Does murine gamma herpes virus 68 infection promote fatty liver formation and hepatic insulin resistance in C57BL/6J mice?
In C57BL/6J mice, MHV68 infection promotes fatty liver formation and hepatic insulin resistance, which can be ameliorated by sirolimus.
A model system for expression of exogenous CAV1 by stable lentiviral transduction of TK6 cells was established. Functional assays demonstrated enhanced early proliferation by CAV1 expression in TK6 cells after irradiation with clinically relevant doses supporting the role of CAV1 as a prosurvival factor.