Considering that both CMV and EBV are human herpesviruses that share common structural characteristics, life cycle (i.e., cellular invasion, replication, and latency), and similar innate and adaptive (particularly CD8+ T cells) responses of the host upon infection [46,47], it is tempting to speculate that PAH could also increase the risk of CMV reactivation once the VGCV prophylaxis was discontinued. This evidence concerns the gene CD8A and pulmonary arterial hypertension.