Brodawki zwykłe
Patofizjologia i mechanizm

Brodawki zwykłe (Verruca vulgaris) są łagodnymi zmianami skórnymi wywołanymi przez HPV, głównie typów 2 i 4. Infekcja rozpoczyna się wniknięciem wirusa do komórek warstwy podstawnej naskórka przez mikrourazy, z okresem inkubacji od 2 do 6 miesięcy. Wirus replikuje się w zróżnicowanych keratynocytach, wykorzystując białka E1, E2, E6 i E7, które indukują niekontrolowaną proliferację komórek i hiperkeratozę. Histopatologicznie obserwuje się hiperkeratozę, akantozę, obecność koilocytów oraz powiększone naczynia krwionośne. Układ immunologiczny, zwłaszcza limfocyty CD8+ i komórki NK, odgrywa kluczową rolę w kontroli infekcji, jednak wirus unika odpowiedzi immunologicznej, co może prowadzić do przewlekłych zakażeń. Cytokiny takie jak IL-1, IL-6, IL-12, IL-17 oraz TNF modulują przebieg infekcji i odpowiedź immunologiczną, a obniżone poziomy IL-17 i IL-22 wiążą się z opornością brodawek. Pacjenci z immunosupresją są bardziej narażeni na cięższy przebieg i trudności terapeutyczne.

Patogeneza brodawek zwykłych

Brodawki zwykłe (Verruca vulgaris) są łagodnymi zmianami skórnymi wywołanymi przez wirusa brodawczaka ludzkiego (Human Papillomavirus – HPV). Spośród ponad 200 znanych typów HPV, brodawki zwykłe najczęściej powodowane są przez HPV typu 2 i 4, a w mniejszym stopniu przez typy 1, 3, 27, 29 i 57.123 Zrozumienie patogenezy brodawek zwykłych jest kluczowe dla opracowania skutecznych metod leczenia i zapobiegania tej powszechnej infekcji wirusowej.

Proces infekcji i wnikania wirusa

Infekcja HPV rozpoczyna się od wniknięcia wirusa do komórek warstwy podstawnej naskórka poprzez mikropęknięcia lub uszkodzenia bariery naskórkowej.45 Urazy, maceracja tkanek oraz osłabiona bariera skórna zwiększają ryzyko zakażenia.67 Po wniknięciu do komórek podstawnych, wirus może pozostawać w stanie latentnym lub rozpocząć aktywną replikację, co prowadzi do rozwoju brodawki. Okres inkubacji wirusa HPV jest stosunkowo długi i wynosi od 2 do 6 miesięcy, choć w niektórych przypadkach może trwać nawet rok.89

Transmisja wirusa zachodzi głównie przez bezpośredni kontakt skóry ze skórą lub przez autoinokulację, gdy osoba przenosi wirusa na inne obszary własnego ciała poprzez dotykanie lub drapanie istniejących brodawek.1011 Wirus może być również przenoszony pośrednio przez kontakt z zanieczyszczonymi powierzchniami lub przedmiotami (np. ręczniki czy podłogi w publicznych łaźniach), choć ten sposób transmisji jest rzadszy.12

Molekularne mechanizmy replikacji wirusa

Po zakażeniu komórek warstwy podstawnej, HPV wykorzystuje maszynerię komórkową gospodarza do replikacji swojego materiału genetycznego. Cykl życiowy wirusa jest ściśle związany z programem różnicowania komórek nabłonkowych.13 W początkowej fazie infekcji wirus utrzymuje swoją obecność w komórkach podstawnych na niskim poziomie, bez wytwarzania pełnych cząstek wirusowych. Aktywna replikacja wirusa zachodzi dopiero w zróżnicowanych keratynocytach warstw powierzchniowych naskórka.14

Kluczową rolę w replikacji wirusa odgrywają białka wirusowe E1 i E2, które stymulują komórki gospodarza do replikacji DNA wirusa.15 Natomiast białka E6 i E7 HPV przejmują kontrolę nad mechanizmami punktów kontrolnych cyklu komórkowego, co prowadzi do niekontrolowanej proliferacji zainfekowanych komórek.16 Ten proces skutkuje charakterystycznym dla brodawek przerostem naskórka (hiperkeratoza/” title=”hiperkeratoza” class=”to-tag” data-termid=”28111″>hiperkeratozą) i hiperplazją komórek.

W zakażonych komórkach dochodzi do nadmiernej produkcji keratyny – twardego białka w zewnętrznej warstwie skóry, co nadaje brodawkom ich charakterystyczną twardą, szorstkią teksturę.1718 Nowe cząsteczki wirusa formują się w górnych warstwach naskórka i są uwalniane wraz z łuszczącymi się komórkami naskórka, co umożliwia dalsze rozprzestrzenianie się zakażenia.19

Zmiany histopatologiczne

Brodawki zwykłe mają charakterystyczny obraz histopatologiczny. Do typowych zmian mikroskopowych należą:2021

  • Pogrubienie warstwy rogowej naskórka (hiperkeratoza)
  • Pogrubienie warstwy kolczystej (akantoza)
  • Pogrubienie warstwy ziarnistej
  • Wydłużenie sopli naskórkowych
  • Powiększone naczynia krwionośne na granicy skórno-naskórkowej
  • Obecność komórek z wakuolizacją cytoplazmy (koilocytów) w górnych warstwach naskórka

22

Koilocyty są charakterystycznym objawem infekcji HPV – są to keratynocyty z małym, obkurczonym jądrem otoczonym okołojądrowym halo (aureolą).23 Ich obecność jest uważana za histologiczny marker infekcji HPV.

Mechanizmy immunologiczne w patogenezie brodawek zwykłych

Odpowiedź immunologiczna na infekcję HPV

Układ immunologiczny odgrywa kluczową rolę w kontroli infekcji HPV i spontanicznej regresji brodawek. HPV posiada jednak mechanizmy umożliwiające mu unikanie odpowiedzi immunologicznej gospodarza, co może prowadzić do przewlekłych zakażeń.24 Wirus zazwyczaj nie wywołuje lizy komórek ani stanu zapalnego, pozostając względnie chroniony przed rozpoznaniem przez układ immunologiczny.

Regresja brodawek zależy od rozwoju efektywnej odpowiedzi immunologicznej komórkowej.25 Antygeny wirusowe są początkowo wychwytywane przez komórki Langerhansa w naskórku, które następnie przemieszczają się do regionalnych węzłów chłonnych, gdzie inicjują odpowiedź immunologiczną.26 Kluczową rolę w eliminacji infekcji HPV odgrywają limfocyty CD8+ cytotoksyczne oraz komórki NK (Natural Killer).2728

Regresja brodawek wiąże się z degeneracją komórek podstawnych, degeneracją naskórka i zakrzepicą naczyniową, co świadczy o aktywnej odpowiedzi immunologicznej skierowanej przeciwko zakażonym komórkom.29

Rola cytokin w patogenezie

Cytokiny odgrywają istotną rolę w odpowiedzi immunologicznej przeciwko HPV. Równowaga między różnymi typami cytokin ma wpływ na przebieg infekcji i możliwość spontanicznej regresji brodawek.30 Interleukiny, takie jak IL-1α, IL-1β, IL-6 i IL-12, uczestniczą w adaptacyjnej odpowiedzi immunologicznej przeciwko HPV.31

Odpowiedź typu Th1 jest kluczowa dla obrony przeciwwirusowej. IL-2 aktywuje komórki immunologiczne, zwłaszcza limfocyty T, natomiast IL-12 reguluje funkcję limfocytów poprzez indukcję ich różnicowania w komórki Th1.32 Podwyższone poziomy IL-6, IL-8 i TNF mogą zaburzać odpowiedź przeciwwirusową, umożliwiając wirusowi przetrwanie w zakażonych komórkach.33

IL-17 może pomagać HPV w unikaniu odpowiedzi immunologicznej gospodarza i długotrwałym utrzymywaniu się w keratynocytach. Niskie poziomy IL-17 w surowicy zaburzają odpowiedź immunologiczną komórek Th1, co zwiększa podatność na zakażenie HPV.34 Badania wykazały, że u pacjentów z opornymi brodawkami występują istotne obniżenia poziomu IL-17 i IL-22 w surowicy, co może odgrywać kluczową rolę w patogenezie opornych brodawek poprzez zaburzenie równowagi układu immunologicznego.35

Zaburzenia immunologiczne a brodawki

Osoby z upośledzoną odpowiedzią immunologiczną komórkową (zarówno pierwotną, jatrogenną, jak i wywołaną przez HIV) są szczególnie narażone na rozwój licznych brodawek, które nie ulegają spontanicznej regresji i są trudne do leczenia.3637 U pacjentów z immunosupresją brodawki występują częściej, są bardziej rozległe i utrzymują się dłużej.3839

Przesunięcie odpowiedzi immunologicznej z typu Th1 na Th2 jest związane z zaburzoną rozpoznawalnością wirusa przez układ immunologiczny, co ułatwia przetrwanie wirusa przez nieokreślony czas i prowadzi do progresji zmian.40

Mechanizmy leczenia brodawek w kontekście patogenezy

Metody destrukcyjne

Metody destrukcyjne powodują niespecyficzne uszkodzenie zakażonych keratynocytów i otaczającej skóry.41 Do tej grupy należą:42

  • Krioterapia – zamrażanie brodawki ciekłym azotem, co powoduje martwicę tkanek. Mechanizm działania obejmuje nie tylko bezpośrednie zniszczenie zakażonych komórek, ale również wywołanie miejscowego podrażnienia, które stymuluje odpowiedź immunologiczną.4344
  • Kwas salicylowy – działa keratolitycznie, niszcząc naskórek zakażony wirusem. Jest nadal leczeniem o najlepiej udokumentowanej skuteczności.45
  • Elektrokoagulacja, chirurgiczne usunięcie i ablacja laserowa – metody te powodują fizyczne usunięcie tkanek zakażonych HPV.46

Warto podkreślić, że metody destrukcyjne nie niszczą samego wirusa, ale usuwają skórę zawierającą wirusa.47 Trwałość i skuteczność leczenia zależy od tego, czy wirus zostanie całkowicie wyeliminowany.

