Pathophysiology

Predisposing factors
Genital warts have a high infectivity. The thinner mucosal surface
is presumably more susceptible to inoculation of virus than
thicker keratinized skin, but in addition lesions are commonest in
sites subject to greatest coital friction in both sexes.
Human papillomavirus transmission has been most closely
studied in the case of anogenital warts. Acquisition most commonly
follows sexual contact but it is generally agreed that anogenital
warts are not always transmitted sexually. Perianal warts
may accompany genital warts, either due to local spread of infection
or to direct contact during anal coitus.
In prospective studies, approximately twothirds of sexual contacts
of patients with genital warts developed lesions themselves
within 24 months; infectivity seemed highest early in the course
of the disease [207,208]. Close inspection by penoscopy of male
sexual contacts of women with genital HPV disease has shown
that 69% [209] or 88% [210] have at least small lesions. Prospective
studies of sexual contacts of patients with genital warts indicated
that the incubation period between contact and diagnosis
of genital warts is 3 weeks to 24 months, with a median of 310
months [207,208].
Occasional nonsexual acquisition of anogenital warts in adults
is assumed to be possible. The sensitivity of PCR analysis has
shown that HPV DNA may be present on underwear and the fingers
of patients with genital warts [211,212] suggesting that transmission
could occur by a number of routes.
Transmission of anogenital warts in children [213215]
Anogenital warts are uncommon in children, but their occurrence
frequently stimulates discussion of the possibility of sexual transmission.
With the lack of largescale prospective studies, the possibility
of bias in referral or in reporting should be considered, and
there remains insufficient information to offer a reliable estimate
of the relative frequency of sexual abuse in such cases.
Infection from the mothers genital tract at delivery [216,217]
is regarded as a frequent source of childhood anogenital warts,
probably including those presenting up to 2 years of age. Genital
papillomavirus transmitted from mother to baby at birth may persist
in childhood [218,219] as shown by the retention of the DNA
and/or a humoral response against the viral proteins. It is thought
that perinatally acquired HPV infection may not manifest as genital
warts for some years.
Postnatally, transmission from adults with genital warts may
occur nonsexually [220] such as by sharing a bath with an infected
adult. A review of reports published between 1976 and 1983 [221]
found that, of the total of 21 cases, the probable route of infection
was believed to be sexual in 11, prepartum or intrapartum in three,
and unknown in seven. In studies of children with anogenital
warts assessed for possible sexual abuse, the mode of acquisition
was thought to be sexual in no more than 5% [222,223].
Thus, on present incomplete information, both sexual and
nonsexual routes are significant in the transmission of childhood
anogenital warts [224]. The long and variable incubation
period, the possibility of latent or subclinical infection in the
source and the problems in eliciting an accurate account of sexual
contact from the child and of confirming it from the perpetrator,
all make it difficult to decide which applies in an individual case.
Absence of other physical evidence of molestation, location of
the warts on fully keratinized skin as opposed to genital or anal
mucosa, a clinical resemblance to common warts and young age of
the child, perhaps up to 12 years at the onset of the warts, would
tend to support nonsexual transmission. Where sexual abuse is
suspected, the case should be referred to a paediatrician or child
abuse specialist. In addition, HPV typing is not routinely of use
but might be forensically useful; the same type in child and in suspected
abuser would be consistent with but not proof of sexual
transmission, while different types would be strong evidence
against the possibility.
The infectivity of maternal genital HPV as regards laryngeal papilloma
in the child seems low; from 51 cases of pregnancy in women
with genital warts, no cases of childhood laryngeal papilloma were
seen [225]. The risk of transmission from mother to child with subsequent
development of disease in the child has been estimated to
be between 1/80 and 1/1500 [226] but only 57% of cases of laryngeal
papilloma in children are diagnosed by 2 years of age [227].
Pathology [35]
Genital warts show extreme acanthosis and papillomatosis, but
the horny layer is parakeratotic and not very thick. Koilocytes
may be limited in distribution and not found in all sections. The
epidermal processes are wide and rounded, with a welldefined
lower border. The connective tissue is frequently very oedematous
and the capillaries tortuous and increased.
Causative organisms
The lowrisk HPVs are most often the cause of anogenital warts,
most commonly HPV6 (in about 4590%) [228230] or HPV11
and less frequently other types as indicated in Table 25.7. HPV1
and HPV2 may occur in genital warts [231,232].
In children, warts in the anogenital area are often more hyperkeratotic
than in adults and may be caused by HPV types associated
with cutaneous disease as well as HPV6 and 11. Studies involving
HPV typing of childhood anogenital warts have produced somewhat
varying conclusions, but overall, approximately 50% have
been found to harbour mucosogenital HPV with the cutaneous
types 2, 27 and 57 also commonly detected [217,233235].

