الفهرس 
o Human Papilloma VirusOnly 14 pages are availabe for public view
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Abstract
The Human papilloma virus (HPV) is a coild, double-stranded DNA virus. HPV infects squamous cells through insertion of DNA into the host genome, causing abnormal cell replication. Typing of HPV is based on the sequence of the E6, E7 oncogenes and L1 major capsid proteins. HPV types possess a genetic difference of greater than 10% in these genes. There are more than 100 genotypes of HPV, composed of 72 pentamers of the L1 major capsid protein. When isolated for testing or immunization, they are also known as virus-like particles.
HPVs are species specific and cause disease manifestations as cutaneous diseases, anogenital diseases, and other types of diseases (eg, respiratory papillomatosis and focal epithelial hyperplasia of the oral cavity). Infection may be clinically obvious or subclinical.
Verrucae have several different forms based upon location (genital, plantar, and palmar warts) and morphology (flat, mosaic, and filiform warts). Lesions may occur singly, in groups, or as coalescing lesions forming plaques. Mosaic warts are plaques of coalescing plantar or palmar warts.
The diagnosis of verrucae is based upon clinical appearance. In plantar warts, if there is doubt, a number15 blade can be used to scrape off any hyperkeratotic debris and reveal thrombosed capillaries, often called seeds. The wart also will obscure normal skin markings. Rarely, a shave biopsy is indicated to confirm the diagnosis.
The HPV infects the basal layer of the skin or mucosa and causes cellular proliferation and vascular growth, resulting in hyperkeratotic or verrucous lesions.
The incubation period of HPV infections is variable and may range from several weeks to more than a year. Spontaneous resolution occurs in one third of patients within 2 years, and over 90% within 5 years. On the other hand, recurrence is common, especially with autoinoculation or reactivation of latent infection.
The type and aggressiveness of therapy for verrucae will depend upon the type of wart, its location, the degree of symptoms, and the patient’s cooperation and immune status. Current therapies for HPV are not specific for the virus. Some work by enhancing innate immunity or by local chemotherapeutic effect, but the majority work by tissue destruction, with the goal of destroying the virus-containing epidermis and preserving as much uninvolved tissue as possible. The least painful methods should be used initially, especially in young children. More aggressive or destructive therapies should be reserved for areas where scarring is not a consideration or for recalcitrant or symptomatic lesions.
Many treatments have been described for viral warts. Common therapeutic approaches include liquid nitrogen, cryosurgery, topically applied acids, chemical and thermal cautery, virucidal agents, cantharidin application, photodynamic therapy, electrosurgery, intralesional bleomycin, 5-fluorouracil, and carbon dioxide laser ablation.
New therapeutic options are based on immunological stimulation such as the immunomodulator imiquimod (5% cream) and interferon which has antiviral, antiproliferative and immunomodulating effect.
Intralesional immunotherapy with a combination of the skin test antigens candida, mumps, and trichophyton is a safe and effective therapy for warts. This approach does not need pretreatment skin testing, thereby saving the patient additional intradermal injections as well as an extra office visit.
A new approach is local immunotherapy of genital warts with bacillus Calmette-Guerin (BCG).
Instillation of BCG into the urinary bladder is an effective treatment of superficial bladder cancer. BCG-mediated anti-tumour activity appears to be a local phenomenon in which cell-mediated immunity, involving cytotoxic T cells, lymphokine-activated killer cells and natural killer cells, is important for the elimination of malignant cells.
Because of the similarity of the immune response against malignant and virally transformed cells, researches have extended the application of BCG to untreated genital condylomata acuminata.
In the present study, we tried to investigate the effectiveness of topical application of BCG in treatment of common and plantar warts.
Our study included 7 patients with common and plantar warts and 2 patients as a control group.
Viable BCG mixed with salicylic acid solution was directly applied to the wart lesions once weekly for 6 weeks. In non-responding or partially responding patients, another course of BCG application was administered for 3 weeks.
Topical application of BCG led to clearance of wart lesions within 6 weeks in 4 of 7 (57%) patients and some warts in one of these patients achieved partial response within 6 weeks and a complete response within another 3 weeks.
In the other 3 patients (43%) there was no response to treatment. None of the patients reported any side effect.
As regarded to the control group, there was no improvement in wart lesions after placebo application.