Entry of a heparan sulphate-binding HRV8 variant strictly depends on dynamin but not on clathrin, caveolin, and flotillin.
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Entry of a heparan sulphate-binding HRV8 variant strictly depends on dynamin but not on clathrin, caveolin, and flotillin. / Khan, Abdul Ghafoor; Pickl-Herk, Angela; Gajdzik, Leszek; Marlovits, Thomas; Fuchs, Renate; Blaas, Dieter.
In: VIROLOGY, Vol. 412, No. 1, 1, 2011, p. 55-67.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Entry of a heparan sulphate-binding HRV8 variant strictly depends on dynamin but not on clathrin, caveolin, and flotillin.
AU - Khan, Abdul Ghafoor
AU - Pickl-Herk, Angela
AU - Gajdzik, Leszek
AU - Marlovits, Thomas
AU - Fuchs, Renate
AU - Blaas, Dieter
PY - 2011
Y1 - 2011
N2 - The major group human rhinovirus type 8 can enter cells via heparan sulphate. When internalized into ICAM-1 negative rhabdomyosarcoma (RD) cells, HRV8 accumulated in the cells but caused CPE only after 3 days when used at high MOI. Adaptation by three blind passages alternating between RD and HeLa cells resulted in variant HRV8v with decreased stability at acidic pH allowing for productive infection in the absence of ICAM-1. HRV8v produced CPE at 10 times lower MOI within 1 day. Confocal fluorescence microscopy colocalization and the use of pharmacological and dominant negative inhibitors revealed that viral uptake is clathrin, caveolin, and flotillin independent. However, it is blocked by dynasore, amiloride, and EIPA. Furthermore, HRV8v induced FITC-dextran uptake and colocalized with this fluid phase marker. Except for the complete inhibition by dynasore, the entry pathway of HRV8v via HS is similar to that of HRV14 in RD cells that overexpress ICAM-1.
AB - The major group human rhinovirus type 8 can enter cells via heparan sulphate. When internalized into ICAM-1 negative rhabdomyosarcoma (RD) cells, HRV8 accumulated in the cells but caused CPE only after 3 days when used at high MOI. Adaptation by three blind passages alternating between RD and HeLa cells resulted in variant HRV8v with decreased stability at acidic pH allowing for productive infection in the absence of ICAM-1. HRV8v produced CPE at 10 times lower MOI within 1 day. Confocal fluorescence microscopy colocalization and the use of pharmacological and dominant negative inhibitors revealed that viral uptake is clathrin, caveolin, and flotillin independent. However, it is blocked by dynasore, amiloride, and EIPA. Furthermore, HRV8v induced FITC-dextran uptake and colocalized with this fluid phase marker. Except for the complete inhibition by dynasore, the entry pathway of HRV8v via HS is similar to that of HRV14 in RD cells that overexpress ICAM-1.
KW - Humans
KW - Cell Line
KW - Membrane Proteins/genetics/metabolism
KW - Caveolins/genetics/metabolism
KW - Clathrin/genetics/metabolism
KW - Cytopathogenic Effect, Viral
KW - Dynamin II/genetics/metabolism
KW - Host-Pathogen Interactions
KW - Intercellular Adhesion Molecule-1/genetics/metabolism
KW - Rhinovirus/genetics/physiology
KW - Serial Passage
KW - Virus Internalization
KW - Humans
KW - Cell Line
KW - Membrane Proteins/genetics/metabolism
KW - Caveolins/genetics/metabolism
KW - Clathrin/genetics/metabolism
KW - Cytopathogenic Effect, Viral
KW - Dynamin II/genetics/metabolism
KW - Host-Pathogen Interactions
KW - Intercellular Adhesion Molecule-1/genetics/metabolism
KW - Rhinovirus/genetics/physiology
KW - Serial Passage
KW - Virus Internalization
M3 - SCORING: Journal article
VL - 412
SP - 55
EP - 67
JO - VIROLOGY
JF - VIROLOGY
SN - 0042-6822
IS - 1
M1 - 1
ER -
