Departments of Pediatrics, The University of Alabama at Birmingham, Birmingham, AL, USA.
Departments of Microbiology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Methods Mol Biol. 2021;2244:403-463. doi: 10.1007/978-1-0716-1111-1_19.
Human cytomegalovirus is the largest human herpesvirus and shares many core features of other herpesviruses such as tightly regulated gene expression during genome replication and latency as well as the establishment of lifelong persistence following infection. In contrast to stereotypic clinical syndromes associated with alpha-herpesvirus infections, almost all primary HCMV infections are asymptomatic and acquired early in life in most populations in the world. Although asymptomatic in most individuals, HCMV is a major cause of disease in hosts with deficits in adaptive and innate immunity such as infants who are infected in utero and allograft recipients following transplantation. Congenital HCMV is a commonly acquired infection in the developing fetus that can result in a number of neurodevelopmental abnormalities. Similarly, HCMV is a major cause of disease in allograft recipients in the immediate and late posttransplant period and is thought to be a major contributor to chronic allograft rejection. Even though HCMV induces robust innate and adaptive immune responses, it also encodes a vast array of immune evasion functions that are thought aid in its persistence. Immune correlates of protective immunity that prevent or modify intrauterine HCMV infection remain incompletely defined but are thought to consist primarily of adaptive responses in the pregnant mother, thus making congenital HCMV a potentially vaccine modifiable disease. Similarly, HCMV infection in allograft recipients is often more severe in recipients without preexisting adaptive immunity to HCMV. Thus, there has been a considerable effort to modify HCMV specific immunity in transplant recipient either through active immunization or passive transfer of adaptive effector functions. Although efforts to develop an efficacious vaccine and/or passive immunotherapy to limit HCMV disease have been underway for nearly six decades, most have met with limited success at best. In contrast to previous efforts, current HCMV vaccine development has relied on observations of unique properties of HCMV in hopes of reproducing immune responses that at a minimum will be similar to that following natural infection. However, more recent findings have suggested that immunity following naturally acquired HCMV infection may have limited protective activity and almost certainly, is not sterilizing. Such observations suggest that either the induction of natural immunity must be specifically tailored to generate protective activity or alternatively, that providing targeted passive immunity to susceptible populations could be prove to be more efficacious.
人巨细胞病毒是最大的人类疱疹病毒,与其他疱疹病毒有许多共同的核心特征,如在基因组复制和潜伏期间严格调控基因表达,以及在感染后建立终身持续性。与与α疱疹病毒感染相关的定型临床综合征相反,几乎所有原发性 HCMV 感染都是无症状的,并且在世界上大多数人群中在生命早期获得。尽管在大多数个体中无症状,但 HCMV 是适应性和先天免疫缺陷宿主(如宫内感染的婴儿和移植后接受同种异体移植物的受者)疾病的主要原因。先天性 HCMV 是发育中的胎儿中常见的获得性感染,可导致多种神经发育异常。同样,HCMV 是移植后即刻和晚期同种异体移植物受者疾病的主要原因,被认为是慢性同种异体排斥的主要原因。尽管 HCMV 诱导强烈的先天和适应性免疫反应,但它也编码大量免疫逃避功能,这些功能被认为有助于其持续性。预防或改变宫内 HCMV 感染的保护性免疫的免疫相关性仍不完全明确,但被认为主要由孕妇的适应性反应组成,因此使先天性 HCMV 成为一种潜在的疫苗可修饰疾病。同样,在没有预先存在的针对 HCMV 的适应性免疫的同种异体移植物受者中,HCMV 感染通常更为严重。因此,人们一直在努力通过主动免疫或适应性效应功能的被动转移来修饰移植受者中的 HCMV 特异性免疫。尽管近六十年以来一直在努力开发有效的疫苗和/或被动免疫疗法来限制 HCMV 疾病,但大多数都取得了有限的成功。与以前的努力相比,目前的 HCMV 疫苗开发依赖于对 HCMV 独特特性的观察,希望复制至少类似于自然感染后产生的免疫反应。然而,最近的发现表明,自然获得性 HCMV 感染后的免疫可能具有有限的保护活性,几乎肯定不是无菌的。这些观察结果表明,要么必须专门调整自然免疫的诱导以产生保护活性,要么向易感人群提供靶向性被动免疫可能更有效。