缺乏合适的动物模型将严重限制登革病毒（DENV）致病机制研究的进展。本研究旨在构建DENV感染小鼠模型，为阐明其致病机制提供实验材料。首先在严重联合免疫缺陷（ SCID）小鼠腹腔内接种人肝癌细胞株HepG2，构建人鼠嵌合体动物模型；移植后10 d腹腔接种DENV，通过检测病毒在体内分布及主要器官的组织学改变，评价该动物模型的实用价值。结果显示，在SCID小鼠成功移植HepG2并感染DENV后，出现病毒血症及主要器官严重损伤等现象，但无后肢麻痹等人类登革热无关症状。本研究成功构建了SCID-HepG2人鼠嵌合模型，该模型能支持DENV复制，并表现出部分人类DENV感染的临床症状，为研究DENV的致病机制提供了有价值的实验材料。

The purpose of the current study is to develop a mouse model for exploration of the pathogenesis of dengue virus (DENV) infection. HepG2 cells were transplanted to severe combined immunodeficiency (SCID) mice intraperitoneally to develop a HepG2-SCID mouse chimera model. To confirm the successful transplantation , the concentration of human albumin (hALB) in the serum was determined by sandwich enzyme-linked immunosorbent assay. Following challenge with intraperitoneal injection of DENV2, HepG2- SCID mice were evaluated by detection of virus distribution and histological changes in major organs. HepG2 cells engrafted into SCID mouse could support the replication of DENV2. HepG2-SCID mouse showed viremia and severe organ injuries. The data suggest that DENV2-infected HepG2-SCID chimera model is developed successfully , which would provide a useful tool for studying pathogenesis of DENV infection.