Materiały źródłowe

• #1 Genital Warts: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/763014-overview

  Genital warts are an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 100 types of double-stranded HPV papovaviruses have been isolated thus far, and, of these, about 35 types have affinity to genital sites. Many have been linked directly to an increased neoplastic risk in men and women. […] Two general categories of genital human papillomavirus (HPV) exist: low-risk benign HPV lesions and high-risk neoplastic HPV lesions. The low-risk strains are responsible for genital warts and recurrent respiratory papillomatosis (RRP), as well as low-grade cervical lesions. Two types, 6 and 11, account for more than 90% of genital warts and most cases of RRP. These are least likely to have malignant potential. […] Thirteen human papillomavirus (HPV) types (ie, 33, 35, 39, 40, 43, 45, 51-56, 58) have a moderate risk for neoplastic conversion; HPV-16 and HPV-18 are considered high risk; more than 70% of cervical, vaginal, and penile cancers are caused from 2 types. This picture is complicated by the proven coexistence of many types in the same patient (10-15%), lack of adequate information on the oncogenic potential of many other types, and ongoing identification of additional HPV-related clinical pathology.

• #2 Genital Warts

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3390234/

  External genital warts, also known as condylomata acuminata, are extremely common, with between 500,000 to one million new cases diagnosed each year in the United States alone. […] To date, more than 120 distinct subtypes of HPV have been identified, with approximately 40 different subtypes capable of infecting the anogenital tract. […] HPV types 6 and 11 rarely give rise to cervical cancers and are thus considered low-risk subtypes. Infection by these genotypes is responsible for 90 percent of the cases of genital wart formation. […] The viral genome is composed of six early-open reading frames (E1, E2, E4, E5, E6, E7) and two late-open reading frames (L1, L2). The early-open E genes are important for regulatory function and encode proteins involved in viral replication and cell transformation. In contrast, the late-open L genes encode viral capsid proteins.

• #3 Detection of specific HPV subtypes responsible for the pathogenesis of condylomata acuminata | Virology Journal | Full Text

  https://virologyj.biomedcentral.com/articles/10.1186/1743-422X-10-137

  The low-risk human papillomavirus types 6 and 11 are responsible for approximately 90% of anogenital wart cases, with approximately 190,000 new and recurrent cases reported in the UK in 2010. […] The aims of the study were to evaluate current strategies used for the monitoring of HPV infection in genital warts and to assess the suitability of laser-capture microdissection (LCM) as a technique to improve the understanding of the natural history of HPV types associated with genital wart lesions. […] Results indicated that swabbing the surface of warts does not accurately reflect potential causative HPV types present within a wart lesion, multiple HPV types being present on the surface of the wart that are absent in the lower layers of tissue isolated by LCM. […] HPV 6 and HPV 11 were present in more than 90% of the lesions examined.

• #4 Ethiology and Pathophysiology of Whart Hpv Infection: A Review Article | Auctores

  https://www.auctoresonline.org/article/ethiology-and-pathophysiology-of-whart-hpv-infection-a-review-article

  Genital Human Papillomavirus (HPV) infection is a self-limiting and often asymptomatic disease. Genital HPV infection is divided into high-risk HPV (HPV 16 and 18) and low-risk HPV (HPV 6 and 11). Low-risk or non-oncogenic HPV produces a clinical picture of anogenital warts, which may be condylomatous, papules, or keratotic. […] The pathogenesis of HPV begins with infection of stem cells in the basal layer of the epithelium. Once inside the cell, the virus requires expression of the E1 and E2 genes to maintain a low genome copy number. These proteins bind to the origin of replication and the virus secretes cellular DNA polymerases and other proteins required for DNA replication. In the suprabasal layer, the expression of genes E1, E2, E5, E6 and E7 contributes to the maintenance of the viral genome and induces cell proliferation, increasing the number of HPV-infected cells in the epithelium, resulting in a higher number of cells that will eventually produce infectious virions.

• #5 Patient education: Genital warts in women (Beyond the Basics) – UpToDate

  https://www.uptodate.com/contents/genital-warts-in-women-beyond-the-basics/print

  Warts may appear weeks to a year or more after being exposed to the virus; it is not usually possible to know when or how you became infected. […] Even with treatment, it is possible that the warts will come back within a few weeks or months. This is because treating the warts does not necessarily get rid of all of the virus (HPV) causing the warts. Some cells in the normal-appearing genital skin and vagina may remain infected with HPV. There is currently no treatment that will permanently get rid of HPV in all infected cells, but most people will clear the virus and the warts with their own immune systems within two years. […] Getting rid of warts does not necessarily mean that the virus causing the warts (HPV) is gone. If warts come back, they usually do so within three to six months of treatment. This problem is more common in people with a weakened immune system (such as diabetes, HIV, or certain medications).

• #6 Condylomata acuminata (anogenital warts) in adults: Epidemiology, pathogenesis, clinical features, and diagnosis – UpToDate

  https://www.uptodate.com/contents/condylomata-acuminata-anogenital-warts-in-adults-epidemiology-pathogenesis-clinical-features-and-diagnosis

  Human papillomavirus (HPV) is transmitted through contact with infected skin or mucosa. The virus invades the cells of the epidermal basal layer through microabrasions. Anogenital HPV infection is almost always acquired through sexual contact. Warts are not required for transmission but are highly infectious because of their high viral load.

