fig1

Figure 1. Illustration depicting the expression of an endogenous retrovirus, HERV-K HML-2, and its role in the spreading of a senescent phenotype in vitro. The diagram illustrates HML-2 expression from the Chr7p22.1a locus, which is stimulated by the binding of transcription factors IRF-1 and NF-κB as a result of innate immune activation or environmental factors. HML-2 transcription and translation of HML-2 open reading frames (ORFs) and the subsequent packaging of its transcripts and proteins into an extracellular vesicle are depicted. The extracellular vesicles produced by senescent cells are then able to act in a paracrine manner and can be endocytosed by a recipient cell, resulting in the spreading of an aging or senescent phenotype (as indicated by the yellow arrow).