The papovaviruses are double-stranded, naked (nonenveloped)

DNA viruses and are characterized by their slow growth. These
viruses typically infect the epithelia of the skin or mucosa, favoring
certain locations such as the hands, feet, face, or genitalia. Over100
subtypes of HPV have been identified, and infections can be categorized
as anogenital lesions (condyloma acuminatum or genital
warts) and nongenital lesions (common warts or verruca). Anogenital
warts will be discussed in chapter 21.
While warts themselves are not cancerous, some strains of HPV
(usually ones not associated with warts) are oncogenic. Cutaneous
warts can be spread through direct person-to-person skin contact
or indirectly through contaminated surfaces and objects (e.g.,
swimming pools, showers). Autoinoculation of the virus from an
existing lesion to adjacent skin is commonly seen on the hands in
the interdigital and periungual areas. The risk of becoming infected
will depend on the immune status of the exposed individual, the
amount of virus present during exposure, and the nature of the
contact.

Papovavirus beranduk ganda, telanjang (tidak dilipat)

Virus DNA dan ditandai oleh pertumbuhannya yang lambat. Ini
Virus biasanya menginfeksi epitel kulit atau mukosa, disukai
Lokasi tertentu seperti tangan, kaki, wajah, atau genitalia. Lebih dari 100
Subtipe HPV telah diidentifikasi, dan infeksi dapat dikategorikan
Sebagai lesi anogenital (condyloma acuminatum atau genital
Kutil) dan lesi nongenital (kutil umum atau veruka). Anogenital
Kutil akan dibahas di Bab 21.
Sementara kutil sendiri tidak bersifat kanker, beberapa jenis HPV
(Biasanya yang tidak terkait dengan kutil) bersifat onkogenik. Kutaneous
Kutil bisa disebarkan melalui kontak langsung dengan orang ke orang
Atau secara tidak langsung melalui permukaan dan objek yang terkontaminasi (misalnya,
Kolam renang, shower). Autoinokulasi virus dari a
Lesi yang ada pada kulit yang berdekatan biasanya terlihat di tangan
Daerah interdigital dan periungual. Risiko terinfeksi
Akan tergantung pada status kekebalan individu yang terpapar
Jumlah virus yang hadir saat pemaparan, dan sifat dari
kontak.
Pathophysiology
HPV is a double-stranded circular DNA genome. Some viral types,
such as types 16, 18, and 31, can cause the p53 protein and RB proteins
to be inactivated and can cause a normal cell to become a cancerous
one. HPV type 16 is thought to be the most oncogenic and can result
in cancers of the vulva, vagina, cervix, penis, and anal area. The virus
infects the squamous cells and creates characteristic koilocytes within
the cell. They initially enter the skin or mucous membrane through
tiny tears or abrasions that may be created through trauma or friction
during sexual contact. The virus enters the basaloid epithelium
and is able to evade immune surveillance. It takes days, months, or
years to develop the condyloma, if at all. Often the body is able to
clear the virus in time through cell-mediated immunity and antibodies
induced by the viral infection itself.

Papillomavirus adalah virus symmetry icosahedral tanpa pelepasan

dengan 72 capsomeres yang mengelilingi genom yang mengandung
DNA melintang beruntai ganda dengan sekitar 8000 pasangan basa.
Genom mereka dibagi menjadi 3 wilayah fungsional utama berikut ini:
Kode wilayah awal (E) untuk 6 gen nonstruktural, beberapa di
antaranya berhubungan dengan transformasi seluler. Kode wilayah
akhir (L) untuk 2 protein struktural, L1 dan L2, yang membentuk kapsid
Wilayah kontrol yang panjang adalah wilayah noncoding yang mengatur
replikasi dan fungsi gen