Nathanson N
Bull World Health Organ. 1975;52(4-6):753-60.
The pathogenesis of arenavirus infection is considered separately for the haemorrhagic fever (HF) syndrome and for lymphocytic choriomeningitis (LCM) virus infection of rodents. Experimental models of HF have received only limited study, mainly because of the virulence of the causal agents. Two useful models (Junin virus in guinea-pigs and Machupo virus in rhesus monkeys) are now available and an attempt is made to delineate crucial questions for future studies, including the physiology of shock, disseminated intravascular coagulation, immune mediation of disease, efficacy of antibody in treatment, and relative utility of attenuated and inactivated vaccines. Immunobiologic problems currently under investigation in LCM virus infection include the mechanism of immune destruction of infected tissues, the H-2 restriction of in vitro T-cell-mediated lysis of infected target cells, the transient immunodepression that accompanies acute primary LCM virus infection, and the mechanism of T-cell-mediated clearance of virus from infected tissues following adoptive immunization of persistently infected carrier mice.
对于出血热（HF）综合征以及啮齿动物的淋巴细胞性脉络丛脑膜炎（LCM）病毒感染，沙粒病毒感染的发病机制是分开考虑的。HF的实验模型研究有限，主要是因为致病原的毒力。目前有两种有用的模型（豚鼠中的胡宁病毒和恒河猴中的马丘波病毒），并尝试为未来研究确定关键问题，包括休克生理学、弥散性血管内凝血、疾病的免疫介导、抗体治疗的疗效以及减毒疫苗和灭活疫苗的相对效用。目前在LCM病毒感染中正在研究的免疫生物学问题包括感染组织免疫破坏的机制、体外T细胞介导的感染靶细胞裂解的H-2限制、急性原发性LCM病毒感染伴随的短暂免疫抑制，以及在对持续感染的携带小鼠进行过继免疫后T细胞介导的从感染组织清除病毒的机制。
