Braunwald J, Nonnenmacher H, Pereira C A, Kirn A
Laboratoire de Virologie de la Faculté de Médecine, Université Louis Pasteur et INSERM U74, Strasbourg, France.
Res Virol. 1991 Jan-Feb;142(1):5-15. doi: 10.1016/0923-2516(91)90022-u.
The administration of a hypercholesterolaemic (HC) diet rendered genetically resistant A/J mice susceptible to mouse hepatitis virus 3 (MHV3) infection. The animals died of acute hepatitis with high viral titres in the liver accompanied by many necrotic foci and high serum transaminase levels. Resistance to virus was re-established by refeeding HC mice with a normal diet for 2 weeks. This modification of pathogenesis was accompanied by an increase in the susceptibility of hepatocyte cultures from HC mice to MHV3 and could be explained by an enhancement in virus adsorption. We hypothesize that the incorporation of cholesterol into the plasma membranes of hepatocytes of HC mice, thereby decreasing the membrane fluidity, may lead to an increase in the availability of virus receptors.
给予高胆固醇血症(HC)饮食会使具有遗传抗性的A/J小鼠易感染小鼠肝炎病毒3型(MHV3)。这些动物死于急性肝炎,肝脏中病毒滴度很高,伴有许多坏死灶和血清转氨酶水平升高。通过给HC小鼠重新喂食正常饮食2周,病毒抗性得以重建。这种发病机制的改变伴随着HC小鼠肝细胞培养物对MHV3易感性的增加,这可以用病毒吸附增强来解释。我们推测,胆固醇掺入HC小鼠肝细胞的质膜中,从而降低膜流动性,可能导致病毒受体的可用性增加。