• #7 Condyloma Acuminatum (Genital Warts): Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/781735-overview

  Condyloma acuminatum (also known as genital warts or anogenital warts) refers to an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 180 types of double-stranded HPV papovavirus have been isolated to date. Many of these have been related directly to an increased neoplastic risk in men and women. […] Approximately 90% of condylomata acuminata are related to HPV types 6 and 11. These 2 types are the least likely to have a neoplastic potential. Risk for neoplastic conversion has been determined to be moderate (types 33, 35, 39, 40, 43, 45, 51-56, 58) or high (types 16, 18), with many other isolated types. […] Cells of the basal layer of the epidermis are invaded by human papillomavirus (HPV). These penetrate through skin and cause mucosal microabrasions. A latent viral phase begins with no signs or symptoms and can last from a month to several years. Following latency, production of viral DNA, capsids, and particles begins. Host cells become infected and develop the morphologic atypical koilocytosis of condyloma acuminatum. […] Multiple simultaneous lesions are common and may involve subclinical states as well-differentiated anatomic sites. Subclinical infections have been established to carry both an infectious and oncogenic potential.

• #8 Ethiology and Pathophysiology of Whart Hpv Infection: A Review Article | Auctores

  https://www.auctoresonline.org/article/ethiology-and-pathophysiology-of-whart-hpv-infection-a-review-article

  Genital Human Papillomavirus (HPV) infection is a self-limiting and often asymptomatic disease. Genital HPV infection is divided into high-risk HPV (HPV 16 and 18) and low-risk HPV (HPV 6 and 11). Low-risk or non-oncogenic HPV produces a clinical picture of anogenital warts, which may be condylomatous, papules, or keratotic. […] The pathogenesis of HPV begins with infection of stem cells in the basal layer of the epithelium. Once inside the cell, the virus requires expression of the E1 and E2 genes to maintain a low genome copy number. These proteins bind to the origin of replication and the virus secretes cellular DNA polymerases and other proteins required for DNA replication. In the suprabasal layer, the expression of genes E1, E2, E5, E6 and E7 contributes to the maintenance of the viral genome and induces cell proliferation, increasing the number of HPV-infected cells in the epithelium, resulting in a higher number of cells that will eventually produce infectious virions.

• #9 Genital wart – Wikipedia

  https://en.wikipedia.org/wiki/Genital_wart

  HPV types 6 and 11 are responsible for causing majority of genital warts whereas HPV types 16, 18, 31, 33, and 35 are also occasionally found. […] The types of HPV that cause cancer are not the same as those that cause warts. […] Although 90% of HPV infections are cleared by the body within two years of infection, it is possible for infected cells to undergo a latency (quiet) period, with the first occurrence or a recurrence of symptoms happening months or years later. […] In individuals with a history of previous HPV infection, the appearance of new warts may be either from a new exposure to HPV, or from a recurrence of the previous infection. […] The presence of wart-like lesions on the genitals of young children has been suggested as an indicator of sexual abuse. However, genital warts can sometimes result from autoinoculation by warts elsewhere on the body, such as from the hands.

• #10 Genital Warts: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/763014-overview

  Human papillomavirus (HPV) invades cells of the basal layer of the epidermis, penetrating skin and mucosal microabrasions in the genital area. […] Following that period, viral DNA, capsids, and particles are produced. Host cells become infected and develop the morphologic atypical koilocytosis of genital warts. […] Multiple simultaneous lesions are common and may involve subclinical states as well as different anatomic sites. Subclinical infections have an infectious and oncogenic potential. However, most infections are transient and clear up within 2 years without intervention. […] 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.

• #11 Condyloma Acuminatum (Genital Warts): Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/781735-overview

  Condyloma acuminatum (also known as genital warts or anogenital warts) refers to an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 180 types of double-stranded HPV papovavirus have been isolated to date. Many of these have been related directly to an increased neoplastic risk in men and women. […] Approximately 90% of condylomata acuminata are related to HPV types 6 and 11. These 2 types are the least likely to have a neoplastic potential. Risk for neoplastic conversion has been determined to be moderate (types 33, 35, 39, 40, 43, 45, 51-56, 58) or high (types 16, 18), with many other isolated types. […] Cells of the basal layer of the epidermis are invaded by human papillomavirus (HPV). These penetrate through skin and cause mucosal microabrasions. A latent viral phase begins with no signs or symptoms and can last from a month to several years. Following latency, production of viral DNA, capsids, and particles begins. Host cells become infected and develop the morphologic atypical koilocytosis of condyloma acuminatum. […] Multiple simultaneous lesions are common and may involve subclinical states as well-differentiated anatomic sites. Subclinical infections have been established to carry both an infectious and oncogenic potential.

• #12 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.

• #13 Genital Warts

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3390234/

  External genital warts, also known as condylomata acuminata, are extremely common, with between 500,000 to one million new cases diagnosed each year in the United States alone. […] To date, more than 120 distinct subtypes of HPV have been identified, with approximately 40 different subtypes capable of infecting the anogenital tract. […] HPV types 6 and 11 rarely give rise to cervical cancers and are thus considered low-risk subtypes. Infection by these genotypes is responsible for 90 percent of the cases of genital wart formation. […] The viral genome is composed of six early-open reading frames (E1, E2, E4, E5, E6, E7) and two late-open reading frames (L1, L2). The early-open E genes are important for regulatory function and encode proteins involved in viral replication and cell transformation. In contrast, the late-open L genes encode viral capsid proteins.