Immunoterapia

Immunoterapia jest innowacyjnym podejściem do leczenia brodawek, które polega na wzmocnieniu odpowiedzi immunologicznej komórkowej.48 Metody immunoterapii obejmują:4950

  • Imikwimod – stymuluje zarówno wrodzoną, jak i komórkową odpowiedź immunologiczną.
  • Intralesional immunotherapy (immunoterapia doogniskowa) – wykorzystanie antygenów, takich jak PPD (Purified Protein Derivative), antygen kandydy, szczepionka MMR lub Mw, do wywołania reakcji nadwrażliwości typu opóźnionego.
  • Dinitrochlorobenzen (DNCB) i difenylocyklopropenon (DCP) – działają jako alergeny kontaktowe, wywołując miejscową reakcję immunologiczną.
  • Cymetydyna – podawana doustnie w celu modulacji odpowiedzi immunologicznej.

Immunoterapia doogniskowa działa poprzez indukcję uwalniania różnych związków prozapalnych, które aktywują komórki prezentujące antygen (APC). Komórki te rozpoznają i przetwarzają HPV zarówno w miejscu iniekcji, jak i w odległych ogniskach infekcji.51 Prowadzi to do rozwoju silnej adaptacyjnej reakcji immunologicznej przeciwko HPV, mediowanej przez cytokiny Th1, takie jak interleukina-4, 5, 8, IFN-γ i TNF-α.52

Mechanizmy spontanicznej regresji

Około 65% brodawek ustępuje samoistnie w ciągu 2 lat, co wskazuje na zdolność układu immunologicznego do ostatecznego opanowania infekcji HPV.5354 Spontaniczna regresja brodawek jest związana z rozwojem odporności komórkowej przeciwko antygenom HPV.55

W brodawkach, które ulegają samoistnej regresji, obserwuje się wyraźne nacieki limfocytarne w skórze właściwej, co potwierdza rolę odpowiedzi immunologicznej komórkowej w tym procesie.56 Warto zauważyć, że brodawki ustępujące samoistnie zazwyczaj nie pozostawiają blizn, w przeciwieństwie do brodawek leczonych metodami destrukcyjnymi.57

Czynniki ryzyka i podatność na zakażenie HPV

Czynniki związane z gospodarzem

Podatność na zakażenie HPV i rozwój brodawek zależy od wielu czynników związanych z gospodarzem:5859

  • Wiek – dzieci i młodzi dorośli są bardziej podatni na rozwój brodawek. Z wiekiem prawdopodobieństwo zachorowania maleje, a istniejące brodawki mogą samoistnie ustąpić.60
  • Stan układu immunologicznego – osoby z osłabionym układem immunologicznym, w tym pacjenci z HIV/AIDS, po przeszczepie narządów lub poddani chemioterapii, są bardziej narażone na rozwój brodawek.61
  • Uszkodzenia skóry – mikrourazy, zadrapania, maceracja skóry zwiększają ryzyko infekcji HPV.62
  • Genetyka – niektóre osoby mogą być genetycznie predysponowane do rozwoju brodawek, mimo rozwinięcia odporności większość osób staje się odporna na wirusa w późnym okresie nastoletnim.63

Czynniki środowiskowe

Do czynników środowiskowych zwiększających ryzyko zakażenia HPV należą:64

  • Bezpośredni kontakt z osobami zakażonymi – bliski kontakt skóry ze skórą z osobą zakażoną HPV.
  • Kontakt z zanieczyszczonymi powierzchniami – podłogi, ręczniki, maty łazienkowe.
  • Środowiska wilgotne – baseny, publiczne prysznice, gdzie wirus może przetrwać dłużej.
  • Środowiska rodzinne – obecność członka rodziny z brodawkami została zidentyfikowana jako czynnik ryzyka, ważniejszy niż korzystanie z basenów czy wspólnych pryszniców.65

Implikacje kliniczne patogenezy brodawek zwykłych

Zrozumienie patogenezy brodawek zwykłych ma istotne implikacje kliniczne:6667

  • Zapobieganie autoinokulacji – ograniczenie samozakażenia jest kluczowe dla skutecznego leczenia brodawek, szczególnie w przypadkach ciężkich i rozsianych.
  • Edukacja pacjentów – zrozumienie etiologii brodawek daje pacjentom wiedzę potrzebną do ograniczenia rozprzestrzeniania się infekcji.
  • Dobór metod leczenia – zrozumienie mechanizmów działania różnych metod terapeutycznych pozwala na indywidualizację leczenia.
  • Profilaktyka – unikanie bezpośredniego kontaktu z brodawkami, noszenie obuwia ochronnego, mycie rąk po kontakcie z brodawkami.68

Warto podkreślić, że cele leczenia brodawek obejmują zniszczenie zmiany, indukcję cytotoksyczności wobec zakażonych komórek i promowanie odpowiedzi immunologicznej przeciwwirusowej w celu zapobiegania nawrotom.69 Najlepsze wyniki osiąga się przy zastosowaniu kombinacji metod destrukcyjnych i immunostymulujących.70

Podsumowanie mechanizmów patogenezy

Patogeneza brodawek zwykłych to złożony proces obejmujący kilka kluczowych etapów:7172

  • Infekcja wstępna – wirus HPV wnika do komórek warstwy podstawnej naskórka przez mikrourazy skóry.
  • Replikacja i integracja – wirus wykorzystuje maszynerię komórkową gospodarza do replikacji swojego DNA, pozostając głównie w górnych warstwach naskórka.
  • Hiperproliferacja – zakażone komórki ulegają nadmiernej proliferacji, co prowadzi do charakterystycznego zgrubienia naskórka i powstania brodawki.
  • Unikanie odpowiedzi immunologicznej – HPV posiada mechanizmy umożliwiające mu unikanie rozpoznania przez układ immunologiczny, co może prowadzić do długotrwałych infekcji.
  • Eliminacja lub przetrwanie – los infekcji HPV zależy od równowagi między mechanizmami unikania odpowiedzi immunologicznej wirusa a zdolnością układu immunologicznego gospodarza do eliminacji zakażonych komórek.

Zrozumienie tych mechanizmów jest kluczowe dla opracowania nowych, bardziej skutecznych strategii leczenia brodawek zwykłych oraz dla edukacji pacjentów na temat zapobiegania rozprzestrzenianiu się infekcji.7374

