Spain-Santana T A, Marglin S, Ennis F A, Rothman A L
Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
J Med Virol. 2001 Oct;65(2):324-30. doi: 10.1002/jmv.2037.
Dengue virus (DV) infection can result in either a mild febrile illness known as dengue fever (DF) or a life-threatening disease called dengue hemorrhagic fever (DHF). DHF is more prevalent in patients undergoing secondary DV infection. This observation has led to the hypothesis that DHF may be the result of immune reactions to the secondary DV infection; an event termed immunopathology. Two cellular factors, MIP-1 alpha and MIP-1 beta, have been found to be induced by infection with DV. MIP-1 induction by DV infection was observed in a myelomonocytic cell line, as well as in peripheral blood mononuclear cells isolated from a dengue naive donor. MIP-1 induction was not due to factors secreted by infected cells. In fact, replication-competent virus was required to induce MIP-1. Evidence is also provided that MIP-1 genes are expressed in patients with dengue disease. It is hypothesized that these chemokines may have roles in the immunopathology of dengue infections and may contribute to fever and bone marrow suppression observed in patients with DV infections.
登革病毒（DV）感染可导致一种称为登革热（DF）的轻度发热疾病，或一种名为登革出血热（DHF）的危及生命的疾病。DHF在二次感染DV的患者中更为普遍。这一观察结果引发了一种假说，即DHF可能是对二次DV感染的免疫反应的结果；这一事件被称为免疫病理学。已发现两种细胞因子，即巨噬细胞炎性蛋白-1α（MIP-1α）和巨噬细胞炎性蛋白-1β（MIP-1β）可由DV感染诱导产生。在髓单核细胞系以及从从未感染过登革热的供体分离出的外周血单个核细胞中，均观察到DV感染诱导的MIP-1。MIP-1的诱导并非由感染细胞分泌的因子所致。事实上，需要具有复制能力的病毒来诱导MIP-1。还提供了证据表明MIP-1基因在登革热疾病患者中表达。据推测，这些趋化因子可能在登革热感染的免疫病理学中发挥作用，并可能导致DV感染患者出现发热和骨髓抑制。