• #14

  https://journals.lww.com/md-journal/fulltext/2024/05240/molecular_mechanisms_of_human_papilloma_virus.6.aspx

  The mechanisms by which HPV exhibits oncogenicity vary depending on the individual type. Low-risk HPV genotypes include HPV 6, 11, 42, 43, and 44. Symptomatic infection by these low-risk genotypes may present as skin lesions such as warts. However, these lesions are often benign and rarely progress to a cancerous type. High-risk HPV genotypes include HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68, and 70. These high-risk HPV genotypes are often associated with cancerous lesions of the cervix. Among them, HPV 16 and 18 are the most prevalent offenders. […] The described invasion of the basal epithelial cell by HPV is a strategic one. Basal epithelial cells divide symmetrically and asymmetrically. The symmetric division of basal epithelial cells allows horizontal replication to produce more of them. Asymmetric division refers to the vertical production of daughter epithelial cells. These daughter cells successively move superiorly towards the superficial epithelium acquiring specialized properties associated with tissue regeneration. HPV exploits these cellular mechanisms for its own replication and propagation.

• #15 Genital Warts

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3390234/

  Specifically, low-risk HPV subtypes will remain separate from the host cell DNA and thus undergo replication independently. In contrast, high-risk HPV subtypes will incorporate their DNA directly into the host cells genetic material. The integration of viral and host cell DNA often results in the dysregulation and uncontrolled activation of the E6 and E7 genes, which promotes the transcription of oncoproteins. These will bind and inactivate tumor suppressor genes p53 and Rb, leading to increased cell proliferation and a greater risk of malignant progression. […] The current options available for the treatment of CA are largely centered upon removal of the warty growth rather than elimination of the underlying viral infection. There is little evidence to suggest that existing treatments are effective in the long-term eradication of genital warts or that they play any significant role in hindering potential malignant wart evolution.

• #16 Genital Warts

  https://www.pawanlal.org/home/index.php/diseases-and-surgery/surgical-diseases-ii/urology/genital-warts-2

  High-risk human papillomaviruses (HPV 16 18 serotypes) cause essentially all cervical cancers, most anal and oropharyngeal cancers, and some vaginal, vulvar, and penile cancers. […] They are caused by a small DNA virus, a papillomavirus belonging to the papovavirus group, which cannot be cultured. Genital warts differ from skin warts histologically and antigenically. Genital warts are nearly always transmitted by sexual contact; autoinoculation from hand to genitals is unusual. The infectivity of sexually acquired warts is about 60%; the incubation period is long, varying from two weeks to eight months. […] Low-risk HPV subtypes will remain separate from the host cell DNA and thus undergo replication independently. In contrast, high-risk HPV subtypes will incorporate their DNA directly into the host cells genetic material. The integration of viral and host cell DNA often results in the dysregulation and uncontrolled activation of the E6 and E7 genes, which promotes the transcription of oncoproteins. These will bind and inactivate tumor suppressor genes p53 and Rb, leading to increased cell proliferation and a greater risk of malignant progression.

• #17 Human papillomavirus infection – Wikipedia

  https://en.wikipedia.org/wiki/Human_papillomavirus_infection

  E6 produces a protein (also called E6) that simultaneously binds to two host cell proteins called p53 and E6-Associated Protein (E6-AP). E6AP is an E3 Ubiquitin ligase, an enzyme whose purpose is to tag proteins with a post-translational modification called Ubiquitin. By binding both proteins, E6 induces E6AP to attach a chain of ubiquitin molecules to p53, thereby flagging p53 for proteosomal degradation. […] Thus, the degradation of p53, induced by E6, promotes unregulated cell division, cell growth and cell survival, all characteristics of cancer.

• #18 Human papillomavirus infection – Wikipedia

  https://en.wikipedia.org/wiki/Human_papillomavirus_infection

  E6 produces a protein (also called E6) that simultaneously binds to two host cell proteins called p53 and E6-Associated Protein (E6-AP). E6AP is an E3 Ubiquitin ligase, an enzyme whose purpose is to tag proteins with a post-translational modification called Ubiquitin. By binding both proteins, E6 induces E6AP to attach a chain of ubiquitin molecules to p53, thereby flagging p53 for proteosomal degradation. […] Thus, the degradation of p53, induced by E6, promotes unregulated cell division, cell growth and cell survival, all characteristics of cancer.

• #19

  https://journals.lww.com/md-journal/fulltext/2024/05240/molecular_mechanisms_of_human_papilloma_virus.6.aspx

  Upon entry into the cell nucleus, HPV begins to exert integrative mechanisms to incorporate itself into cellular DNA. HPV RNA encoding the E6 and E7 oncogenes is initiated via the viral upstream regulatory region. The E6 oncoprotein will bind to p53 and disable its normal function for tumor suppression. This affects the host cell ability to undergo programmed cell death and growth arrest. This inactivation of p53 forces the host cell to enter the S phase of the cell cycle. The E7 oncoprotein will bind to the retinoblastoma protein, causing the release of the transcription factor E2F. The release of E2F activates cyclin-dependent kinases. Subsequent expression of the E1 and E2 oncogenes allows genomic instability at the integration locus. Persistence of the S phase of the cell cycle leads to uninhibited proliferation and differentiation of infected cells, eventually leading to dysplasia.

• #20 Core Concepts – Human Papillomavirus Infection – Self-Study Lessons – National STD Curriculum

  https://www.std.uw.edu/go/comprehensive-study/hpv

  The HPV types that infect humans have a known specificity for mucosal and cutaneous epithelium. Infection with HPV occurs at the basal cell layer of stratified squamous epithelial cells. Infection stimulates cellular proliferation in the epithelium, and the infected cells display a broad spectrum of changes, with a spectrum of cellular outcomes that include inapparent infection, benign hyperplasia (papilloma), precancerous lesions, and invasive carcinoma. To effectively replicate, HPV must utilize the host cellular machinery. During the process, the viral protein product encoded by E6 binds to the p53 tumor suppressor gene product, which results in the premature degradation of the p53 protein. The E7 protein binds to a tumor suppressor protein—the retinoblastoma protein—and inhibits its function. The E6 and E7 proteins mediate much of the HPV oncogenic potential by assisting the cell in evading host immunity, a process that facilitates virion production in differentiating epithelial cells.

