Yaghobi R, Geramizadeh B, Zamani S, Rahsaz M, Azarpira N, Karimi M H, Ayatolahi M, Hossein Aghdai M, Nikeghbalian S, Bahador A, Salahi H, Malek-Hosseini S A
Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran, ; Organ Transplant Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Int J Organ Transplant Med. 2011;2(3):108-15.
Pathogenesis of neonatal hepatitis relates to various underlying causes including viral infections. Both hepatotropic and non-hepatotropic viruses may induce liver failures in infants before birth, during delivery, or shortly after birth.
The tissue impact of HCMV, HSV, HBV, HCV, and rotavirus and adenovirus infections was evaluated in studied infants with neonatal hepatitis.
The history of viral infections was analyzed in paraffin-embedded biopsy and autopsy tissues of 22 infants with neonatal hepatitis between years 1996 and 2007, retrospectively. The tissue molecular presentation of HBV, HCV, HCMV, HSV, adenovirus, and rotavirus was evaluated by different qualitative simple and nested PCR and RT-PCR protocols. Immunohistochemistry (IHC) method was used for studying the antigenic prevalence of HSV-1, 2; HBV, HCMV and adenovirus infections. Also the laboratory liver indices of all patients with neonatal hepatitis were analyzed.
The HBV and HSV genomes were detected in 3 (14%) of 22 infants. The rotavirus and HCV-RNA and also the HCMV-DNA were detected separately in 1 (4%) of 26 paraffin-embedded autopsy and biopsy tissues. The HBV and HSV-1 specific antigens were separately diagnosed in 1 (4%) of 26 neonatal samples by IHC protocols. Also the HSV-2 antigen was seen in 5 (23%) of 22 liver autopsy and biopsy specimens. Co-infections with HCMV, HSV, HBV, HCV, and rotavirus were detected in these infants with hepatitis.
Diagnosis of single and mixed molecular and antigenic traces of HCMV, HSV, HBV, HCV and rotavirus underlines the etiologic role of these viruses in clinical pathogenesis of neonatal hepatitis.
新生儿肝炎的发病机制与包括病毒感染在内的多种潜在病因有关。嗜肝病毒和非嗜肝病毒均可在婴儿出生前、分娩期间或出生后不久诱发肝衰竭。
在患有新生儿肝炎的研究婴儿中评估人巨细胞病毒(HCMV)、单纯疱疹病毒(HSV)、乙型肝炎病毒(HBV)、丙型肝炎病毒(HCV)、轮状病毒和腺病毒感染对组织的影响。
回顾性分析1996年至2007年间22例患有新生儿肝炎的婴儿石蜡包埋活检和尸检组织中的病毒感染史。采用不同的定性简单和巢式PCR及逆转录PCR方案评估HBV、HCV、HCMV、HSV、腺病毒和轮状病毒的组织分子表现。采用免疫组织化学(IHC)方法研究HSV-1、2;HBV、HCMV和腺病毒感染的抗原流行情况。此外,还分析了所有新生儿肝炎患者的实验室肝脏指标。
在22例婴儿中的3例(14%)检测到HBV和HSV基因组。在26份石蜡包埋的尸检和活检组织中的1份(4%)分别检测到轮状病毒和HCV-RNA以及HCMV-DNA。通过IHC方案在26份新生儿样本中的1份(4%)分别诊断出HBV和HSV-1特异性抗原。在22份肝脏尸检和活检标本中的5份(23%)也发现了HSV-2抗原。在这些肝炎婴儿中检测到HCMV、HSV、HBV、HCV和轮状病毒的合并感染。
HCMV、HSV、HBV、HCV和轮状病毒单一及混合分子和抗原痕迹的诊断强调了这些病毒在新生儿肝炎临床发病机制中的病因学作用。