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  1. 09.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Wart – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK431047/
    Warts are prevalent benign lesions caused by the human papillomavirus (HPV) that occur in the mucosa and skin. […] Warts are caused by the human papillomavirus (HPV), with over 100 types of HPV identified. HPV may occur at any site. The primary manifestations of HPV infection include common warts, genital warts, flat warts, deep palmoplantar warts (Myrmecia), focal epithelial hyperplasia, Epidermodysplasia verruciformis, and Plantar cysts. […] Events that disrupt the normal epithelial barrier increase the likelihood of developing warts. […] Common warts are associated with HPV types 2, 4 (most common), followed by types 1, 3, 27, 29, and 57. […] Out of the 100 subtypes of HPV, a few of them have the propensity to induce cancer. These subtypes include HPV strains 6, 11, 16, 18, 31, and 35. Malignant transformation tends to occur in individuals with genital warts and those who are immunocompromised. HPV strains 5, 8, 20, and 47 also have malignant potential in individuals with epidermodysplasia verruciformis.
  • #2 Nongenital Warts: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1133317-overview
    Warts are benign proliferations of skin and mucosa caused by the human papillomavirus (HPV). Currently, more than 100 types of HPV have been identified. Certain HPV types tend to infect skin at particular anatomic sites; however, warts of any HPV type may occur at any site. The primary clinical manifestations of HPV infection include common warts, genital warts, flat warts, and deep palmoplantar warts (myrmecia). […] Warts can affect any area on the skin and mucous membranes. The HPV virus infects the epithelium, and systemic dissemination of the virus does not occur. Viral replication occurs in differentiated epithelial cells in the upper level of the epidermis; however, viral particles can be found in the basal layer. […] Warts are caused by HPV, which is a double-stranded, circular, supercoiled DNA virus enclosed in an icosahedral capsid and comprising 72 capsomers. More than 100 types of HPV have been identified. Note the following wart types and HPV types: Common warts – HPV types 2 and 4 (most common), followed by types 1, 3, 27, 29, and 57.
  • #3 Wart – Wikipedia
    https://en.wikipedia.org/wiki/Wart
    Common warts have a characteristic appearance under the microscope. They have thickening of the stratum corneum (hyperkeratosis), thickening of the stratum spinosum (acanthosis), thickening of the stratum granulosum, rete ridge elongation, and large blood vessels at the dermoepidermal junction. […] Warts are caused by the human papillomavirus (HPV). There are about 130 known types of human papillomaviruses. HPV infects the squamous epithelium, usually of the skin or genitals, but each HPV type is typically only able to infect a few specific areas of the body. Many HPV types can produce a benign growth, often called a „wart” or „papilloma”, in the area they infect. […] Common warts HPV types 2 and 4 (most common); also types 1, 3, 26, 29, and 57 and others.
  • #4 Plantar Warts: Epidemiology, Pathophysiology, and Clinical Management
    https://www.degruyterbrill.com/document/doi/10.7556/jaoa.2018.024/html?lang=en&srsltid=AfmBOoqQL1T6uhM6uwzNSccLw67fZYvk_Xios8qN2yaFK6JddrSqgeQY
    Verrucae plantaris (plantar warts) are common cutaneous lesions of the plantar aspect of the foot that are caused by the human papillomavirus (HPV). […] Plantar warts, or verrucae plantaris, are cutaneous lesions on the plantar aspect of the foot that are caused by the infection of keratinocytes with the human papillomavirus (HPV). […] Once a plantar wart is established, it sheds HPV via desquamated epithelial cells. The viral particles can subsequently infect other sites and hosts. […] Current treatment methods have been used with variable success, as the lesions are notoriously resistant to treatment and recur frequently. […] Once infection occurs, 3 outcomes are possible: clearance of the infection with resultant immunity to that particular HPV type, latent infection, or clinically manifested infection as a plantar wart.
  • #5 Destructive therapies for cutaneous warts: A review of the evidence
    https://www1.racgp.org.au/ajgp/2022/october/destructive-therapies-for-cutaneous-warts
    Common warts (Verruca vulgaris), plantar warts (Verruca plantaris) and flat/plane warts (Verruca plana), collectively known as cutaneous warts, are benign growths of the skin caused by the human papillomavirus (HPV). […] A break in the epidermal barrier of the skin allows entry of HPV and subsequent infection of basal epithelial cells. HPV replicates alongside the natural lifecycle of epithelial cells, and is eventually released from desquamated keratinocytes on the surface of warts, potentially infecting other sites via direct contact or through fomites. […] Damaging or destroying the infected epithelium causes HPV cell death. The subsequent antigen exposure and presentation might also induce an immune response.
  • #6 Wart – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK431047/
    Warts are prevalent benign lesions caused by the human papillomavirus (HPV) that occur in the mucosa and skin. […] Warts are caused by the human papillomavirus (HPV), with over 100 types of HPV identified. HPV may occur at any site. The primary manifestations of HPV infection include common warts, genital warts, flat warts, deep palmoplantar warts (Myrmecia), focal epithelial hyperplasia, Epidermodysplasia verruciformis, and Plantar cysts. […] Events that disrupt the normal epithelial barrier increase the likelihood of developing warts. […] Common warts are associated with HPV types 2, 4 (most common), followed by types 1, 3, 27, 29, and 57. […] Out of the 100 subtypes of HPV, a few of them have the propensity to induce cancer. These subtypes include HPV strains 6, 11, 16, 18, 31, and 35. Malignant transformation tends to occur in individuals with genital warts and those who are immunocompromised. HPV strains 5, 8, 20, and 47 also have malignant potential in individuals with epidermodysplasia verruciformis.
  • #7 Warts – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/viral-skin-diseases/warts
    Warts are cutaneous lesions caused by human papillomavirus (HPV) infection; there are over 100 HPV subtypes (1). […] Trauma and maceration facilitate initial epidermal inoculation. Spread can then occur by autoinoculation. Local and systemic immune factors also appear to influence spread; immunosuppressed patients (especially those with suppressed cellular immunity, [eg, HIV infection or a kidney transplant or those with a history of tumor-suppressive immunotherapy]) are at particular risk of developing generalized lesions that are difficult to treat. […] Cellular immunity by CD8+ T-cells is crucial for established infection to regress. However, intact humoral immunity can also provide resistance to HPV infection. […] Common warts (verrucae vulgaris) are caused by HPV types 1, 2, 4, and 7 and occasionally other types in immunosuppressed patients (eg, 75 to 77).
  • #8 Common warts – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/common-warts/symptoms-causes/syc-20371125
    Common warts are caused by a virus and are transmitted by touch. It can take 2 to 6 months for a wart to develop. […] Common warts are caused by the human papillomavirus, also called HPV. There are more than 100 types of this common virus, but only a few cause warts on the hands. Some strains of HPV are spread through sexual contact. But most are spread by casual skin contact or shared objects, such as towels or washcloths. The virus usually spreads through breaks in the skin, such as hangnails or scrapes. Biting your nails also can cause warts to spread on your fingertips and around your nails. […] Each person’s immune system responds to HPV differently. So not everyone who comes in contact with HPV develops warts.
  • #9 Cutaneous warts (common, plantar, and flat warts) – UpToDate
    https://www.uptodate.com/contents/cutaneous-warts-common-plantar-and-flat-warts/print
    Human papillomaviruses (HPVs) infect epithelial tissues of skin and mucous membranes. The most common clinical manifestations of HPV infection are warts (verrucae). There are over 200 distinct HPV subtypes; some tend to infect specific body sites. HPV type 1 commonly infects the soles of the feet and produces plantar warts, while HPV types 6 and 11 infect the anogenital area and cause anogenital warts. […] Infection with human papillomavirus (HPV) occurs by direct skin contact, with maceration or sites of trauma predisposing patients to inoculation. Latent HPV infection also may occur in normal skin. The reservoir for HPV appears to be individuals with clinical or subclinical infection. […] The incubation period is approximately two to six months.
  • #10 Warts, verrucas, human papillomavirus infection
    https://dermnetnz.org/topics/viral-wart
    Warts are due to infection by the human papillomavirus (HPV), a double-stranded DNA virus. There are more than 150 known HPV types, only some of which infect the skin, giving rise to a variety of clinical presentations. Infection begins in the basal layer of the epidermis, causing proliferation of the keratinocytes (skin cells) and hyperkeratosis, and production of infectious virus particles the wart. The most common HPV types infecting the skin are types 1, 2, 3, 4, 10, 27, 29, and 57. […] HPV is spread by direct skin-to-skin contact or autoinoculation; if a wart is scratched or picked, a wart may develop under the fingernail (subungual wart) or virus may be spread to another area of skin. Autoinoculation of the virus in a scratch can result in a line of warts (pseudo-koebnerisation) The incubation period can be as long as twelve months, depending on the amount of virus inoculated. […] Treatments do not kill the virus, but work by removing virus-containing skin. Persistence with the treatment and patience is essential! Remember HPV infects the basal cell layer of the epidermis so warts recur rapidly if the virus has not been eradicated.
  • #11 Etiology, Autoinoculation, and Transmission: What Wart Patients Need to Know
    https://practicaldermatology.com/topics/infections-infectious-disease/etiology-autoinoculation-and-transmission-what-wart-patients-need-to-know/23613/
    Educating the patient about wart etiology, autoinoculation, and transmission can greatly enhance patient satisfaction and improve outcomes. […] Many patients don’t know that warts are caused by a virus, and they have little understanding of how warts are transmitted. A clear understanding of wart etiology empowers the patient, giving them the knowledge to limit autoinoculation and transmission. […] Limiting autoinoculation is key to successfully treating warts, especially in severe and widespread cases. If clear predisposing factors for having warts are identified or suspected, you now have a great opportunity to educate the patient and form a plan to prevent future outbreaks. […] One of the fears of wart patients, especially those with widespread warts, is that their warts will continue to spread out of control and to other parts of the body.
  • #12 Common Warts: Symptoms, Causes & Treatments | Ada Health
    https://ada.com/conditions/common-warts/
    Common warts are caused by an infection with certain types of human papillomavirus (HPV) an umbrella term for a large group of viruses causing different conditions. […] HPV infects the skin through small cuts, scrapes, or weak spots, with warts appearing approximately two to six months later. The virus causes the protein keratin to develop in excess on the surface of the skin, resulting in the appearance of a wart. […] Common warts are particularly prevalent in children and young adults, as well as people with weakened immune systems as a result of conditions such as HIV/AIDS, certain other severe and long-lasting medical conditions, receiving certain kinds of chemotherapy, or after procedures such as organ transplantation and the ensuing treatment. […] HPV is contagious and is passed on through direct skin-to-skin contact or indirect contact with objects or surfaces. Damaged or wet skin is most likely to pick up the virus, meaning locations such as swimming pools and showers, especially public ones, are particularly common sources of infection.
