Wang Y, Burnier M, Detrick B, Hooks J J
Immunology and Virology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Invest Ophthalmol Vis Sci. 1996 Jan;37(1):250-4.
Retinal inflammatory and degenerative processes in humans and animals frequently are associated with genetic factors. The murine coronavirus, mouse hepatitis virus (MHV), JHM strain, induces a biphasic retinal disease in adult BALB/c mice. The genetic constitution of the host and the virus serotype can be critical factors in determining the outcome of a virus infection. The purpose of this study was to evaluate the possible role of host genetics in murine coronavirus-induced retinal disease.
JHM virus was inoculated by the intravitreal route into BALB/c, CD-1, and A/J mice. At varying times after inoculation, eye tissues were evaluated histologically. Antibody responses to the virus were evaluated by neutralization assays.
JHM virus induces a biphasic retinal disease in BALB/c mice. In the early phase, 1 to 7 days after inoculation, retinal vasculitis is observed. The second phase, characterized by retinal degeneration in the absence of inflammation, is seen by day 10 and progresses for several months. There is a similar biphasic disease process in JHM virus-infected A/J mice. However, retinal changes are less severe than those seen in BALB/c mice. Retinal tissue damage induced by JHM virus in CD-1 mice is different. Only the early phase of the disease, consisting of retinal vasculitis, was observed. These CD-1 mice do not develop the retinal degenerative disease. In fact, after day 10, the retina has a normal appearance. These differences in retinal tissue damage are seen over a wide range of infectivity of the virus inocula. Virus concentrations ranging from 10(1.4) to 10(4.4) TCID50/5 microliters were capable of inducing both inflammation and degeneration in BALB/c mice, whereas, the highest concentration of virus (10(4.4) TCID50/5 microliters) in CD-1 mice resulted in only the early inflammatory changes.
The authors show that the genetics of the host can profoundly affect the nature of retinal tissue damage. These studies substantiate the concept that a virus can indeed trigger retinal degenerative processes in genetically susceptible hosts.
人类和动物的视网膜炎症及退行性病变常与遗传因素相关。鼠冠状病毒，即小鼠肝炎病毒（MHV）JHM株，可在成年BALB/c小鼠中诱发双相性视网膜疾病。宿主的遗传构成和病毒血清型可能是决定病毒感染结果的关键因素。本研究的目的是评估宿主遗传学在鼠冠状病毒诱导的视网膜疾病中可能发挥的作用。
通过玻璃体内注射途径将JHM病毒接种到BALB/c、CD-1和A/J小鼠体内。在接种后的不同时间，对眼组织进行组织学评估。通过中和试验评估对该病毒的抗体反应。
JHM病毒在BALB/c小鼠中诱发双相性视网膜疾病。在早期阶段，接种后1至7天，可观察到视网膜血管炎。第二阶段的特征是在无炎症的情况下出现视网膜变性，在第10天可见，并持续数月。在JHM病毒感染的A/J小鼠中也有类似的双相疾病过程。然而，视网膜变化比在BALB/c小鼠中所见的要轻。JHM病毒在CD-1小鼠中诱导的视网膜组织损伤有所不同。仅观察到疾病的早期阶段，即由视网膜血管炎组成。这些CD-1小鼠不会发展为视网膜退行性疾病。事实上，并在第10天后，视网膜外观正常。在病毒接种物的广泛感染范围内均可见到这些视网膜组织损伤的差异。病毒浓度范围从10(1.4)至10(4.4) TCID50/5微升能够在BALB/c小鼠中诱导炎症和变性，而在CD-1小鼠中最高浓度的病毒（10(4.4) TCID50/5微升）仅导致早期炎症变化。
作者表明宿主遗传学可深刻影响视网膜组织损伤的性质。这些研究证实了病毒确实可在遗传易感宿主中引发视网膜退行性病变这一概念。
