Podell M, Hayes K, Oglesbee M, Mathes L
Department of Veterinary Clinical Sciences, Center for Retrovirus Research, The Ohio State University, Columbus 43210, U.S.A.
J Acquir Immune Defic Syndr Hum Retrovirol. 1997 Aug 15;15(5):332-40. doi: 10.1097/00042560-199708150-00002.
Experimental intravenous challenge of five adult cats with the feline immunodeficiency virus Maryland isolate (FIV-MD) was investigated for its ability to induce neurologic abnormalities associated with the onset of immunodeficiency. Five 8-month-old cats were inoculated with 1000 median tissue culture infective dose of FIV-MD isolate, with five age-matched cats serving as uninfected controls. All FIV-MD-infected cats tested positive for serum antiviral antibodies and plasma viral DNA as detected by polymerase chain reaction at 2, 4, 10, and 16 months postinfection (PI). At 10 and 16 months PI, there was a significant reduction in the CD4/CD8 lymphocyte ratio, with all cats having a CD4/CD8 ratio of 1 or less. Total protein electrophoretic analysis of cerebrospinal fluid demonstrated a significantly increased albumin quotient at 4 and 16 months PI, representing a disrupted blood-brain barrier (BBB). At 16 months PI, all cats demonstrated a preferential increase in frontal cortical slow-wave activity compared with control cats. Serial evaluation of brainstem auditory evoked potential recordings revealed a prolongation of the interpeak latencies times over the study time. At least one abnormality was found over time in visual and somatosensory evoked potential testing in three and four infected cats, respectively. Comparing lymphocyte subtype ratios with neurologic testing revealed that every FIV-MD-infected cat exhibited an abnormality in at least one neurologic functional test with a concurrent CD4/CD8 count ratio of 1 or less. Overall, this study demonstrated that FIV-MD infection in adult cats results in a delayed-onset, progressive encephalopathy that parallels the decline in the CD4/CD8 lymphocyte ratio. Compared with prior information from pediatric FIV-MD-infected cats, these results indicate that age of infection influences the onset and severity of disease and may be associated with CD4 cell depletion in FIV-MD-infected cats, as seen in HIV-1-infected humans.
研究了用猫免疫缺陷病毒马里兰分离株(FIV-MD)对五只成年猫进行实验性静脉内攻击,以观察其诱导与免疫缺陷发作相关的神经学异常的能力。五只8个月大的猫接种了1000个组织培养感染剂量中位数的FIV-MD分离株,五只年龄匹配的猫作为未感染对照。所有感染FIV-MD的猫在感染后(PI)2、4、10和16个月时,血清抗病毒抗体和血浆病毒DNA经聚合酶链反应检测均呈阳性。在感染后10个月和16个月时,CD4/CD8淋巴细胞比率显著降低,所有猫的CD4/CD8比率均为1或更低。脑脊液的总蛋白电泳分析显示,在感染后4个月和16个月时,白蛋白商显著增加,表明血脑屏障(BBB)遭到破坏。在感染后16个月时,与对照猫相比,所有猫额叶皮质慢波活动均有优先增加。对脑干听觉诱发电位记录的系列评估显示,在研究期间峰间潜伏期延长。分别在三只和四只感染猫的视觉和体感诱发电位测试中,随时间推移至少发现了一项异常。将淋巴细胞亚型比率与神经学测试进行比较发现,每只感染FIV-MD的猫在至少一项神经功能测试中均表现出异常,同时CD4/CD8计数比率为1或更低。总体而言,本研究表明,成年猫感染FIV-MD会导致迟发性、进行性脑病,这与CD4/CD8淋巴细胞比率的下降平行。与先前关于感染FIV-MD的幼猫的信息相比,这些结果表明感染年龄会影响疾病的发作和严重程度,并且可能与感染FIV-MD的猫的CD4细胞耗竭有关,这在感染HIV-1的人类中也有体现。