  • #13 Azthena logo with the word Azthena
    https://www.news-medical.net/health/What-are-Warts.aspx
    HPV is a small double-stranded DNA virus with a genome of approximately 8,000 base pairs. All types of the virus show tropism for cells of the stratified squamous epithelium; however, the difference in affinity can be observed for various anatomical sites. For example, HPV 1 is a typical representative of skin HPV type that shows a high rate of replication in the keratinized epithelium. Conversely, HPV 16 is a mucosal HPV type with a preference for genital regions. […] The life cycle of HPV is linked to the cell differentiation program of the host cell. Initial infection requires access of infectious particles to cells in the basal layer. Note that there is no viral replication at this site and that the virus instead just keeps its genome by amplification of low copy numbers. Replication and the synthesis of proteins occur in the differentiated keratinocytes of the suprabasal layer.
  • #14 Plantar Warts: Epidemiology, Pathophysiology, and Clinical Management
    https://www.degruyterbrill.com/document/doi/10.7556/jaoa.2018.024/html?lang=en&srsltid=AfmBOoqQL1T6uhM6uwzNSccLw67fZYvk_Xios8qN2yaFK6JddrSqgeQY
    After infection, if the virus is not cleared, the host basal keratinocyte is stimulated to divide and replicate viral DNA via HPV E1 and E2 proteins. […] The induction of cellular replication throughout the process of viral genome amplification leads to the hyperkeratinized papule that constitutes a plantar wart. […] Plantar warts tend to develop at areas of increased pressure on the sole of the foot, including the heel and metatarsal heads. […] Thus, once a plantar wart develops, the host is susceptible to additional warts developing. […] Wart regression relies on the development of an effective cellular immune response. […] However, plantar warts may develop in an otherwise healthy person when HPV gains entry to the epithelium and evades the host’s immune response. […] The viral antigen is first taken up by Langerhans cells of the epidermis, which then enter the regional lymphatic drainage and thereby enter a lymph node.
  • #15 Plantar Warts: Epidemiology, Pathophysiology, and Clinical Management
    https://www.degruyter.com/document/doi/10.7556/jaoa.2018.024/html?lang=en
    After infection, if the virus is not cleared, the host basal keratinocyte is stimulated to divide and replicate viral DNA via HPV E1 and E2 proteins. […] The induction of cellular replication throughout the process of viral genome amplification leads to the hyperkeratinized papule that constitutes a plantar wart. […] Plantar warts tend to develop at areas of increased pressure on the sole of the foot, including the heel and metatarsal heads. […] Thus, once a plantar wart develops, the host is susceptible to additional warts developing. […] Wart regression relies on the development of an effective cellular immune response. […] However, plantar warts may develop in an otherwise healthy person when HPV gains entry to the epithelium and evades the host’s immune response. […] The viral antigen is first taken up by Langerhans cells of the epidermis, which then enter the regional lymphatic drainage and thereby enter a lymph node.
  • #16 Pathology Outlines – Warts (verrucae)
    https://www.pathologyoutlines.com/topic/skinnontumorwarts.html
    Common viral infection of skin and mucosal epithelial cells (Ann Ig 2018;30:28) […] Caused by human papilloma virus (HPV) (Ann Ig 2018;30:28) […] HPV invades the epidermal basal cells through microabrasions; induces hyperplasia and hyperkeratosis […] E6 and E7 HPV proteins hijack the checkpoint mechanisms of the cell cycle → uncontrolled proliferation […] Viral genome replication with increased levels of the E1, E2, E4 and E5 proteins […] The virions are sloughed off with the dead squamous cells of the host epithelium for further transmission (Front Biosci (Landmark Ed) 2018;23:1587) […] More than 200 types of HPV (J Dtsch Dermatol Ges 2019;17:613) […] Common and plantar warts: usually HPV 1, 2, 4 and 7 (J Dtsch Dermatol Ges 2019;17:613) […] Genital warts: 90% caused by HPV 6 and 11 (Infect Dis Clin North Am 2013;27:765) […] Koilocytes are a characteristic histologic finding.
  • #17 Warts and verrucas | NHS inform
    https://www.nhsinform.scot/illnesses-and-conditions/skin-hair-and-nails/warts-and-verrucas/
    Warts are caused by certain strains of the human papilloma virus (HPV). […] HPV causes too much keratin (a hard protein) to develop in the top skin layer (epidermis). The extra keratin produces the rough, hard texture of a wart. […] There are lots of different strains of HPV and these cause different types of warts.
  • #18 Warts: Causes, types, and treatments
    https://www.medicalnewstoday.com/articles/155039
    The human papillomavirus (HPV) family causes warts. These growths can appear anywhere on the body and are transmissible through touch. There are more than 100 types of HPV. […] HPV causes the excessive and rapid growth of keratin, which is a hard protein on the top layer of the skin. This results in warts forming. […] Different HPV strains cause different warts. These strains can transmit through close skin-to-skin contact and contact with items recently exposed to HPV. […] The virus can spread to other parts of the body through scratching or biting a wart. […] People with a compromised or suppressed immune system have a higher risk for contracting an HPV strain leading to warts.
  • #19 Pathology Outlines – Warts (verrucae)
    https://www.pathologyoutlines.com/topic/skinnontumorwarts.html
    Common viral infection of skin and mucosal epithelial cells (Ann Ig 2018;30:28) […] Caused by human papilloma virus (HPV) (Ann Ig 2018;30:28) […] HPV invades the epidermal basal cells through microabrasions; induces hyperplasia and hyperkeratosis […] E6 and E7 HPV proteins hijack the checkpoint mechanisms of the cell cycle → uncontrolled proliferation […] Viral genome replication with increased levels of the E1, E2, E4 and E5 proteins […] The virions are sloughed off with the dead squamous cells of the host epithelium for further transmission (Front Biosci (Landmark Ed) 2018;23:1587) […] More than 200 types of HPV (J Dtsch Dermatol Ges 2019;17:613) […] Common and plantar warts: usually HPV 1, 2, 4 and 7 (J Dtsch Dermatol Ges 2019;17:613) […] Genital warts: 90% caused by HPV 6 and 11 (Infect Dis Clin North Am 2013;27:765) […] Koilocytes are a characteristic histologic finding.
  • #20 Wart – Wikipedia
    https://en.wikipedia.org/wiki/Wart
    Common warts have a characteristic appearance under the microscope. They have thickening of the stratum corneum (hyperkeratosis), thickening of the stratum spinosum (acanthosis), thickening of the stratum granulosum, rete ridge elongation, and large blood vessels at the dermoepidermal junction. […] Warts are caused by the human papillomavirus (HPV). There are about 130 known types of human papillomaviruses. HPV infects the squamous epithelium, usually of the skin or genitals, but each HPV type is typically only able to infect a few specific areas of the body. Many HPV types can produce a benign growth, often called a „wart” or „papilloma”, in the area they infect. […] Common warts HPV types 2 and 4 (most common); also types 1, 3, 26, 29, and 57 and others.
  • #21 Azthena logo with the word Azthena
    https://www.news-medical.net/health/What-are-Warts.aspx
    The development of lesions and their type both correlate with the quantity of detected viral particles. In younger particles, there is a higher amount of viruses in comparison to old ones. Furthermore, plantar warts contain a higher viral load as compared to common warts. It must be noted that in benign lesions, the replication of the HPV genome is extrachromosomal. […] The histopathological characteristics of viral warts are acanthosis, papillomatosis, and hyperkeratosis, with the confluence of the epidermal ridges in the center of the lesion and koilocytes. Some authors have also suggested that certain histological features are specific to each type of HPV; thus, a histopathological examination would help in identifying different viral types.
  • #22 Verruca vulgaris (common wart) pathology
    https://dermnetnz.org/topics/verruca-vulgaris-pathology
    Verruca vulgaris (common viral wart) is a keratotic lesion caused by specific human papillomavirus (HPV) types. […] Characteristic vacuolated keratinocytes (koilocytes), which have a small shrunken nucleus surrounded by a perinuclear halos, are seen in the upper epidermis (figure 3). […] PCR may be used to identify the HPV type.
  • #23 Verruca vulgaris (common wart) pathology
    https://dermnetnz.org/topics/verruca-vulgaris-pathology
    Verruca vulgaris (common viral wart) is a keratotic lesion caused by specific human papillomavirus (HPV) types. […] Characteristic vacuolated keratinocytes (koilocytes), which have a small shrunken nucleus surrounded by a perinuclear halos, are seen in the upper epidermis (figure 3). […] PCR may be used to identify the HPV type.
  • #24 Update on human papilloma virus – part I: epidemiology, pathogenesis, and clinical spectrum | Anais Brasileiros de Dermatologia
    https://www.anaisdedermatologia.org.br/en-update-on-human-papilloma-virus-articulo-S0365059620306620
    The prevalence of CWs in the general population is estimated at around 5% and is the result of continuous and repeated infection by multiple types. […] HPV infection occurs when viral particles reach exposed basal cells, usually by microtrauma in the epithelium. […] The viral replication cycle has three phases: an initial amplification of DNA, with the participation of proteins E1 and E2; a phase of maintenance of viral replication that occurs in the proliferating infected cells; and a phase of genome amplification and formation of new viruses that occurs when the cells complete their differentiation. […] HPV, in general, completes its life cycle in epithelial cells; does not produce viremia, cell lysis, or inflammation; and remains protected from the immune system through mechanisms of evasion of the innate immune response, in addition to delaying the adaptive immune response.
  • #25 Plantar Warts: Epidemiology, Pathophysiology, and Clinical Management
    https://www.degruyterbrill.com/document/doi/10.7556/jaoa.2018.024/html?lang=en&srsltid=AfmBOoqQL1T6uhM6uwzNSccLw67fZYvk_Xios8qN2yaFK6JddrSqgeQY
    After infection, if the virus is not cleared, the host basal keratinocyte is stimulated to divide and replicate viral DNA via HPV E1 and E2 proteins. […] The induction of cellular replication throughout the process of viral genome amplification leads to the hyperkeratinized papule that constitutes a plantar wart. […] Plantar warts tend to develop at areas of increased pressure on the sole of the foot, including the heel and metatarsal heads. […] Thus, once a plantar wart develops, the host is susceptible to additional warts developing. […] Wart regression relies on the development of an effective cellular immune response. […] However, plantar warts may develop in an otherwise healthy person when HPV gains entry to the epithelium and evades the host’s immune response. […] The viral antigen is first taken up by Langerhans cells of the epidermis, which then enter the regional lymphatic drainage and thereby enter a lymph node.
  • #26 Plantar Warts: Epidemiology, Pathophysiology, and Clinical Management
    https://www.degruyter.com/document/doi/10.7556/jaoa.2018.024/html?lang=en
