In women with genital warts caused by low‑risk HPV, the body naturally ramps up several beta‑defensins (hBD‑1, hBD‑2, hBD‑3) and a protein called psoriasin, but it does not increase the antimicrobial peptide LL‑37. This suggests LL‑37 isn’t a key player in fighting these lesions, while beta‑defensins may be more important.

Infections with a low-risk type of human papillomavirus (HPV) may lead to genital warts. HPV targets the basal cell layer of epithelial cells. The first line of defense is the innate immune system, which provides nonspecific protection against a variety of pathogens. The antimicrobial peptides (AMPs) α- and β-defensins, cathelicidins, psoriasin, and RNase7 are central mediators. The expression of various α- and β-defensins, cathelicidin LL-37, psoriasin, and RNase7 was studied in biopsy samples from 35 patients with genital warts and 25 healthy women using quantitative real-time polymerase chain reaction and immunohistochemical analysis. We found a significantly higher expression of the β-defensins hBD-1 (P = .03), hBD-2 (P < 0.01), and hBD-3 (P < .001), and psoriasin (P = .001) in condylomata acuminata, compared with normal controls. The RNA and protein levels of RNase7 did not differ between infected and uninfected samples (P = .55). The α-defensins HNP 1-3, HD5, and HD6 and the cathelicidin LL-37 were scarcely detectable in normal and infected tissue. The differing expression of AMPs in HPV-infected, compared with noninfected, vulvovaginal biopsy samples suggests that these peptides are important in the local immune response. Curiously, hBD-1 shows a significant induction whereas RNase7 does not, which suggests differing regulation of AMPs over the course of bacterial and viral infections.