Maglennon Gareth Adam, Doorbar John
Pathology & Infectious Diseases, The Royal Veterinary College, North Mymms, AL9 7TA, UK.
Open Virol J. 2012;6:190-7. doi: 10.2174/1874357901206010190. Epub 2012 Dec 28.
The presence of viral DNA in the absence of disease has suggested that papillomaviruses, like many other viruses, can exist as latent infections in the skin or other epithelial sites. In animal models, where detailed investigation has been carried out, papillomavirus DNA can be found at sites of previous infection following immune regression, with the site of latent infection being the epithelial basal layer. Such studies suggest that immune surveillance can restrict viral gene expression in the basal and parabasal layers without efficiently suppressing viral genome replication, most probably through the action of memory T-cells in the skin or dermis. Although gradual papillomavirus genome loss appears to occur over time at latent sites, immunosuppression can arrest this, and can lead to an elevation in viral genome copy number in experimental systems. In addition to immune-mediated latency, it appears that a similar situation can be achieved following infection at low virus titres and/or infection at epithelial sites where the virus life cycle is not properly supported. Such silent of asymptomatic infections do not necessarily involve the host immune system and may be controlled by different mechanisms. It appears that virus reactivation can be triggered by mechanical irritation, wounding or by UV irradiation which changes the local environment. Although the duration of papillomavirus latency in humans is not yet known, it is likely that some of the basic principles will resemble those elucidated in these model systems, and that persistence in the absence of disease may be the default outcome for at least some period of time following regression.
在没有疾病的情况下检测到病毒DNA，这表明乳头瘤病毒与许多其他病毒一样，可作为潜伏感染存在于皮肤或其他上皮部位。在已进行详细研究的动物模型中，免疫消退后可在先前感染部位发现乳头瘤病毒DNA，潜伏感染部位为上皮基底层。此类研究表明，免疫监视可限制基底层和副基底层中的病毒基因表达，但无法有效抑制病毒基因组复制，这很可能是通过皮肤或真皮中记忆T细胞的作用实现的。虽然随着时间推移，潜伏部位的乳头瘤病毒基因组似乎会逐渐丢失，但免疫抑制可阻止这种情况发生，并可导致实验系统中病毒基因组拷贝数增加。除了免疫介导的潜伏外，在低病毒滴度感染和/或在病毒生命周期未得到适当支持的上皮部位感染后，似乎也会出现类似情况。这种无症状感染不一定涉及宿主免疫系统，可能由不同机制控制。似乎病毒再激活可由机械刺激、创伤或紫外线照射引发，这些因素会改变局部环境。虽然人类乳头瘤病毒潜伏的持续时间尚不清楚，但很可能一些基本原理与这些模型系统中所阐明的原理相似，并且在消退后的至少一段时间内，在没有疾病的情况下持续存在可能是默认结果。