    After infection, if the virus is not cleared, the host basal keratinocyte is stimulated to divide and replicate viral DNA via HPV E1 and E2 proteins. […] The induction of cellular replication throughout the process of viral genome amplification leads to the hyperkeratinized papule that constitutes a plantar wart. […] Plantar warts tend to develop at areas of increased pressure on the sole of the foot, including the heel and metatarsal heads. […] Thus, once a plantar wart develops, the host is susceptible to additional warts developing. […] Wart regression relies on the development of an effective cellular immune response. […] However, plantar warts may develop in an otherwise healthy person when HPV gains entry to the epithelium and evades the host’s immune response. […] The viral antigen is first taken up by Langerhans cells of the epidermis, which then enter the regional lymphatic drainage and thereby enter a lymph node.
  • #27 Warts – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/viral-skin-diseases/warts
    Warts are cutaneous lesions caused by human papillomavirus (HPV) infection; there are over 100 HPV subtypes (1). […] Trauma and maceration facilitate initial epidermal inoculation. Spread can then occur by autoinoculation. Local and systemic immune factors also appear to influence spread; immunosuppressed patients (especially those with suppressed cellular immunity, [eg, HIV infection or a kidney transplant or those with a history of tumor-suppressive immunotherapy]) are at particular risk of developing generalized lesions that are difficult to treat. […] Cellular immunity by CD8+ T-cells is crucial for established infection to regress. However, intact humoral immunity can also provide resistance to HPV infection. […] Common warts (verrucae vulgaris) are caused by HPV types 1, 2, 4, and 7 and occasionally other types in immunosuppressed patients (eg, 75 to 77).
  • #28 Common Wart (Verruca vulgaris)
    https://www.webpathology.com/images/dermpath/non-neoplastic-dermpath—ii/skin-infections—viral/41296
    HPV lesions are generally self-limited but can persist for several years. They eventually regress in most cases due to cell-mediated immunity. Regression is associated with basal cell degeneration, epidermal degeneration, and vascular thrombosis. […] Patients with defective cell-mediated immunity (primary, iatrogenic, or HIV-induced) are particularly at risk for developing large crops of warts that don’t regress spontaneously and are difficult to treat.
  • #29 Common Wart (Verruca vulgaris)
    https://www.webpathology.com/images/dermpath/non-neoplastic-dermpath—ii/skin-infections—viral/41296
    HPV lesions are generally self-limited but can persist for several years. They eventually regress in most cases due to cell-mediated immunity. Regression is associated with basal cell degeneration, epidermal degeneration, and vascular thrombosis. […] Patients with defective cell-mediated immunity (primary, iatrogenic, or HIV-induced) are particularly at risk for developing large crops of warts that don’t regress spontaneously and are difficult to treat.
  • #30 Interleukins in the Pathogenesis of Warts: Insight from the Last Decade—A Narrative Review
    https://www.mdpi.com/2077-0383/14/6/2057
    Human papillomavirus (HPV) is the etiological agent of a wide spectrum of diseases, from benign lesions to neoplasms. […] The immune response to HPV is regulated by the dynamic interaction between numerous interleukins that exert pro- or anti-inflammatory effects. […] This review compiles data from the last 10 years on the involvement of interleukins in the pathogenesis of warts, with the aim of providing new perspectives on this topic. […] Elucidating the role of interleukins will not only increase our knowledge of the pathogenesis of HPV infection but will also provide the foundation for the development of new therapies. […] The disruption of the immune response and its shift from a Th1 response to a Th2 response are associated with altered virus recognition by the immune system, facilitating the persistence of the virus for an indefinite period and resulting in the progression of the lesions.
  • #31 Interleukins in the Pathogenesis of Warts: Insight from the Last Decade—A Narrative Review
    https://www.mdpi.com/2077-0383/14/6/2057
    IL-1α and β, IL-6, and IL-12 are involved in the adaptive immune response against HPV. […] The Th1 immune response is essential for an antiviral defense; therefore, ILs such as IL-2 activate immune cells, especially T cells. […] Increased levels of IL-6, IL-8, and TNF alter the antiviral response, allowing the virus to persist in infected cells. […] IL-12 regulates the function of lymphocytes by inducing their differentiation into Th1 cells, while IL-23 is an activator of IL-17. […] IL-17 can help HPV evade the host immune response and persist for a long time in keratinocytes. […] Low serum IL-17 levels alter the immune response mediated by Th1 cells, which increases susceptibility to HPV infection. […] IL-33 levels in lesional tissue were higher than in non-lesional tissue. […] Increased levels of IL-33 may represent a defense mechanism of the body against HPV infection. […] The role of ILs in the pathogenesis of HPV is supported by the results of studies that evaluated their levels before and after therapy. […] These studies found that the levels of IL-1, IL-2, IL-4, IL-12, and IL-18 increased, while the levels of IL-10 and IL-17 decreased after therapy.
  • #32 Interleukins in the Pathogenesis of Warts: Insight from the Last Decade—A Narrative Review
    https://www.mdpi.com/2077-0383/14/6/2057
    IL-1α and β, IL-6, and IL-12 are involved in the adaptive immune response against HPV. […] The Th1 immune response is essential for an antiviral defense; therefore, ILs such as IL-2 activate immune cells, especially T cells. […] Increased levels of IL-6, IL-8, and TNF alter the antiviral response, allowing the virus to persist in infected cells. […] IL-12 regulates the function of lymphocytes by inducing their differentiation into Th1 cells, while IL-23 is an activator of IL-17. […] IL-17 can help HPV evade the host immune response and persist for a long time in keratinocytes. […] Low serum IL-17 levels alter the immune response mediated by Th1 cells, which increases susceptibility to HPV infection. […] IL-33 levels in lesional tissue were higher than in non-lesional tissue. […] Increased levels of IL-33 may represent a defense mechanism of the body against HPV infection. […] The role of ILs in the pathogenesis of HPV is supported by the results of studies that evaluated their levels before and after therapy. […] These studies found that the levels of IL-1, IL-2, IL-4, IL-12, and IL-18 increased, while the levels of IL-10 and IL-17 decreased after therapy.
  • #33 Interleukins in the Pathogenesis of Warts: Insight from the Last Decade—A Narrative Review
    https://www.mdpi.com/2077-0383/14/6/2057
    IL-1α and β, IL-6, and IL-12 are involved in the adaptive immune response against HPV. […] The Th1 immune response is essential for an antiviral defense; therefore, ILs such as IL-2 activate immune cells, especially T cells. […] Increased levels of IL-6, IL-8, and TNF alter the antiviral response, allowing the virus to persist in infected cells. […] IL-12 regulates the function of lymphocytes by inducing their differentiation into Th1 cells, while IL-23 is an activator of IL-17. […] IL-17 can help HPV evade the host immune response and persist for a long time in keratinocytes. […] Low serum IL-17 levels alter the immune response mediated by Th1 cells, which increases susceptibility to HPV infection. […] IL-33 levels in lesional tissue were higher than in non-lesional tissue. […] Increased levels of IL-33 may represent a defense mechanism of the body against HPV infection. […] The role of ILs in the pathogenesis of HPV is supported by the results of studies that evaluated their levels before and after therapy. […] These studies found that the levels of IL-1, IL-2, IL-4, IL-12, and IL-18 increased, while the levels of IL-10 and IL-17 decreased after therapy.
  • #34 Interleukins in the Pathogenesis of Warts: Insight from the Last Decade—A Narrative Review
    https://www.mdpi.com/2077-0383/14/6/2057
    IL-1α and β, IL-6, and IL-12 are involved in the adaptive immune response against HPV. […] The Th1 immune response is essential for an antiviral defense; therefore, ILs such as IL-2 activate immune cells, especially T cells. […] Increased levels of IL-6, IL-8, and TNF alter the antiviral response, allowing the virus to persist in infected cells. […] IL-12 regulates the function of lymphocytes by inducing their differentiation into Th1 cells, while IL-23 is an activator of IL-17. […] IL-17 can help HPV evade the host immune response and persist for a long time in keratinocytes. […] Low serum IL-17 levels alter the immune response mediated by Th1 cells, which increases susceptibility to HPV infection. […] IL-33 levels in lesional tissue were higher than in non-lesional tissue. […] Increased levels of IL-33 may represent a defense mechanism of the body against HPV infection. […] The role of ILs in the pathogenesis of HPV is supported by the results of studies that evaluated their levels before and after therapy. […] These studies found that the levels of IL-1, IL-2, IL-4, IL-12, and IL-18 increased, while the levels of IL-10 and IL-17 decreased after therapy.
  • #35 Serum level of IL22 and IL17 in recalcitrant common warts
    https://ejmm.journals.ekb.eg/article_371119.html
    Recalcitrant warts are defined as warts persistent for longer than two years in spite of proper use of appropriate treatment. […] The aim of this study was to measure the level of IL-22 and Il-17 in recalcitrant common warts and healthy controls in an attempt to explain their role in wart pathogenesis. […] Cases with recalcitrant warts were associated with significant decreases in serum IL-22 level, and this low level may have a potential function in improving the cell-mediated immune response towards HPV infections. Patients with recalcitrant warts were associated with significant reductions in serum IL-17 value; IL-17 deficiency plays a main role in recalcitrant wart pathogenesis via disturbance of the balance of the immune system and deficiency of immune cells. As a result, IL-17 may have an essential role in the antiviral immune response to HPV infection.
  • #36 Common Wart (Verruca vulgaris)
    https://www.webpathology.com/images/dermpath/non-neoplastic-dermpath—ii/skin-infections—viral/41296
    HPV lesions are generally self-limited but can persist for several years. They eventually regress in most cases due to cell-mediated immunity. Regression is associated with basal cell degeneration, epidermal degeneration, and vascular thrombosis. […] Patients with defective cell-mediated immunity (primary, iatrogenic, or HIV-induced) are particularly at risk for developing large crops of warts that don’t regress spontaneously and are difficult to treat.
  • #37 Genital Warts: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/763014-overview
    Genital warts are caused by several of the epidermotropic human papillomaviruses (HPVs). HPV-6 and HPV-11 most commonly are isolated; however, many of the more than 60 types of HPV may cause condyloma. […] Mortality is secondary to malignant transformation to a carcinoma. This oncogenic potential, which is rare with HPV-6 and HPV-11 (the most commonly isolated viruses), reportedly triples the risk of genitourinary cancer among infected males. […] HPV infection appears to be more common and worse in patients with various types of immunologic deficiencies. Recurrence rate, size, discomfort, and risk of oncologic progression are highest among these patients.
  • #38 Plantar Warts: Epidemiology, Pathophysiology, and Clinical Management
    https://www.degruyter.com/document/doi/10.7556/jaoa.2018.024/html?lang=en