• #21

  https://journals.lww.com/md-journal/fulltext/2024/05240/molecular_mechanisms_of_human_papilloma_virus.6.aspx

  Upon entry into the cell nucleus, HPV begins to exert integrative mechanisms to incorporate itself into cellular DNA. HPV RNA encoding the E6 and E7 oncogenes is initiated via the viral upstream regulatory region. The E6 oncoprotein will bind to p53 and disable its normal function for tumor suppression. This affects the host cell ability to undergo programmed cell death and growth arrest. This inactivation of p53 forces the host cell to enter the S phase of the cell cycle. The E7 oncoprotein will bind to the retinoblastoma protein, causing the release of the transcription factor E2F. The release of E2F activates cyclin-dependent kinases. Subsequent expression of the E1 and E2 oncogenes allows genomic instability at the integration locus. Persistence of the S phase of the cell cycle leads to uninhibited proliferation and differentiation of infected cells, eventually leading to dysplasia.

• #22 SciELO Brazil – Sexually transmitted papillomavirus infections: epidemiology pathogenesis, clinic, morphology, important differential diagnostic aspects, current diagnostic and treatment options Sexually transmitted papillomavirus infections: epidemiolog

  https://www.scielo.br/j/abd/a/TKSXnk4f3c4VXWcbfnTwWpp/?lang=en

  Minor wounds in the anogenital region caused during intercourse favor invasion by papilloma viruses into the basal layer of the epidermis. The activation of certain viral proteins after a specific latent period leads to intensified proliferative activity of the affected cells. The integration of viral proteins in human cells disturbs cellular homeostasis. The expression of E6 and E7 genes leads to immortalization of keratinocytes and stimulates cellular proliferation. Simultaneously, cellular differentiation and aging are stopped or retarded. The different association of certain clinical lesions with certain papilloma viral strains (e.g., condylomata acuminata with HPV-6 and -11, or HPV-16 and -18 with cervical carcinomas), correlates to some extent with the different activities of E6 and E7 gene products, which, are oncogenic. The more the differentiation processes in the affected keratinocytes progresses, the more the expression of the viral proteins is strengthened, and they consequently form the viral particle. The cellular nuclei of the above keratinizing epidermal layer contain highly concentrated viral particles which, upon separating from the tissue, are highly infectious. It is not clear to what extent external factors play an auxiliary role in the clinical manifestation of certain HPV associated lesions. […] The presence of immune defects in certain groups of patients is able to favour the early clinical manifestation, the infiltrative proliferating growth, and, in the cancer-inducing strains, to potentate the malignant transformation of the lesions.

• #23 Genital Warts: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/763014-overview

  Human papillomavirus (HPV) invades cells of the basal layer of the epidermis, penetrating skin and mucosal microabrasions in the genital area. […] Following that period, viral DNA, capsids, and particles are produced. Host cells become infected and develop the morphologic atypical koilocytosis of genital warts. […] Multiple simultaneous lesions are common and may involve subclinical states as well as different anatomic sites. Subclinical infections have an infectious and oncogenic potential. However, most infections are transient and clear up within 2 years without intervention. […] 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.

• #24 Chapter 11: Human Papillomavirus | Pink Book | CDC

  https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-11-human-papillomavirus.html

  HPV infection occurs at the basal epithelium. Although incidence of infection is high, most infections resolve spontaneously within a year or two. A small proportion of infected persons become persistently infected; persistent infection is the most important risk factor for the development of cervical cancer. […] The pathogenesis of other types of HPV-related cancers may follow a similar course, although less is known about their respective precursor lesions: anal HSIL has been identified as a precursor to anal cancer, vulvar HSIL has been identified as a precursor to vulvar cancer, and vaginal HSIL has been identified as a precursor to vaginal cancer. […] Infection with one type of HPV does not prevent infection with another type. Of persons infected with HPV that infects the mucosal epithelium, 5% to 30% are infected with multiple types of the virus.

• #25 Patient education: Genital warts in women (Beyond the Basics) – UpToDate

  https://www.uptodate.com/contents/genital-warts-in-women-beyond-the-basics/print

  Warts may appear weeks to a year or more after being exposed to the virus; it is not usually possible to know when or how you became infected. […] Even with treatment, it is possible that the warts will come back within a few weeks or months. This is because treating the warts does not necessarily get rid of all of the virus (HPV) causing the warts. Some cells in the normal-appearing genital skin and vagina may remain infected with HPV. There is currently no treatment that will permanently get rid of HPV in all infected cells, but most people will clear the virus and the warts with their own immune systems within two years. […] Getting rid of warts does not necessarily mean that the virus causing the warts (HPV) is gone. If warts come back, they usually do so within three to six months of treatment. This problem is more common in people with a weakened immune system (such as diabetes, HIV, or certain medications).

• #26 Genital Warts: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/763014-overview

  Human papillomavirus (HPV) invades cells of the basal layer of the epidermis, penetrating skin and mucosal microabrasions in the genital area. […] Following that period, viral DNA, capsids, and particles are produced. Host cells become infected and develop the morphologic atypical koilocytosis of genital warts. […] Multiple simultaneous lesions are common and may involve subclinical states as well as different anatomic sites. Subclinical infections have an infectious and oncogenic potential. However, most infections are transient and clear up within 2 years without intervention. […] 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.

