Gujar Shashi A, Michalak Tomasz I
Molecular Virology and Hepatology Research Group, Division of BioMedical Science, Faculty of Medicine, Health Sciences Centre, Memorial University, St. John's, Newfoundland, Canada A1B 3V6.
J Virol. 2009 Apr;83(8):3861-76. doi: 10.1128/JVI.02521-08. Epub 2009 Feb 4.
Although the virological features of serologically silent hepadnaviral primary occult infection (POI) have been relatively well recognized in the woodchuck model of hepatitis B virus infection, the characteristics of accompanying immune responses remain unknown. In this study, the kinetics of woodchuck hepatitis virus (WHV)-specific and generalized (mitogen-induced) T-cell proliferative responses and cytokine expression profiles in circulating lymphoid cells and the liver, along with WHV-specific antibody responses, were investigated during experimentally induced POI and subsequent challenge with a liver-pathogenic dose (>10(3) virions) or liver-nonpathogenic dose (50 virions) of the same virus. The data revealed that POI, which does not prompt WHV surface antigenemia, antiviral antibody response, and hepatitis or protect from challenge with a liver-pathogenic virus dose, was accompanied by the appearance of a strong WHV-specific T-cell response directed against multiple viral epitopes that intermittently persisted at low levels for up to 10-months during follow-up. Furthermore, immediately after exposure to a liver-nonpathogenic dose of WHV, lymphocytes acquired a heightened capacity to proliferate in response to mitogenic stimuli and displayed augmented expression of alpha interferon, interleukin-12 (IL-12), and IL-2, but not tumor necrosis factor alpha. Overall, the kinetics of WHV-specific and mitogen-induced T-cell proliferative and cytokine responses in POI were closely comparable to those seen in infection induced by liver-pathogenic viral doses. The data demonstrated that virus-specific T-cell proliferative reactivity is a very sensitive indicator of exposure to hepadnavirus, even to small amounts inducing serologically mute infection. They also showed that hepadnaviral POI is not only a molecularly but also an immunologically identifiable and distinctive entity.
尽管在乙型肝炎病毒感染的土拨鼠模型中,血清学沉默的嗜肝DNA病毒原发性隐匿感染(POI)的病毒学特征已得到相对充分的认识,但其伴随的免疫反应特征仍不清楚。在本研究中,我们调查了实验诱导的POI期间以及随后用相同病毒的肝致病性剂量(>10³个病毒体)或肝非致病性剂量(50个病毒体)进行攻击后,土拨鼠肝炎病毒(WHV)特异性和全身性(丝裂原诱导)T细胞增殖反应的动力学、循环淋巴细胞和肝脏中细胞因子表达谱以及WHV特异性抗体反应。数据显示,POI不引发WHV表面抗原血症、抗病毒抗体反应和肝炎,也不能保护免受肝致病性病毒剂量的攻击,但伴随着针对多个病毒表位的强烈WHV特异性T细胞反应的出现,在随访期间这种反应以低水平间歇性持续长达10个月。此外,在接触肝非致病性剂量的WHV后,淋巴细胞对丝裂原刺激的增殖能力增强,并显示出α干扰素、白细胞介素12(IL-12)和IL-2的表达增加,但肿瘤坏死因子α未增加。总体而言,POI中WHV特异性和丝裂原诱导的T细胞增殖及细胞因子反应的动力学与肝致病性病毒剂量诱导的感染中所见的动力学密切可比。数据表明,病毒特异性T细胞增殖反应性是接触嗜肝DNA病毒的非常敏感的指标,即使是诱导血清学沉默感染的少量病毒。它们还表明,嗜肝DNA病毒POI不仅在分子上,而且在免疫学上都是可识别且独特的实体。