    This response should lead to eradication of the infection and prevent a plantar wart from occurring or lead to regression of established plantar warts. […] Plantar warts have a very high viral load, which increases the rate of viral shedding and the likelihood of contaminating adjacent body surfaces, inanimate communal surfaces, or close contacts. […] Plantar warts present a significant problem to athletes, as the pain can affect the athlete’s ability to ambulate. […] Immunocompromised patients have higher rates of plantar warts, along with increased severity and duration of the lesions. […] Therefore, it is imperative that physicians consider that patients who present with large numbers of plantar warts or treatment-resistant plantar warts may have an underlying immunodeficiency and that patients with an established immunodeficiency and plantar warts may harbor a malignant neoplasm within the lesion. […] Because all currently available plantar wart management modalities address the lesion itself, none adequately manage the risk of transmission, which is intrinsic to the pathophysiologic mechanism by which the plantar wart develops and sheds viral particles.
  • #39 Common Warts: Symptoms, Causes & Treatments | Ada Health
    https://ada.com/conditions/common-warts/
    Common warts are caused by an infection with certain types of human papillomavirus (HPV) an umbrella term for a large group of viruses causing different conditions. […] HPV infects the skin through small cuts, scrapes, or weak spots, with warts appearing approximately two to six months later. The virus causes the protein keratin to develop in excess on the surface of the skin, resulting in the appearance of a wart. […] Common warts are particularly prevalent in children and young adults, as well as people with weakened immune systems as a result of conditions such as HIV/AIDS, certain other severe and long-lasting medical conditions, receiving certain kinds of chemotherapy, or after procedures such as organ transplantation and the ensuing treatment. […] HPV is contagious and is passed on through direct skin-to-skin contact or indirect contact with objects or surfaces. Damaged or wet skin is most likely to pick up the virus, meaning locations such as swimming pools and showers, especially public ones, are particularly common sources of infection.
  • #40 Interleukins in the Pathogenesis of Warts: Insight from the Last Decade—A Narrative Review
    https://www.mdpi.com/2077-0383/14/6/2057
    Human papillomavirus (HPV) is the etiological agent of a wide spectrum of diseases, from benign lesions to neoplasms. […] The immune response to HPV is regulated by the dynamic interaction between numerous interleukins that exert pro- or anti-inflammatory effects. […] This review compiles data from the last 10 years on the involvement of interleukins in the pathogenesis of warts, with the aim of providing new perspectives on this topic. […] Elucidating the role of interleukins will not only increase our knowledge of the pathogenesis of HPV infection but will also provide the foundation for the development of new therapies. […] The disruption of the immune response and its shift from a Th1 response to a Th2 response are associated with altered virus recognition by the immune system, facilitating the persistence of the virus for an indefinite period and resulting in the progression of the lesions.
  • #41 Treatment of Warts in Children: An Update | Actas Dermo-Sifiliográficas
    https://actasdermo.org/en-treatment-warts-in-children-an-articulo-S1578219016301329
    The main goal when treating warts is to eradicate the lesions, while attempting to minimize pain, avoid scarring, and prevent recurrence. Choice of treatment will depend on the location, size, number, and type of warts, as well as on the age and level of cooperation of the patient. The experience of the treating physician may also have an influence. […] There are many types of treatment for warts. The fact that so many treatments exist is indicative of their varying degrees of effectiveness, with success rates ranging between 32% and 93%. […] Destructive methods are those that cause nonspecific damage to infected keratinocytes and surrounding skin. Although these methods are associated with high recurrence, the fact that they are simple to use and relatively cheap explains why they are the most widely used treatments in routine practice.
  • #42 Destructive therapies for cutaneous warts: A review of the evidence
    https://www1.racgp.org.au/ajgp/2022/october/destructive-therapies-for-cutaneous-warts
    Common warts (Verruca vulgaris), plantar warts (Verruca plantaris) and flat/plane warts (Verruca plana), collectively known as cutaneous warts, are benign growths of the skin caused by the human papillomavirus (HPV). […] A break in the epidermal barrier of the skin allows entry of HPV and subsequent infection of basal epithelial cells. HPV replicates alongside the natural lifecycle of epithelial cells, and is eventually released from desquamated keratinocytes on the surface of warts, potentially infecting other sites via direct contact or through fomites. […] Damaging or destroying the infected epithelium causes HPV cell death. The subsequent antigen exposure and presentation might also induce an immune response.
  • #43 Treatment of Warts in Children: An Update | Actas Dermo-Sifiliográficas
    https://actasdermo.org/en-treatment-warts-in-children-an-articulo-S1578219016301329
    Salicylic acid is a keratolytic agent that destroys the epidermis infected by the virus. It is available in different vehicles at concentrations of between 10% and 30%. Topical salicylic acid is still the treatment with the best evidence base and it is the only option approved by the US Food and Drug Administration for warts. […] Cryotherapy consists of freezing the wart with liquid nitrogen for 10 to 20 seconds every 2 to 3 weeks. Although the exact mechanism of action is unknown, the freezing is thought to cause local irritation, thereby stimulating an immune response. […] Cantharidin is a blistering agent produced by beetles of the order Meloidae Coleoptera. It is used at a concentration of 0.7% or 1% and once applied should be covered with an occlusive dressing for 24 hours. […] Surgical treatment of warts involves the radical eradication of lesions by conventional surgery, electrosurgery, or curettage.
  • #44 Common warts – Symptoms, Causes, Diagnosis and Treatment | MedPark Hospital
    https://www.medparkhospital.com/en-US/disease-and-treatment/common-warts
    Common warts (verruca vulgaris) are skin bumps with rough surfaces and tiny black specks. […] The cause of common warts is exposure to and infection by the HPV virus. It can take up to 6 months for them to appear after viral exposure. […] The human papillomavirus (HPV) is the cause of common warts. The viral infection can occur through breaks in the skin, such as a scrape or hangnail. […] Proper treatment can remove your wart and boost your immunity to fight the virus. […] Cryotherapy can also stimulate your immunity to fight the HPV virus.
  • #45 Treatment of Warts in Children: An Update | Actas Dermo-Sifiliográficas
    https://actasdermo.org/en-treatment-warts-in-children-an-articulo-S1578219016301329
    Salicylic acid is a keratolytic agent that destroys the epidermis infected by the virus. It is available in different vehicles at concentrations of between 10% and 30%. Topical salicylic acid is still the treatment with the best evidence base and it is the only option approved by the US Food and Drug Administration for warts. […] Cryotherapy consists of freezing the wart with liquid nitrogen for 10 to 20 seconds every 2 to 3 weeks. Although the exact mechanism of action is unknown, the freezing is thought to cause local irritation, thereby stimulating an immune response. […] Cantharidin is a blistering agent produced by beetles of the order Meloidae Coleoptera. It is used at a concentration of 0.7% or 1% and once applied should be covered with an occlusive dressing for 24 hours. […] Surgical treatment of warts involves the radical eradication of lesions by conventional surgery, electrosurgery, or curettage.
  • #46 Warts – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/viral-skin-diseases/warts
    Common warts are sharply demarcated, rough, round or irregular, firm, and light gray, yellow, brown, or gray-black nodules 2 to 10 mm in diameter. They appear most often on sites subject to trauma (eg, fingers, elbows, knees, face) but may spread elsewhere. […] Topical irritant treatments have mechanisms of action that involve directing an immune response to the irritant locally, which targets the HPV lesion as well (1). […] In immunocompetent patients, common warts usually spontaneously regress within 2 to 4 years, but some linger for many years. […] Numerous treatments are available. Destructive methods include electrocautery, cryosurgery with liquid nitrogen, and laser surgery. Salicylic acid preparations are also commonly used. […] Recalcitrant warts can be treated with other intralesional and oral agents.
  • #47 Warts, verrucas, human papillomavirus infection
    https://dermnetnz.org/topics/viral-wart
    Warts are due to infection by the human papillomavirus (HPV), a double-stranded DNA virus. There are more than 150 known HPV types, only some of which infect the skin, giving rise to a variety of clinical presentations. Infection begins in the basal layer of the epidermis, causing proliferation of the keratinocytes (skin cells) and hyperkeratosis, and production of infectious virus particles the wart. The most common HPV types infecting the skin are types 1, 2, 3, 4, 10, 27, 29, and 57. […] HPV is spread by direct skin-to-skin contact or autoinoculation; if a wart is scratched or picked, a wart may develop under the fingernail (subungual wart) or virus may be spread to another area of skin. Autoinoculation of the virus in a scratch can result in a line of warts (pseudo-koebnerisation) The incubation period can be as long as twelve months, depending on the amount of virus inoculated. […] Treatments do not kill the virus, but work by removing virus-containing skin. Persistence with the treatment and patience is essential! Remember HPV infects the basal cell layer of the epidermis so warts recur rapidly if the virus has not been eradicated.
  • #48 Immunotherapy with PPD in treatment of warts: An open labelled study from western Uttar Pradesh – IP Indian J Clin Exp Dermatol
    https://www.ijced.org/article-details/8428
    Warts are the viral infection of the skin caused by Human Papilloma virus, which manifest in the form of verrucous growth over the surface of skin. HPV is a DNA virus that infects skin or mucosal cells. It infects the basal layer of epithelium, possibly the stem cells, but viral replication takes place only in fully differentiated keratinocytes i.e. cells of the stratum spinosum and stratum granulosum. All papilloma virus types have a tropism for stratified squamous epithelial cells, but they vary in their specificity for different anatomical sites like cervix, skin etc. […] Currently, a newer form of therapy is in trend which is known as immunotherapy. This involves the amplification or activation of the patients immune system with the help of immunomodulators. Intralesional immunotherapy uses purified protein derivative, candida antigen, trychophytin skin test antigen. MMR vaccine, or Mw vaccine, to treat warts.
  • #49 Treatment of Warts in Children: An Update | Actas Dermo-Sifiliográficas
    https://actasdermo.org/en-treatment-warts-in-children-an-articulo-S1578219016301329
    Immunotherapy drugs are used to elicit humoral and/or cellular immune responses and thereby eliminate the viral infection responsible for warts. […] Cimetidine is administered orally at daily doses of 20 to 40 mg/d, with a maximum dose of 600 mg per day. […] Candida antigen is a substance derived from purified extracts of Candida albicans. It is typically injected intralesionally, either pure or diluted to a concentration of 50% in lidocaine. […] The exact mechanism of action of imiquimod is unknown, but it is assumed to involve stimulation of both innate and cell-mediated immunity. […] Zinc sulfate appears to act as an immunomodulating agent via the polyclonal activation of lymphocytes. […] Diphenylcyclopropenone is an allergic contact sensitizer used to treat resistant warts. […] 5-fluorouracil is a fluorinated pyrimidine that is effective against viral warts because it blocks DNA and RNA synthesis of viral particles and reduces epidermal proliferation.