• #27 Ethiology and Pathophysiology of Whart Hpv Infection: A Review Article | Auctores

  https://www.auctoresonline.org/article/ethiology-and-pathophysiology-of-whart-hpv-infection-a-review-article

  In benign HPV lesions, cell proliferation increases leading to increased nutrition, resulting in competition for nutrients and oxygen. Both HR-HPV and LR-HPV E7 proteins increase the level of the transcription factor Hypoxia-inducible factor-1 (HIF-1), and induce increased expression of HIF-1 target genes under hypoxic conditions. Increased HIF-1 activity results in increased transcription of a subset of genes that support angiogenesis, and the induction of this angiogenesis is critical for the persistence and growth of HPV lesions such as genital warts.

• #28 Human Papillomavirus (HPV) Infection – Infectious Diseases – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/infectious-diseases/sexually-transmitted-infections-stis/human-papillomavirus-hpv-infection

  Genital warts may persist and spread widely in patients with decreased cell-mediated immunity (eg, due to pregnancy or HIV infection). […] Some data suggest HPV plays a role in the pathogenesis of some bladder cancers. […] Condylomata acuminata are benign anogenital warts most often caused by HPV types 6 and 11, as are laryngeal and oropharyngeal warts. Low- and high-grade intraepithelial neoplasia and carcinoma may be caused by HPV. […] Virtually all cervical cancer is caused by HPV; about 70% is caused by types 16 and 18, and many of the rest result from types 31, 33, 45, 52, and 58. […] HPV types that affect mainly the anogenital area can be transmitted to the oropharynx by orogenital contact; type 16 appears responsible for many cases of oropharyngeal cancer. […] HPV is transmitted from lesions during contact with skin or mucosa. The types that affect the anogenital region are usually transmitted sexually by vaginal or anal intercourse, but digital, oral, and nonpenetrative genital contact may be involved. […] Genital warts are more common among immunocompromised patients. Growth rates vary, but pregnancy, immunosuppression, or maceration of the skin may accelerate the growth and spread of warts.

• #29 Ethiology and Pathophysiology of Whart Hpv Infection: A Review Article | Auctores

  https://www.auctoresonline.org/article/ethiology-and-pathophysiology-of-whart-hpv-infection-a-review-article

  In benign HPV lesions, cell proliferation increases leading to increased nutrition, resulting in competition for nutrients and oxygen. Both HR-HPV and LR-HPV E7 proteins increase the level of the transcription factor Hypoxia-inducible factor-1 (HIF-1), and induce increased expression of HIF-1 target genes under hypoxic conditions. Increased HIF-1 activity results in increased transcription of a subset of genes that support angiogenesis, and the induction of this angiogenesis is critical for the persistence and growth of HPV lesions such as genital warts.

• #30 Human Papillomavirus Infection: Management and Treatment | IntechOpen

  https://www.intechopen.com/chapters/72773

  Human papillomaviruses (HPVs) are a large and diverse group of viruses with 174 completely characterised types, with new HPV types being continuously found. HPVs infect epithelial cells in genital mucosa (Alphapapillomaviruses only), oral mucosa or skin (representatives of all five genera). The most common clinical manifestation is verruca, with different morphological forms. The histology shows acanthosis, elongation of dermal papillae, presence of vacuolated cells and koilocytes. Subclinical manifestations are invisible to the human eye. These subclinical lesions are flat and multiple. Their clinical insignificance facilitates their spread, and in women their persistence is possibly related to genital cancer. […] The known spontaneous remission of HPV-induced warts, which is attributed to cell-bound mechanisms, underscores the role of the immune system, including an increase in Th1 cytokines and infiltration of T cells (CD4+, CD8+) around the diseased tissue.

• #31 Genital Warts | Craig Singer MD Dermatology

  https://singerderm.com/genital-warts/

  Genital warts are caused by human papillomavirus (HPV) and are almost always spread by sexual contact (including oral, anal, and vaginal intercourse), but on occasion may be spread at the time of birth or through autoinoculation. HPV is highly contagious. Sexual contact with an HPV infected individual results in a 75% chance of contracting the virus and developing genital warts. HPV may be transmitted even if the infected person has no signs or symptoms of genital warts. […] The majority of people exposed to HPV become infected with HPV, but most infections resolve spontaneously. The incubation period of HPV (i.e the time from exposure until the time warts appear) varies from weeks to months, but on average is 2-3 months after initial contact. Sometimes, genital warts appear years after exposure. Other times, people exposed to HPV never develop visible genital warts (i.e. subclinical infection). Therefore it is difficult to know when a person first became infected.

• #32 The Forgotten HPV: External Genital Warts

  https://www.skintherapyletter.com/family-practice/hpv-external-genital-warts-fp/

  Infection with HPV occurs by direct inoculation of the virus into the epidermal layers of the skin through epithelial defects. Skin maceration is an important factor in transmission. […] Genital infections are predominantly obtained through sexual contact, which can then be transmitted vertically to newborns by passage through the infected birth canal. […] The rate of infectivity between sexual partners is estimated to be 60%.

• #33 Approaches to Treatment: External Genital Warts (Slide with Transcript)

  https://www.medscape.org/viewarticle/567995

  EGWs are highly contagious. One can be exposed to warts or HPV causing EGW during oral, vaginal, or anal sex with an infected partner. You can also get these by skin-to-skin contact during vaginal or anal sex. Like many sexually transmitted infections, genital HPV infections often do not have the signs and symptoms that you can see or feel. So a lot of times patients won’t know that they have been exposed to a genital HPV virus. […] The papillary structures can be very early signs of EGW. People think of the warts as being distinct, with white caps on them, but they can be any color and any size. If they take up — stimulate — the lanocytes, they can be pigmented. If they have a lot of angiogenesis, or formation of blood vessels, they can be red. They can appear fleshy in color. Many have keratin-producing characteristics as they grow, and that will makes them look white or whitish in color.

