Based on this, we found that both cell-associated virus and secreted virus from HSV-1-infected Oct-1 KO cells were significantly less efficient in initiating the next round of infection in wild type (wt) HEp-2 cells, implying that the presence of Oct-1 in prior infection is critical for the two primary modes of HSV-1 transmission, cell-free release (CFR) and cell–cell spread (CCS; Rice, 2021). Here, POU2F1 is linked to infection.