Whether and how certain transposable elements with viral origins, such as endogenous retroviruses (ERVs) dormant in our genomes, can become awakened and contribute to the aging process is largely unknown. In human senescent cells, we found that HERVK (HML-2), the most recently integrated human ERVs, are unlocked to transcribe viral genes and produce retrovirus-like particles (RVLPs). These HERVK RVLPs constitute a transmissible message to elicit senescence phenotypes in young cells, which can be blocked by neutralizing antibodies. The activation of ERVs was also observed in organs of aged primates and mice as well as in human tissues and serum from the elderly. Their repression alleviates cellular senescence and tissue degeneration and, to some extent, organismal aging. These findings indicate that the resurrection of ERVs is a hallmark and driving force of cellular senescence and tissue aging.

某些具有病毒起源的转座元件，例如休眠在我们基因组中的内源性逆转录病毒（ERV），是否以及如何能够被唤醒并促进衰老过程，在很大程度上尚不清楚。在人类衰老细胞中，我们发现 HERVK (HML-2)（最近整合的人类 ERV）被解锁以转录病毒基因并产生逆转录病毒样颗粒 (RVLP)。这些 HERVK RVLP 构成了一种可传递的信息，可在年轻细胞中引发衰老表型，而这种信息可以被中和抗体阻断。在老年灵长类动物和小鼠的器官以及老年人的人体组织和血清中也观察到了 ERV 的激活。它们的抑制减轻了细胞衰老和组织退化，并在某种程度上减轻了有机体的衰老。这些发现表明，ERV 的复活是细胞衰老和组织衰老的标志和驱动力。