• #34 Genital wart – Wikipedia

  https://en.wikipedia.org/wiki/Genital_wart

  HPV types 6 and 11 are responsible for causing majority of genital warts whereas HPV types 16, 18, 31, 33, and 35 are also occasionally found. […] The types of HPV that cause cancer are not the same as those that cause warts. […] Although 90% of HPV infections are cleared by the body within two years of infection, it is possible for infected cells to undergo a latency (quiet) period, with the first occurrence or a recurrence of symptoms happening months or years later. […] In individuals with a history of previous HPV infection, the appearance of new warts may be either from a new exposure to HPV, or from a recurrence of the previous infection. […] The presence of wart-like lesions on the genitals of young children has been suggested as an indicator of sexual abuse. However, genital warts can sometimes result from autoinoculation by warts elsewhere on the body, such as from the hands.

• #35 Non-sexual HPV transmission and role of vaccination for a better future (Review)

  https://www.spandidos-publications.com/10.3892/etm.2020.9316

  The horizontal transmission of HPV includes fomites, fingers, and mouth, skin contact (other than sexual). […] Self-inoculation is described in studies as a potential HPV transmission route. […] Vertical transmission from mother to newborn is another HPV transmittal route. […] The possibility of vertical HPV infection was discussed as early as 1950, in a study on infantile anogenital warts, congenital conjunctival papilloma, and juvenile laryngeal papillomatosis. […] Data show there is a correlation between the HPV DNA load of the mother and the ability to transfer it to newborns. […] Hygiene measures are proven to be inefficient in preventing HPV transmission, as the studies which have evaluated samples of HPV on contaminated medical equipment (after conventional disinfection) have found them to still be positive, especially for type 16. […] According to this study, we can argue for the self-inoculation and horizontal transmission of HPV.

• #36 Genital Warts – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441884/

  Genital warts (condyloma acuminatum) are a sexually transmitted infection caused by the human papillomavirus (HPV) types 6 and 11. These are spread by skin-to-skin contact, usually during sex. […] HPV is transmitted primarily through penetrative sex. While HPV also can be transmitted via non-penetrative sexual activity, it is less common. […] HPV infection appears to be the cause of most cases of anal cancer (about 90%) and virtually all cases of cervical cancer in women, with HPV type 16 accounting for about 50% of these. […] Although treatments can remove warts, they do not remove HPV. Warts may sometimes spontaneously regress. Traditional theories postulate that the virus remains in the body for a lifetime. However, it is now believed that the virus may be either cleared or suppressed to levels below what polymerase chain reaction (PCR) tests can measure.

• #37 Non-sexual HPV transmission and role of vaccination for a better future (Review)

  https://www.spandidos-publications.com/10.3892/etm.2020.9316

  The horizontal transmission of HPV includes fomites, fingers, and mouth, skin contact (other than sexual). […] Self-inoculation is described in studies as a potential HPV transmission route. […] Vertical transmission from mother to newborn is another HPV transmittal route. […] The possibility of vertical HPV infection was discussed as early as 1950, in a study on infantile anogenital warts, congenital conjunctival papilloma, and juvenile laryngeal papillomatosis. […] Data show there is a correlation between the HPV DNA load of the mother and the ability to transfer it to newborns. […] Hygiene measures are proven to be inefficient in preventing HPV transmission, as the studies which have evaluated samples of HPV on contaminated medical equipment (after conventional disinfection) have found them to still be positive, especially for type 16. […] According to this study, we can argue for the self-inoculation and horizontal transmission of HPV.

• #38 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. […] No treatment is universally effective at eradicating viral warts.

• #39 Genital Warts: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/763014-overview

  Genital warts are an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 100 types of double-stranded HPV papovaviruses have been isolated thus far, and, of these, about 35 types have affinity to genital sites. Many have been linked directly to an increased neoplastic risk in men and women. […] Two general categories of genital human papillomavirus (HPV) exist: low-risk benign HPV lesions and high-risk neoplastic HPV lesions. The low-risk strains are responsible for genital warts and recurrent respiratory papillomatosis (RRP), as well as low-grade cervical lesions. Two types, 6 and 11, account for more than 90% of genital warts and most cases of RRP. These are least likely to have malignant potential. […] Thirteen human papillomavirus (HPV) types (ie, 33, 35, 39, 40, 43, 45, 51-56, 58) have a moderate risk for neoplastic conversion; HPV-16 and HPV-18 are considered high risk; more than 70% of cervical, vaginal, and penile cancers are caused from 2 types. This picture is complicated by the proven coexistence of many types in the same patient (10-15%), lack of adequate information on the oncogenic potential of many other types, and ongoing identification of additional HPV-related clinical pathology.

• #40 Management of Genital Warts | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/1215/p2335.html

  Genital warts caused by human papillomavirus infection are encountered commonly in primary care. Evidence guiding treatment selection is limited, but treatment guidelines recently have changed. […] Genital warts are the visible manifestation of infection by one or more of the nearly 100 recognized human papillomaviruses (HPVs). Visible genital warts typically are caused by HPV types 6 and 11, which rarely are associated with invasive squamous cell carcinoma of the external genitalia. HPV types 16, 18, 31, 33, and 35 have been found in genital warts and are associated with squamous intraepithelial neoplasia; types 16 and 18 are associated most strongly with malignant potential. These virus types also are associated with vaginal, anal, and cervical intraepithelial dysplasia, and squamous cell carcinoma.