  • #50 Treatment of Warts in Children: An Update | Actas Dermo-Sifiliográficas
    https://actasdermo.org/en-treatment-warts-in-children-an-articulo-S1578219016301329
    Bleomycin has antibacterial, antiviral, and cytotoxic activity, and by blocking cellular and viral DNA synthesis, it causes acute tissue necrosis that stimulates an immune response. […] Cidofovir is an antiviral agent that acts via competitive inhibition of viral polymerase DNA. […] Podophyllin is an antimitotic agent derived from the plant Podophyllum peltatum. […] Local hyperthermia is a simple treatment, particularly for multiple lesions. […] The mechanism of action underlying the use of duct tape to treat warts is not known, but like other treatments, it would appear to involve the stimulation of the immune system in response to local irritation. […] Polyphenon E is a green tea leaf extract that appears to induce cell cycle arrest, activate apoptosis, inhibit HPV transcription, and stimulate cell-mediated immunity.
  • #51 Immunotherapy with PPD in treatment of warts: An open labelled study from western Uttar Pradesh – IP Indian J Clin Exp Dermatol
    https://www.ijced.org/article-details/8428
    In Intralesional immunotherapy, a delayed hypersensitivity response develops to the injected antigen and the wart tissue. It is usually seen that there is development of TH1 cytokines which activate cytotoxic and NK cells to eradicate the HPV infection. […] Intralesional immunotherapy carries an advantage of developing or augmenting the host immune response to the wart antigen. So, it is helpful for destroying the wart infection at the disease as well as at the remote site. It confers immunity to wart antigen for future also, so it is helpful in reducing the chance of recurrence also. […] How the PPD clears the wart, its mechanism is not very well established but various studies suggest that when PPD is injected into the wart tissue, it induces the release of various pro-inflammatory chemicals. These in turn, cause activation of APC (antigen presenting cell), which recognize and then process the HPV at the local site.
  • #52 Immunotherapy with PPD in treatment of warts: An open labelled study from western Uttar Pradesh – IP Indian J Clin Exp Dermatol
    https://www.ijced.org/article-details/8428
    This leads to the development of robust adaptive immune reaction against mycobacterium tuberculosis as well as against HPV infection. It is mediated by Th1 cytokines such as interleukin-4, 5,8, IFN- and TNF-?. An increase in IL-12 as a process in boosting the cell mediated immunity also contributes to the mechanism of action. […] In our study, the response to PPD at the site of injection was noticed in 2nd to 3nd visit while the response at remote site was seen in 5th to 6th visit. The gap in response between the injection site and remote site was of 4 weeks i.e. at injection site and remote site, it may be due to time taken for induction of CMI. It suggests that immune response is not restricted only to the site of injection.
  • #53 Nongenital Warts: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1133317-overview
    Approximately 65% of warts disappear spontaneously within 2 years. When warts resolve on their own, no scarring is seen. However, scarring can occur as a result of different treatment methods. Growth of periungual or subungual warts may result in permanent nail dystrophy. […] Treatment failures and wart recurrences are common, more so among immunocompromised patients. Normal appearing perilesional skin may harbor HPV, which helps explain recurrences. […] Malignant change in nongenital warts is rare but has been reported and is termed verrucous carcinoma. Verrucous carcinoma is considered to be a slow-growing, locally invasive, well-differentiated squamous cell carcinoma that may be easily mistaken for a common wart. It can occur anywhere on the skin but is most common on the plantar surfaces. Although this type of cancer rarely metastasizes, it can be locally destructive.
  • #54 Warts – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/viral-skin-diseases/warts
    Common warts are sharply demarcated, rough, round or irregular, firm, and light gray, yellow, brown, or gray-black nodules 2 to 10 mm in diameter. They appear most often on sites subject to trauma (eg, fingers, elbows, knees, face) but may spread elsewhere. […] Topical irritant treatments have mechanisms of action that involve directing an immune response to the irritant locally, which targets the HPV lesion as well (1). […] In immunocompetent patients, common warts usually spontaneously regress within 2 to 4 years, but some linger for many years. […] Numerous treatments are available. Destructive methods include electrocautery, cryosurgery with liquid nitrogen, and laser surgery. Salicylic acid preparations are also commonly used. […] Recalcitrant warts can be treated with other intralesional and oral agents.
  • #55 Immunotherapy using purified protein derivative in the treatment of warts: An open uncontrolled trial – Indian Journal of Dermatology, Venereology and Leprology
    https://ijdvl.com/immunotherapy-using-purified-protein-derivative-in-the-treatment-of-warts-an-open-uncontrolled-trial/
    Warts are caused by human papillomaviruses (HPVs) which infect keratinocytes. […] Spontaneous regression is known to occur in warts due to the development of cell-mediated immunity (CMI) to the virus and such lesions demonstrate prominent lymphocytic infiltration in the dermis. […] An immune response is essential for clearance of warts. […] Immunotherapy is an innovative approach to treat warts which relies on the principle of enhancement of cell-mediated immunity. […] Injection of PPD stimulates cell mediated immunity non-specifically through activation of Th1 cytokines, natural killer cells and cytotoxic T cells and is found to be effective against all types of warts such as verruca plana, verruca vulgaris and plantar warts irrespective of the serotype of HPV. […] It is believed that injection of PPD not only stimulates the local immunity but also leads to circulation of activated T cells in the body leading to clearance of injected as well as non-injected, distant warts.
  • #56 Immunotherapy using purified protein derivative in the treatment of warts: An open uncontrolled trial – Indian Journal of Dermatology, Venereology and Leprology
    https://ijdvl.com/immunotherapy-using-purified-protein-derivative-in-the-treatment-of-warts-an-open-uncontrolled-trial/
    Warts are caused by human papillomaviruses (HPVs) which infect keratinocytes. […] Spontaneous regression is known to occur in warts due to the development of cell-mediated immunity (CMI) to the virus and such lesions demonstrate prominent lymphocytic infiltration in the dermis. […] An immune response is essential for clearance of warts. […] Immunotherapy is an innovative approach to treat warts which relies on the principle of enhancement of cell-mediated immunity. […] Injection of PPD stimulates cell mediated immunity non-specifically through activation of Th1 cytokines, natural killer cells and cytotoxic T cells and is found to be effective against all types of warts such as verruca plana, verruca vulgaris and plantar warts irrespective of the serotype of HPV. […] It is believed that injection of PPD not only stimulates the local immunity but also leads to circulation of activated T cells in the body leading to clearance of injected as well as non-injected, distant warts.
  • #57 Wart – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK431047/
    Warts, in general, are benign, but there are reports that sometimes they may become malignant and develop into what is known as verrucous carcinoma. The verrucous carcinoma is a slow-growing tumor and is classified as a well-differentiated squamous cell malignancy that is often mistaken for a common wart. […] The virus is known to replicate in the upper level of the epithelium, but the virus particles also can be found in the basal layer. […] The majority of warts do not cause symptoms. However, they do cause cosmetic disfigurement and, in a rare patient, may cause localized pain. […] Close to two-thirds of warts resolve spontaneously over several years, so the efficacy of treatments is difficult to discern. Warts usually do not cause residual scarring when they disappear on their own. However, almost every type of topical treatment available has the potential to cause moderate to severe scarring. […] Malignant change is rare with common warts but rarely one may encounter transformation to verrucous carcinoma, which is most common on the plantar surface.
  • #58 Common warts – Symptoms and causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/common-warts/symptoms-causes/syc-20371125
    Common warts are caused by a virus and are transmitted by touch. It can take 2 to 6 months for a wart to develop. […] Common warts are caused by the human papillomavirus, also called HPV. There are more than 100 types of this common virus, but only a few cause warts on the hands. Some strains of HPV are spread through sexual contact. But most are spread by casual skin contact or shared objects, such as towels or washcloths. The virus usually spreads through breaks in the skin, such as hangnails or scrapes. Biting your nails also can cause warts to spread on your fingertips and around your nails. […] Each person’s immune system responds to HPV differently. So not everyone who comes in contact with HPV develops warts.
  • #59 Warts Information | Mount Sinai – New York
    https://www.mountsinai.org/health-library/condition/warts
    Warts are caused by various strains of a common virus in humans, the human papillomavirus (HPV). […] They are more likely to occur if the skin has been broken or damaged in some way. […] The following factors increase your risk of developing warts: Direct contact with warts or the fluid in warts (notably genital warts), using communal facilities (such as locker rooms), skin trauma, diseases or drugs that weaken your immune system. […] Even with treatment, some warts may return. Genital warts are more likely to return because there is no cure for the virus that causes them, and because warts are more difficult to control in a moist environment.
  • #60 „Warts” the Matter?
    https://www.dermla.com/sbcblog/warts-the-matter/
    A virus called human papillomavirus, or HPV for short, can infect the top layer of the skin and lead to an unfortunate growth known as a wart. HPV usually infiltrates a broken area of skin causing the top layer to grow rapidly and form a wart. […] Warts are easily spread by direct contact with a HPV. Some people are more susceptible while still others never get them at all. Doctors theorize thats because some peoples immune systems make them less likely to get the viruses that cause warts. […] Age can determine the incidence of warts. They occur more frequently in children and young adults. As one ages, warts are less likely to develop and any you have may simply disappear. […] Warts can itch or bleed. Its best to avoid scratching or picking them in order not to infect them with bacteria and/or spread the virus to another part of the body. […] Actually, the length of time that transpires between exposure to a HPV virus and the appearance of a wart varies, but warts generally grow very slowly and may take many months to develop.
  • #61 Common Warts: Symptoms, Causes & Treatments | Ada Health
    https://ada.com/conditions/common-warts/
