congenital viral infections of the brain lessons learned from lymphocytic choriomeningitis virus in the neonatal rat先天性病毒感染大脑的教训在新生大鼠淋巴细胞性脉络丛脑膜炎病毒.pdfVIP

Review Congenital Viral Infections of the Brain: Lessons Learned from Lymphocytic Choriomeningitis Virus in the Neonatal Rat * Daniel J. Bonthius , Stanley Perlman ABSTRACT and not become evident until after the first few months or years of life. Factors important in determining outcome he fetal brain is highly vulnerable to teratogens, include pathogen identity, gestational timing of infection, T including many infectious agents. As a consequence pathogen load, tissue tropism, inflammatory response, and of prenatal infection, many children suffer severe immune status of the mother and fetus. and permanent brain injury and dysfunction. Because most For example, human infection with the rubella virus during animal models of congenital brain infection do not strongly the first 11 weeks of gestation results in teratogenic changes mirror human disease, the models are highly limited in their in most fetuses that survive the acute infection, with abilities to shed light on the pathogenesis of these diseases. abnormalities commonly detected in the heart, eye, and The animal model for congenital lymphocytic central nervous system [2]. At later times in gestation (11–16 choriomeningitis virus (LCMV) infection, however, does not weeks), infection is less likely to result in congenital suffer from this limitation. LCMV is a well-known human anomalies, but may still result in hearing loss, mental pathogen. When the infection occurs during pregnancy, the retardation, and growth deficits [3]. Sequelae from congenital virus can infect the fetus, and the d