Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.2.2.7 (heparinase)
 1,270 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human papillomavirus type 33 (HPV-33) pseudovirus infection is a slow process dependent on the initial interaction with cell-surface heparan sulfate (T. Giroglou, L. Florin, F. Schafer, R. E. Streeck, and M. Sapp, 2001a, J. Virol. 75, 1565-1570). We have now further dissected the initial steps of pseudovirus uptake using removal of cell-surface proteoglycans and selective inhibition of entry pathways. Treatment of cells with heparinase I, but not with phosphoinositol-specific phospholipase C (PIPLC), prevented binding of papillomavirus-like particles and infection with HPV-33 pseudovirions, indicating that GPI-linked proteoglycans (glypicans) are not required for productive infection. The slow entry of pseudovirions was inhibited by cytochalasin D and nocodazole in a concentration-dependent manner, suggesting actin polymerization and intact microtubuli be required. Inhibitors of the caveolae-mediated uptake did not significantly affect pseudoinfection. Interestingly, pseudoinfection was blocked by selective inhibitors of endosomal acidification up to 12 h postinfection. Together, our results suggest that binding of HPV pseudovirions to heparan sulfate proteoglycans, most likely syndecans, is followed by delayed internalization via the endosomal pathway.
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PMID:Analysis of the infectious entry pathway of human papillomavirus type 33 pseudovirions. 1220 31