A viral wart is an intra-epidermal proliferation caused by the human papillomavirus (HPV). More than 150 genotypes of HPV exist; types 1, 2, 4, 27 and 57 most often produce the cutaneous lesions termed common warts, plantar warts, flat warts and mosaic warts. The virus enters through micro-abrasions and remains strictly within the epithelium; no systemic viraemia occurs. The infected keratinocyte shows delayed maturation and excessive production of keratin, yielding the clinically rough, thickened papule. Transmission occurs by direct skin contact or indirectly via contaminated floors, towels and footwear. Occlusion, maceration and atopic dermatitis increase susceptibility, while intact, well-moisturised skin offers considerable protection.
Who Develops Viral Warts?
Viral warts affect all ages, but peak incidence is between 6 and 14 years. Immunocompromised patients—organ transplant recipients on long-term azathioprine or ciclosporin, individuals with human immunodeficiency virus infection and those on biologic therapies—have higher incidence, larger lesions and lower rates of spontaneous resolution. Diabetes mellitus, peripheral vascular disease and occupations involving chronic water exposure also predispose to persistence.
How Do Viral Warts Appear Clinically?
Common warts (verruca vulgaris) present as firm, grey-brown papules with a papillomatous surface, most often on the dorsal hands and periungual skin. Plantar warts (verruca plantaris) interrupt the normal dermatoglyphics, display central punctate thrombosed capillaries and are painful on lateral compression. Flat warts (verruca plana) are 1–3 mm, skin-coloured or slightly hyperpigmented, flat-topped papules that appear in clusters on the face and extremities. Filiform warts exhibit a narrow, elongated stalk and are typically located on the lips, eyelids and nares. Mosaic warts are confluent plaques on the soles formed by multiple small plantar warts coalescing.
Dermoscopy performed with the IBOOLO DE-4100 in polarised mode shows densely packed, punctate red-to-black haemorrhagic dots corresponding to thrombosed capillaries, each surrounded by a white halo. These dots lie within papillomatous elevations separated by white furrows. No pigment network is present, and interruption of skin lines at the border helps distinguish plantar warts from callus.
Why Do Some Warts Resolve Spontaneously While Others Persist?
Resolution depends on the development of a cell-mediated immune response. Children develop HPV-specific T-helper-1 lymphocytes more readily than adults, explaining the higher rate of spontaneous clearance in the young. Immunosuppression, repeated micro-trauma and high viral load impede this response. Genotype also matters: HPV-1 and HPV-2 lesions often regress within two years, whereas HPV-57 and HPV-60 lesions are more persistent. Smoking and ultraviolet exposure further delay clearance.
Can Dermoscopy Aid in Diagnosis and Monitoring?
Yes. Dermoscopy with the IBOOLO DE-4100 clarifies the differential diagnosis. In viral warts, the polarised image reveals the characteristic "red-black pepper" pattern of thrombosed capillaries surrounded by white halos, distinguishing the lesion from seborrhoeic keratosis, which shows comedo-like openings and milia-like cysts, and from squamous cell carcinoma, which displays irregular vessels and ulceration.
What Treatments Are Available?
Therapeutic choice balances lesion type, patient preference, age and immune status. First-line options include daily application of 15–40 % salicylic acid formulations, which induce keratolysis and expose HPV-infected cells to the immune system. Regular soaking, gentle paring and occlusion improve efficacy. Cryotherapy with liquid nitrogen at –196 °C, applied for 10–30 seconds every 2–3 weeks, achieves 60–80 % clearance for common and plantar warts after 2–6 sessions. Pain, blistering and post-inflammatory hypopigmentation are common adverse effects.
For recalcitrant lesions, pulsed-dye laser (585 nm) targets haemoglobin within wart capillaries, causing selective photothermolysis with minimal scarring. CO₂laser ablation provides rapid tissue vaporisation and excellent haemostasis but requires local anaesthesia and carries a small risk of scarring. Intralesional immunotherapy with Candida antigen, MMR vaccine or purified protein derivative stimulates delayed-type hypersensitivity and is effective for multiple or periungual warts. Topical imiquimod 5 % cream is useful for flat facial warts and immunocompromised patients, applied three nights weekly for up to sixteen weeks.
Surgical curettage or shave excision is reserved for solitary, large or diagnostically uncertain lesions and must be followed by electrocautery to reduce recurrence. Cantharidin 0.7 % induces intra-epidermal blistering and is painless on application, making it suitable for children. Trichloroacetic acid 80–90 % offers chemical cauterisation for periungual and mosaic warts.
What Simple Measures Prevent Spread?
Since HPV survives in moist environments, patients should wear protective footwear in communal showers and swimming pools. Towels, nail clippers and razors must not be shared. Existing warts should be covered with a waterproof plaster during sports. Regular hand washing and prompt treatment of minor skin injuries reduce autoinoculation. Individuals with atopic dermatitis benefit from daily emollients to maintain barrier function.
When Should Medical Review Be Sought?
Any wart that enlarges rapidly, bleeds, ulcerates, or resists standard therapy warrants dermoscopic and histological review to exclude verrucous carcinoma or squamous cell carcinoma. Immunocompromised patients with numerous or giant warts require early specialist referral, as treatments are less effective and recurrence rates are high. Plantar warts causing significant pain or interfering with gait should be assessed for underlying bursitis or secondary infection.