Cytomegalovirus (CMV) is a β-herpesvirus. Latent infections are common in all populations. However age-associated increases in levels of CMV-reactive antibody are testament to repeated reactivations and periods of viral replication. CMV has been associated with several diseases of aging, including vasculopathy and neurocognitive impairment. These conditions occur at a younger age in persons with particularly high burdens of CMV - transplant recipients and people living with HIV. Here we define the “clinical footprints” as immunopathologies triggered by CMV that develop over many years.

A high burden of CMV also drives accumulation of multifunctional terminally-differentiated αβ T-cells, a novel population of Vδ2 ⁻ γδ T-cells, and a population of CD56^lo NK cells lacking a key regulatory molecule. An understanding of these “immunological footprints” of CMV may reveal how they collectively promote the “clinical footprints” of the virus. This is explored here in transplant recipients, HIV patients and healthy aging.

巨细胞病毒（CMV）是一种β疱疹病毒。潜伏感染在所有人群中都很普遍。但是，与年龄相关的CMV反应性抗体水平的增加证明了重复激活和病毒复制的时间。CMV与多种衰老疾病相关，包括血管病变和神经认知功能障碍。这些情况发生在年龄较小的CMV负担特别重的人-移植受者和HIV感染者中。在这里，我们将“临床足迹”定义为由CMV触发并发展了多年的免疫病理学。

高CMV负担还推动了多功能终末分化αβT细胞，新的Vδ2 ^- γδT细胞群体以及缺乏关键调控分子的CD56 ^lo NK细胞群体的积累 。对CMV的这些“免疫足迹”的理解可能揭示了它们如何共同促进病毒的“临床足迹”。这是在移植接受者，HIV患者和健康衰老中进行的。