Human rhinovirus 14 enters rhabdomyosarcoma cells expressing icam-1 by a clathrin-, caveolin-, and flotillin-independent pathway.
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Human rhinovirus 14 enters rhabdomyosarcoma cells expressing icam-1 by a clathrin-, caveolin-, and flotillin-independent pathway. / Khan, Abdul Ghafoor; Pickl-Herk, Angela; Gajdzik, Leszek; Marlovits, Thomas; Fuchs, Renate; Blaas, Dieter.
In: J VIROL, Vol. 84, No. 8, 8, 2010, p. 3984-3992.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Human rhinovirus 14 enters rhabdomyosarcoma cells expressing icam-1 by a clathrin-, caveolin-, and flotillin-independent pathway.
AU - Khan, Abdul Ghafoor
AU - Pickl-Herk, Angela
AU - Gajdzik, Leszek
AU - Marlovits, Thomas
AU - Fuchs, Renate
AU - Blaas, Dieter
PY - 2010
Y1 - 2010
N2 - Intercellular adhesion molecule 1 (ICAM-1) mediates binding and entry of major group human rhinoviruses (HRVs). Whereas the entry pathway of minor group HRVs has been studied in detail and is comparatively well understood, the pathway taken by major group HRVs is largely unknown. Use of immunofluorescence microscopy, colocalization with specific endocytic markers, dominant negative mutants, and pharmacological inhibitors allowed us to demonstrate that the major group virus HRV14 enters rhabdomyosarcoma cells transfected to express human ICAM-1 in a clathrin-, caveolin-, and flotillin-independent manner. Electron microscopy revealed that many virions accumulated in long tubular structures, easily distinguishable from clathrin-coated pits and caveolae. Virus entry was strongly sensitive to the Na(+)/H(+) ion exchange inhibitor amiloride and moderately sensitive to cytochalasin D. Thus, cellular uptake of HRV14 occurs via a pathway exhibiting some, but not all, characteristics of macropinocytosis and is similar to that recently described for adenovirus 3 entry via alpha(v) integrin/CD46 in HeLa cells.
AB - Intercellular adhesion molecule 1 (ICAM-1) mediates binding and entry of major group human rhinoviruses (HRVs). Whereas the entry pathway of minor group HRVs has been studied in detail and is comparatively well understood, the pathway taken by major group HRVs is largely unknown. Use of immunofluorescence microscopy, colocalization with specific endocytic markers, dominant negative mutants, and pharmacological inhibitors allowed us to demonstrate that the major group virus HRV14 enters rhabdomyosarcoma cells transfected to express human ICAM-1 in a clathrin-, caveolin-, and flotillin-independent manner. Electron microscopy revealed that many virions accumulated in long tubular structures, easily distinguishable from clathrin-coated pits and caveolae. Virus entry was strongly sensitive to the Na(+)/H(+) ion exchange inhibitor amiloride and moderately sensitive to cytochalasin D. Thus, cellular uptake of HRV14 occurs via a pathway exhibiting some, but not all, characteristics of macropinocytosis and is similar to that recently described for adenovirus 3 entry via alpha(v) integrin/CD46 in HeLa cells.
KW - Humans
KW - Cell Line, Tumor
KW - Microscopy, Fluorescence
KW - Microscopy, Electron
KW - Microscopy, Confocal
KW - Membrane Proteins/metabolism
KW - Sodium Channel Blockers/pharmacology
KW - Clathrin/metabolism
KW - Virus Internalization
KW - Amiloride/pharmacology
KW - Caveolins/metabolism
KW - Cytochalasin D/pharmacology
KW - Intercellular Adhesion Molecule-1/biosynthesis
KW - Muscle Cells/virology
KW - Rhinovirus/physiology
KW - Humans
KW - Cell Line, Tumor
KW - Microscopy, Fluorescence
KW - Microscopy, Electron
KW - Microscopy, Confocal
KW - Membrane Proteins/metabolism
KW - Sodium Channel Blockers/pharmacology
KW - Clathrin/metabolism
KW - Virus Internalization
KW - Amiloride/pharmacology
KW - Caveolins/metabolism
KW - Cytochalasin D/pharmacology
KW - Intercellular Adhesion Molecule-1/biosynthesis
KW - Muscle Cells/virology
KW - Rhinovirus/physiology
M3 - SCORING: Journal article
VL - 84
SP - 3984
EP - 3992
JO - J VIROL
JF - J VIROL
SN - 0022-538X
IS - 8
M1 - 8
ER -
