Establishment of AIDS Animal Model with SIVmac239 Infected Chinese Rhesus Monkey

In the present research,two Chinese rhesus monkeys were inoculated intravenously with 5000 TCID50 of SIVmac239. The changes in the numbers of CD4+ T lymphocyte in peripheral blood,plasma viral loads,proviral DNA and humoral antibodies against virus were periodically monitored during 121 days. At the early stage of infection,proviral DNA had been detected in PBMCs,and infectious SIVmac239 virus had been isolated from PBMCs. At the same period,the numbers of CD4+ T lymphocytes were significantly decreased,and maintained at low level during the 121-day period of infection. Plasma viral loads reached the peak at week 2 post-inoculation and kept at a steady state subsequently. Moreover,antibodies against viral proteins were detected from plasma. All the results showed that the two Chinese rhesus monkeys had been infected with SIVmac239 successfully. This animal model can be applied for further AIDS researches.

Neonatal rhesus monkeys as an animal model for rotavirus infection

AIM To establish a rotavirus(RV)-induced diarrhea model using RV SA11 in neonatal rhesus monkeys for the study of the pathogenic and immune mechanisms of RV infection and evaluation of candidate vaccines.METHODS Neonatal rhesus monkeys with an average age of 15-20 d and an average weight of 500 g ± 150 g received intragastric administration of varying doses of SA11 RV( 107 PFUs/mL, 106 PFUs/mL, or 105 PFUs/mL, 10 mL/animal) to determine whether the SA11 strain can effectively infect these animals by observing their clinical symptoms, fecal shedding of virus antigen by ELISA, distribution of RV antigen in the organs by immunofluorescence, variations of viral RNA load in the organs by qRT-PCR, histopathological changes in the small intestine by HE staining, and apoptosis of small intestinal epithelial cells by TUNEL assay.RESULTS The RV monkey model showed typical clinical diarrhea symptoms in the 108 PFUs SA11 group, where we observed diarrhea 1-4 d post infection(dpi) and viral antigen shed in the feces from 1-7 dpi. RV was found in jejunal epithelial cells. We observed a viral load of approximately 5.85 × 103 copies per 100 mg in the jejunum at 2 dpi, which was increased to 1.09 × 105 copies per 100 mg at 3 dpi. A relatively high viral load was also seen in mesenteric lymph nodes at 2 dpi and 3 dpi. The following histopathological changes were observed in the small intestine following intragastric administration of SA11 RV: vacuolization, edema, and atrophy. Apoptosis in the jejunal villus epithelium was also detectable at 3 dpi.CONCLUSION Our results indicate that we have successfully established a RV SA11 strain diarrhea model in neonatal rhesus monkeys. Future studies will elucidate the mechanisms underlying the pathogenesis of RV infection, and we will use the model to evaluate the protective effect of candidate vaccines.

Coxsackievirus B3 HFMD animal models in Syrian hamster and rhesus monkey

Coxsackievirus B3(CVB3)is the pathogen causing hand,foot and mouth disease(HFMD),which manifests across a spectrum of clinical severity from mild to severe.However,CVB3-infected mouse models mainly demonstrate viral myocarditis and pancreatitis,failing to replicate human HFMD symptoms.Although several enteroviruses have been evaluated in Syrian hamsters and rhesus monkeys,there is no comprehensive data on CVB3.In this study,we have first tested the susceptibility of Syrian hamsters to CVB3 infection via different routes.The results showed that Syrian hamsters were successfully infected with CVB3 by intraperitoneal injection or nasal drip,leading to nasopharyngeal colonization,acute severe pathological injury,and typical HFMD symptoms.Notably,the nasal drip group exhibited a longer viral excretion cycle and more severe pathological damage.In the subsequent study,rhesus monkeys infected with CVB3 through nasal drips also presented signs of HFMD symptoms,viral excretion,serum antibody conversion,viral nucleic acids and antigens,and the specific organ damages,particularly in the heart.Surprisingly,there were no significant differences in myocardial enzyme levels,and the clinical symptoms resembled those often associated with common,mild infections.In summary,the study successfully developed severe Syrian hamsters and mild rhesus monkey models for CVB3-induced HFMD.These models could serve as a basis for understanding the disease pathogenesis,conducting pre-trial prevention and evaluation,and implementing post-exposure intervention.

超声乳化术后联合及不联合人工晶状体植入术建立后囊膜混浊兔眼模型的比较

背景后发性白内障（PCO）的防治是目前研究的热点问题之一。建立PCO动物模型常用的方法为超声乳化术后植入或不植入人工晶状体（IOL），但二者造模的效果评价尚不一致。目的比较兔眼PCO模型建立过程中植入与不植入IOL对PCO的影响。方法选择新西兰白兔20只，用随机数字表法将实验动物分为超声乳化联合IOL植入组和超声乳化不植入IOL组，每组10只兔，两组兔右眼超声乳化手术过程一致，术后共随访3个月，裂隙灯下观察2个组术后晶状体的反应及PCO情况，按OdrichPCO分级系统对术眼PCO情况进行分级。结果术后1～3d，超声乳化联合IOL植入组术眼结膜充血、角膜水肿和房水混浊的严重程度均明显比超声乳化不植入IOL组严重，而术后2周至3个月2个组兔眼的炎性反应均消失；术后1d至3个月，2个组兔术眼的瞳孔直径变化及PCO分级一致。术后2个月，超声乳化不植入IOL组及超声乳化联合IOL植入组兔眼1～3级PCO者分别为8只眼和9只眼，0级PCO者分别为2只眼和1只眼，组间差异无统计学意义（P=0．39）。裂隙灯下检查发现2个组实验眼均于术后1个月开始出现PCO，术后2个月PCO的范围扩大并快速发展，术后3个月形成致密纤维化层。结论采用超声乳化联合IOL植入术建立PCO模型的效果与不植入IOL者相同，但后者术后早期的前房炎性反应较轻，可作为研究PCO的理想动物模型。

猕猴眼内人工晶状体植入手术体会

目的 使用猕猴进行人工晶状体植入手术 ,寻求理想的动物模型。方法 15只猕猴 3 0眼 ,施行现代白内障囊外摘出联合后房型人工晶状体植入术。结果 猕猴眼手术与人眼手术相近。结论 猕猴为眼科最理想的实验动物模型。