Human herpesvirus 6 envelope cholesterol is required for virus entry.

In this study, the role of cholesterol in the envelope of human herpesvirus 6 (HHV-6) was examined by using methyl-beta-cyclodextrin (MbetaCD) depletion. When cholesterol was removed from HHV-6 virions with MbetaCD, infectivity was abolished, but it could be rescued by the addition of exogenous cholesterol. HHV-6 binding was affected slightly by MbetaCD treatment. In contrast, envelope cholesterol depletion markedly affected HHV-6 infectivity and HHV-6-induced cell fusion. These results suggest that the cholesterol present in the HHV-6 envelope plays a prominent role in the fusion process and is a key component in viral entry.