• #41 Genital warts overview – wikidoc

  https://www.wikidoc.org/index.php/Genital_warts_overview

  Genital warts are the most easily recognized sign of genital HPV infection. They can be caused by strains 6, 11, 30, 42, 43, 44, 45, 51, 52 and 54 of genital HPV; types 6 and 11 are responsible for 90% of genital warts cases. […] Although treatments can remove the warts, they do not remove the HPV virus, so warts can recur after treatment. Traditional theories postulated that the virus remained in the body for a lifetime. However, new studies using sensitive DNA techniques have shown that through immunological response the virus can either be cleared or suppressed to levels below what PCR tests can measure. […] The gradual development of an effective immune response is thought to be the likely mechanism for HPV DNA clearance. […] The state of the immune system determines the chances of removing the virus entirely and can be affected by factors such as HIV infection, certain medications, stress, or illness.

• #42 Genital Warts: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/763014-overview

  Genital warts are an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 100 types of double-stranded HPV papovaviruses have been isolated thus far, and, of these, about 35 types have affinity to genital sites. Many have been linked directly to an increased neoplastic risk in men and women. […] Two general categories of genital human papillomavirus (HPV) exist: low-risk benign HPV lesions and high-risk neoplastic HPV lesions. The low-risk strains are responsible for genital warts and recurrent respiratory papillomatosis (RRP), as well as low-grade cervical lesions. Two types, 6 and 11, account for more than 90% of genital warts and most cases of RRP. These are least likely to have malignant potential. […] Thirteen human papillomavirus (HPV) types (ie, 33, 35, 39, 40, 43, 45, 51-56, 58) have a moderate risk for neoplastic conversion; HPV-16 and HPV-18 are considered high risk; more than 70% of cervical, vaginal, and penile cancers are caused from 2 types. This picture is complicated by the proven coexistence of many types in the same patient (10-15%), lack of adequate information on the oncogenic potential of many other types, and ongoing identification of additional HPV-related clinical pathology.

• #43 Genital wart – Wikipedia

  https://en.wikipedia.org/wiki/Genital_wart

  HPV types 6 and 11 are responsible for causing majority of genital warts whereas HPV types 16, 18, 31, 33, and 35 are also occasionally found. […] The types of HPV that cause cancer are not the same as those that cause warts. […] Although 90% of HPV infections are cleared by the body within two years of infection, it is possible for infected cells to undergo a latency (quiet) period, with the first occurrence or a recurrence of symptoms happening months or years later. […] In individuals with a history of previous HPV infection, the appearance of new warts may be either from a new exposure to HPV, or from a recurrence of the previous infection. […] The presence of wart-like lesions on the genitals of young children has been suggested as an indicator of sexual abuse. However, genital warts can sometimes result from autoinoculation by warts elsewhere on the body, such as from the hands.

• #44 Genital Warts: Causes, Symptoms, Treatment & Prevention

  https://my.clevelandclinic.org/health/diseases/4209-genital-warts

  Certain types of HPV cause genital warts. […] Certain strains of human papillomavirus (HPV) cause genital warts. […] Certain types of HPV cause genital warts. Genital warts spread through skin-to-skin contact during sex. […] The strain of HPV that cause genital warts is low-risk. The HPV strains that cause cancer arent the same ones that cause genital warts. […] Genital warts and the virus that causes them (HPV) are both contagious. […] Treatment to remove genital warts doesnt cure you from HPV. Even if you dont have an active outbreak and your warts were removed, you can still spread HPV. […] Genital warts and HPV are common STIs. These types of warts, and the HPV types that cause them, dont increase your risk for getting cancer.

• #45 Prevalence and distribution of HPV types in genital warts in Xi’an, China: a prospective study | BMJ Open

  https://bmjopen.bmj.com/content/9/5/e023897

  Genital warts are a kind of sexually transmitted diseases caused by certain types of human papillomavirus (HPV). The main clinical manifestation of genital warts is benign hyperplasia of the skin and mucous membrane in the genitalia, anus and perineum. HPV is the most common sexually transmitted infection globally, and most people are infected at some point in their lives. To date, 201 different HPV types have been identified. More than 40 of these types can infect the mucous membrane of the anus and genitalia and have been classified as probably low-risk or possibly high-risk and high-risk, depending on their ability to lead to malignant progression. A variety of HPV types can cause genital warts, but HPV6 and 11 together account for about 90% of all cases. HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59 are considered carcinogenic, but 70% of cervical cancers are caused by HPV16 and 18. The results of this study suggest that low-risk HPV types are major pathogens of genital warts, but high-risk HPV type infections and multiple HPV type coinfections are also common in genital warts. HPV6, 11, 52 and 16 are the four most common HPV types in genital wart in Xian, China.

• #46 Prevalence and distribution of HPV types in genital warts in Xi’an, China: a prospective study | BMJ Open

  https://bmjopen.bmj.com/content/9/5/e023897

  The detectable rates of low-risk HPV types peaked in the ages of 15-19 and 55-59 years, while those of high-risk HPV types peaked in the age of 55-59 years. […] Our study found that the detectable rates of low-risk and high-risk HPV types were 45.4% and 34.5% in genital warts in Xian, China. The above reports and our study indicate that low-risk HPV types are major pathogens of genital warts, but high-risk HPV types in genital warts are also common and can act as reservoirs of cancer-related HPV types to threaten local populations.

• #47 Genital/Anogenital Warts | Johns Hopkins ABX Guide

  https://www.hopkinsguides.com/hopkins/view/Johns_Hopkins_ABX_Guide/540244/all/Genital_Anogenital_Warts

  All anogenital warts are caused by human papillomavirus (HPV) infection. […] Most (90%) anogenital warts are benign, caused by HPV subtypes 6 and 11, which are „low-risk” (for malignancy) HPV subtypes. […] These other „intermediate risk” HPV subtypes, including 16, 18, 31, 33, and 35, are associated with high-grade squamous intraepithelial neoplasia (HG-SIL) and are occasionally found in warts, particularly in persons with concurrent HIV infection.