    Common warts are caused by an infection with certain types of human papillomavirus (HPV) an umbrella term for a large group of viruses causing different conditions. […] HPV infects the skin through small cuts, scrapes, or weak spots, with warts appearing approximately two to six months later. The virus causes the protein keratin to develop in excess on the surface of the skin, resulting in the appearance of a wart. […] Common warts are particularly prevalent in children and young adults, as well as people with weakened immune systems as a result of conditions such as HIV/AIDS, certain other severe and long-lasting medical conditions, receiving certain kinds of chemotherapy, or after procedures such as organ transplantation and the ensuing treatment. […] HPV is contagious and is passed on through direct skin-to-skin contact or indirect contact with objects or surfaces. Damaged or wet skin is most likely to pick up the virus, meaning locations such as swimming pools and showers, especially public ones, are particularly common sources of infection.
  • #62 Viral Warts: Causes and Treatment | Doctor
    https://patient.info/doctor/viral-warts-excluding-verrucae
    Warts are caused by HPV. There are well over one hundred types of HPV. Types 1, 2, 3, 4, 10, 27 and 57 are most often implicated in the aetiology of cutaneous warts. Infection of keratinocytes causes hyperkeratinisation and epidermal thickening. […] HPV infection is acquired from direct contact with an affected individual or from the environment (eg, from contaminated floors or surfaces). It appears the virus can survive outside the body for a significant length of time, probably months or even years. […] Trauma and wetness are contributory in contracting warts. The virus is more likely to spread around other parts of the body if the wart is damaged by trauma or scratching.
  • #63 Viral Warts > Fact Sheets > Yale Medicine
    https://www.yalemedicine.org/conditions/viral-warts
    Common warts, flat warts, and plantar warts are viral infections of the skin (most originating from the human papillomavirus or HPV family, but not the strains associated with cancer). […] Viruses like to infect through cuts in the skin, says Yale Medicine dermatologist Christopher Bunick, MD, PhD. Picking of the warts (or biting them) can lead to spread of the virus, including around the mouths of kids. […] Viral warts affect children and teens more than adults because their immune systems havent developed the antibodies to fight strains of HPV that cause warts. […] Skin-to-skin contact, or skin that comes in contact with things that have been touched by others, is often what spreads the virus. […] Though most people become immune to the viruses over time, usually by the end of the teenage years, some people may develop warts into adulthood, possibly because of certain genetic susceptibilities.
  • #64 Warts (common, flat & plantar) – including symptoms, treatment and prevention | SA Health
    https://www.sahealth.sa.gov.au/wps/wcm/connect/public+content/sa+health+internet/conditions/infectious+diseases/warts/warts+common+flat+and+plantar+-+including+symptoms+treatment+and+prevention
    Warts are lumpy growths in the skin caused by infection with human papilloma viruses (HPV), of which there are more than 100 known types. […] The wart virus is thought to be transmitted by direct skin to skin contact or by contact with contaminated surfaces, for example floors. […] About 65% of warts will go away by themselves within 2 years. If treatment is necessary, the following may be used: liquid nitrogen, chemical paint applications, surgical removal, laser therapy. […] Wart infection can be prevented by the following measures: avoid direct contact with warts, wear shoes, wash hands after any contact with warts.
  • #65 Treatment of Warts in Children: An Update | Actas Dermo-Sifiliográficas
    https://actasdermo.org/en-treatment-warts-in-children-an-articulo-S1578219016301329
    Human papillomavirus (HPV) is a DNA virus that belongs to the papillomavirus genus within the Papovaviridae family. There are at least 189 different strains of papillomavirus and 151 of these have been detected in human DNA. HPV affects the skin and mucosa of humans, producing benign proliferations known as warts. Some types of HPV have been associated with the development of malignant epithelial lesions in immunosuppressed patients or patients with anogenital warts, but this possibility is very rare during childhood. […] Warts are transmitted directly through contact with infected skin or indirectly through contaminated surfaces. An affected family member or classmate has been identified as a risk factor for acquiring warts, even more so than the use of swimming pools or communal showers.
  • #66 Etiology, Autoinoculation, and Transmission: What Wart Patients Need to Know
    https://practicaldermatology.com/topics/infections-infectious-disease/etiology-autoinoculation-and-transmission-what-wart-patients-need-to-know/23613/
    Educating the patient about wart etiology, autoinoculation, and transmission can greatly enhance patient satisfaction and improve outcomes. […] Many patients don’t know that warts are caused by a virus, and they have little understanding of how warts are transmitted. A clear understanding of wart etiology empowers the patient, giving them the knowledge to limit autoinoculation and transmission. […] Limiting autoinoculation is key to successfully treating warts, especially in severe and widespread cases. If clear predisposing factors for having warts are identified or suspected, you now have a great opportunity to educate the patient and form a plan to prevent future outbreaks. […] One of the fears of wart patients, especially those with widespread warts, is that their warts will continue to spread out of control and to other parts of the body.
  • #67 Etiology, Autoinoculation, and Transmission: What Wart Patients Need to Know
    https://practicaldermatology.com/topics/infections-infectious-disease/etiology-autoinoculation-and-transmission-what-wart-patients-need-to-know/23613/
    There is also evidence from genital wart studies that warts are more infectious in their first two to three months and much less likely to spread after 12 months. […] Understanding and listening to the patient’s experience with warts allows us to fine-tune our treatment choices and shows the patient that we empathize with and understand their situation. The goal is to have the wart patient understand not only their treatment, but also wart etiology and how to avoid autoinoculation and limit transmission.
  • #68 Warts (common, flat & plantar) – including symptoms, treatment and prevention | SA Health
    https://www.sahealth.sa.gov.au/wps/wcm/connect/public+content/sa+health+internet/conditions/infectious+diseases/warts/warts+common+flat+and+plantar+-+including+symptoms+treatment+and+prevention
    Warts are lumpy growths in the skin caused by infection with human papilloma viruses (HPV), of which there are more than 100 known types. […] The wart virus is thought to be transmitted by direct skin to skin contact or by contact with contaminated surfaces, for example floors. […] About 65% of warts will go away by themselves within 2 years. If treatment is necessary, the following may be used: liquid nitrogen, chemical paint applications, surgical removal, laser therapy. […] Wart infection can be prevented by the following measures: avoid direct contact with warts, wear shoes, wash hands after any contact with warts.
  • #69 Common warts – Symptoms, diagnosis and treatment | BMJ Best Practice
    https://bestpractice.bmj.com/topics/en-gb/615
    Common warts, also known as verrucae vulgaris, are caused by human papillomavirus infection and affect most people during their lifetimes. […] The goals of treatment are to destroy the lesion, induce cytotoxicity against infected cells, and promote antiviral immune responsiveness to prevent recurrence. […] Best outcomes are achieved with a combination of destructive and immune sensitisation approaches.
  • #70 Common warts – Symptoms, diagnosis and treatment | BMJ Best Practice
    https://bestpractice.bmj.com/topics/en-gb/615
    Common warts, also known as verrucae vulgaris, are caused by human papillomavirus infection and affect most people during their lifetimes. […] The goals of treatment are to destroy the lesion, induce cytotoxicity against infected cells, and promote antiviral immune responsiveness to prevent recurrence. […] Best outcomes are achieved with a combination of destructive and immune sensitisation approaches.
  • #71 Nongenital Warts: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1133317-overview
    Warts are benign proliferations of skin and mucosa caused by the human papillomavirus (HPV). Currently, more than 100 types of HPV have been identified. Certain HPV types tend to infect skin at particular anatomic sites; however, warts of any HPV type may occur at any site. The primary clinical manifestations of HPV infection include common warts, genital warts, flat warts, and deep palmoplantar warts (myrmecia). […] Warts can affect any area on the skin and mucous membranes. The HPV virus infects the epithelium, and systemic dissemination of the virus does not occur. Viral replication occurs in differentiated epithelial cells in the upper level of the epidermis; however, viral particles can be found in the basal layer. […] Warts are caused by HPV, which is a double-stranded, circular, supercoiled DNA virus enclosed in an icosahedral capsid and comprising 72 capsomers. More than 100 types of HPV have been identified. Note the following wart types and HPV types: Common warts – HPV types 2 and 4 (most common), followed by types 1, 3, 27, 29, and 57.
  • #72 Warts: How To Identify, Causes, Types, Treatment & Prevention
    https://my.clevelandclinic.org/health/diseases/15045-warts
    Warts are skin growths that develop due to strains of the human papillomavirus (HPV). […] The human papillomavirus (HPV) causes warts. There are over 100 subtypes (strains) of HPV, but only a few types can cause warts on certain parts of your body. […] Certain strains of the human papillomavirus (HPV) cause warts. The virus can enter your skin through small cuts and cause extra cell growth. The outer layer of your skin turns thicker and harder, forming a wart. Warts are more likely to infect moist and soft skin or injured skin. […] All warts come from HPV, but not all forms of HPV cause warts. The type of HPV that can progress to cancer (like cervical cancer) doesn’t cause warts.
  • #73 Etiology, Autoinoculation, and Transmission: What Wart Patients Need to Know
    https://practicaldermatology.com/topics/infections-infectious-disease/etiology-autoinoculation-and-transmission-what-wart-patients-need-to-know/23613/
    Educating the patient about wart etiology, autoinoculation, and transmission can greatly enhance patient satisfaction and improve outcomes. […] Many patients don’t know that warts are caused by a virus, and they have little understanding of how warts are transmitted. A clear understanding of wart etiology empowers the patient, giving them the knowledge to limit autoinoculation and transmission. […] Limiting autoinoculation is key to successfully treating warts, especially in severe and widespread cases. If clear predisposing factors for having warts are identified or suspected, you now have a great opportunity to educate the patient and form a plan to prevent future outbreaks. […] One of the fears of wart patients, especially those with widespread warts, is that their warts will continue to spread out of control and to other parts of the body.
  • #74 Etiology, Autoinoculation, and Transmission: What Wart Patients Need to Know
    https://practicaldermatology.com/topics/infections-infectious-disease/etiology-autoinoculation-and-transmission-what-wart-patients-need-to-know/23613/
    There is also evidence from genital wart studies that warts are more infectious in their first two to three months and much less likely to spread after 12 months. […] Understanding and listening to the patient’s experience with warts allows us to fine-tune our treatment choices and shows the patient that we empathize with and understand their situation. The goal is to have the wart patient understand not only their treatment, but also wart etiology and how to avoid autoinoculation and limit transmission.