Chronic viral infections represent a unique challenge to the infected host. Persistently replicating viruses outcompete or subvert the initial antiviral response, allowing the establishment of chronic infections that result in continuous stimulation of both the innate and adaptive immune compartments. This causes a profound reprogramming of the host immune system, including attenuation and persistent low levels of type I interferons, progressive loss (or exhaustion) of CD8(+) T cell functions, and specialization of CD4(+) T cells to produce interleukin-21 and promote antibody-mediated immunity and immune regulation. Epigenetic, transcriptional, posttranscriptional, and metabolic changes underlie this adaptation or recalibration of immune cells to the emerging new environment in order to strike an often imperfect balance between the host and the infectious pathogen. In this review we discuss the common immunological hallmarks observed across a range of different persistently replicating viruses and host species, the underlying molecular mechanisms, and the biological and clinical implications.

中文翻译：

---

慢性病毒感染期间的先天性和适应性免疫调节。

慢性病毒感染代表了对感染宿主的独特挑战。持久复制的病毒胜过或破坏了最初的抗病毒反应，从而导致建立了慢性感染，从而导致连续刺激先天和适应性免疫区室。这会导致宿主免疫系统发生深刻的重编程，包括I型干扰素的衰减和持续低水平，CD8（+）T细胞功能的进行性丧失（或衰竭）以及CD4（+）T细胞的特化以产生白介素- 21，促进抗体介导的免疫和免疫调节。表观遗传的，转录的，转录后的 代谢变化是免疫细胞对新出现的新环境的适应或重新校准的基础，目的是在宿主和传染性病原体之间达到通常不完美的平衡。在这篇综述中，我们讨论了在一系列不同的持续复制的病毒和宿主物种中观察到的常见免疫学标志，潜在的分子机制以及生物学和临床意义。