Duck hepatitis B virus requires cholesterol for endosomal escape during virus entry.
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Duck hepatitis B virus requires cholesterol for endosomal escape during virus entry. / Funk, Anneke; Mouna, Mhamdi; Hohenberg, Heinz; Heeren, Jörg; Reimer, Rudolph; Lambert, Carsten; Prange, Reinhild; Sirma, Hüseyin.
In: J VIROL, Vol. 82, No. 21, 21, 2008, p. 10532-10542.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Duck hepatitis B virus requires cholesterol for endosomal escape during virus entry.
AU - Funk, Anneke
AU - Mouna, Mhamdi
AU - Hohenberg, Heinz
AU - Heeren, Jörg
AU - Reimer, Rudolph
AU - Lambert, Carsten
AU - Prange, Reinhild
AU - Sirma, Hüseyin
PY - 2008
Y1 - 2008
N2 - The identity and functionality of biological membranes are determined by cooperative interaction between their lipid and protein constituents. Cholesterol is an important structural lipid that modulates fluidity of biological membranes favoring the formation of detergent-resistant microdomains. In the present study, we evaluated the functional role of cholesterol and lipid rafts for entry of hepatitis B viruses into hepatocytes. We show that the duck hepatitis B virus (DHBV) attaches predominantly to detergent-soluble domains on the plasma membrane. Cholesterol depletion from host membranes and thus disruption of rafts does not affect DHBV infection. In contrast, depletion of cholesterol from the envelope of both DHBV and human HBV strongly reduces virus infectivity. Cholesterol depletion increases the density of viral particles and leads to changes in the ultrastructural appearance of the virus envelope. However, the dual topology of the viral envelope protein L is not significantly impaired. Infectivity and density of viral particles are partially restored upon cholesterol replenishment. Binding and entry of cholesterol-deficient DHBV into hepatocytes are not significantly impaired, in contrast to their release from endosomes. We therefore conclude that viral but not host cholesterol is required for endosomal escape of DHBV.
AB - The identity and functionality of biological membranes are determined by cooperative interaction between their lipid and protein constituents. Cholesterol is an important structural lipid that modulates fluidity of biological membranes favoring the formation of detergent-resistant microdomains. In the present study, we evaluated the functional role of cholesterol and lipid rafts for entry of hepatitis B viruses into hepatocytes. We show that the duck hepatitis B virus (DHBV) attaches predominantly to detergent-soluble domains on the plasma membrane. Cholesterol depletion from host membranes and thus disruption of rafts does not affect DHBV infection. In contrast, depletion of cholesterol from the envelope of both DHBV and human HBV strongly reduces virus infectivity. Cholesterol depletion increases the density of viral particles and leads to changes in the ultrastructural appearance of the virus envelope. However, the dual topology of the viral envelope protein L is not significantly impaired. Infectivity and density of viral particles are partially restored upon cholesterol replenishment. Binding and entry of cholesterol-deficient DHBV into hepatocytes are not significantly impaired, in contrast to their release from endosomes. We therefore conclude that viral but not host cholesterol is required for endosomal escape of DHBV.
M3 - SCORING: Zeitschriftenaufsatz
VL - 82
SP - 10532
EP - 10542
JO - J VIROL
JF - J VIROL
SN - 0022-538X
IS - 21
M1 - 21
ER -
