 1 (HPEV-1) is a key member of the parechovirus genus.
- Previous studies suggested alpha(V) integrins as potential cellular receptors for HPEV-1.
- Early events in HPEV-1 infection, including entry mechanisms, remain poorly understood.
Purpose of the Study:
- To elucidate the entry mechanisms of HPEV-1 into host cells.
- To identify specific cellular receptors involved in HPEV-1 attachment.
- To determine the endocytic pathway utilized by HPEV-1 for cellular entry.
Main Methods:
- Blocking experiments using monoclonal antibodies against integrin subunits.
- Double-labeling immunofluorescence microscopy to track viral entry.
- Colocalization studies with markers for clathrin-coated vesicles, caveolae, early and late endosomes.
- Assessment of microtubule involvement using nocodazole treatment.
Main Results:
- Antibodies against alpha(V) and beta(3) integrin subunits significantly inhibited HPEV-1 infection.
- HPEV-1 colocalized with early endosomes (EEA1) at 5 min p.i. and late endosomes (mannose-6-phosphate receptor) at 30 min p.i.
- No colocalization with caveolin-1 was observed, indicating the caveolin route is not used.
- Microtubule depolymerization affected viral translocation but not replication, suggesting early genome release.
Conclusions:
- HPEV-1 utilizes alpha(V) integrins as cellular receptors for attachment.
- The virus enters host cells via the clathrin-dependent endocytic pathway.
- Microtubule-dependent transport is involved in moving the virus to late endosomes, but viral RNA may be released earlier in the infection process.