• #48 Genital Warts

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3390234/

  Specifically, low-risk HPV subtypes will remain separate from the host cell DNA and thus undergo replication independently. In contrast, high-risk HPV subtypes will incorporate their DNA directly into the host cells genetic material. The integration of viral and host cell DNA often results in the dysregulation and uncontrolled activation of the E6 and E7 genes, which promotes the transcription of oncoproteins. These will bind and inactivate tumor suppressor genes p53 and Rb, leading to increased cell proliferation and a greater risk of malignant progression. […] The current options available for the treatment of CA are largely centered upon removal of the warty growth rather than elimination of the underlying viral infection. There is little evidence to suggest that existing treatments are effective in the long-term eradication of genital warts or that they play any significant role in hindering potential malignant wart evolution.

• #49 Management of Genital Warts | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/1215/p2335.html

  Some evidence suggests that treatment also may reduce the persistence of HPV DNA in genital tissue, and therefore may reduce infectivity. However, there is currently no evidence that treatment of genital warts has a favorable impact on the incidence of cervical and genital cancer, and there have been no controlled studies on the effects of treatment of external genital warts and HPV transmission rates. […] The mechanism of action for each treatment method is summarized in Table 1, and treatment courses and cycles are summarized in Table 2. […] The choice of initial treatment modality should be guided by a number of considerations, including wart morphology, size, number, and location. Many treatment recommendations are based on expert opinion from consensus guidelines; few studies have directly compared different treatments. […] Patients with suppressed cell immunity associated with organ transplantation, HIV infection, or other conditions may have a poorer response to treatment for genital warts, increased relapse rates, and a higher risk of dysplasia.

• #50 Genital wart – Wikipedia

  https://en.wikipedia.org/wiki/Genital_wart

  The diagnosis of genital warts is most often made visually, but may require confirmation by biopsy in some cases. […] Because genital warts are caused by low-risk HPV types, DNA tests cannot be used for diagnosis of genital warts or other low-risk HPV infections. […] HPV vaccines have excellent safety profiles and are highly efficacious, or have met immunobridging standards. […] They prevent genital warts, with the quadrivalent and nonavalent vaccines providing virtually complete protection. […] Existing treatments are directed towards the removal of visible warts, but these may also regress on their own without any therapy. […] There is no evidence to suggest that removing visible warts reduces transmission of the underlying HPV infection.

• #51 Genital Warts – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441884/

  Genital warts (condyloma acuminatum) are a sexually transmitted infection caused by the human papillomavirus (HPV) types 6 and 11. These are spread by skin-to-skin contact, usually during sex. […] HPV is transmitted primarily through penetrative sex. While HPV also can be transmitted via non-penetrative sexual activity, it is less common. […] HPV infection appears to be the cause of most cases of anal cancer (about 90%) and virtually all cases of cervical cancer in women, with HPV type 16 accounting for about 50% of these. […] Although treatments can remove warts, they do not remove HPV. Warts may sometimes spontaneously regress. Traditional theories postulate that the virus remains in the body for a lifetime. However, it is now believed that the virus may be either cleared or suppressed to levels below what polymerase chain reaction (PCR) tests can measure.

• #52 Management of Genital Warts | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/1215/p2335.html

  Some evidence suggests that treatment also may reduce the persistence of HPV DNA in genital tissue, and therefore may reduce infectivity. However, there is currently no evidence that treatment of genital warts has a favorable impact on the incidence of cervical and genital cancer, and there have been no controlled studies on the effects of treatment of external genital warts and HPV transmission rates. […] The mechanism of action for each treatment method is summarized in Table 1, and treatment courses and cycles are summarized in Table 2. […] The choice of initial treatment modality should be guided by a number of considerations, including wart morphology, size, number, and location. Many treatment recommendations are based on expert opinion from consensus guidelines; few studies have directly compared different treatments. […] Patients with suppressed cell immunity associated with organ transplantation, HIV infection, or other conditions may have a poorer response to treatment for genital warts, increased relapse rates, and a higher risk of dysplasia.

• #53 Patient education: Genital warts in women (Beyond the Basics) – UpToDate

  https://www.uptodate.com/contents/genital-warts-in-women-beyond-the-basics/print

  Warts may appear weeks to a year or more after being exposed to the virus; it is not usually possible to know when or how you became infected. […] Even with treatment, it is possible that the warts will come back within a few weeks or months. This is because treating the warts does not necessarily get rid of all of the virus (HPV) causing the warts. Some cells in the normal-appearing genital skin and vagina may remain infected with HPV. There is currently no treatment that will permanently get rid of HPV in all infected cells, but most people will clear the virus and the warts with their own immune systems within two years. […] Getting rid of warts does not necessarily mean that the virus causing the warts (HPV) is gone. If warts come back, they usually do so within three to six months of treatment. This problem is more common in people with a weakened immune system (such as diabetes, HIV, or certain medications).

• #54 Approaches to Treatment: External Genital Warts (Slide with Transcript)

  https://www.medscape.org/viewarticle/567995

  In EGW, absolutely not. They really need to be identified, diagnosed generally by simple examination — visual examination — and treated with options we’re going to discuss. Just because someone has types 11 and 6 (low oncogenic potential) does not necessarily mean they have the types 16 and 18 that cause 70% of cervical cancers. […] Generally, recurrences are in the range of at least 30% to 40% following primary treatment. […] But in general terms, these HPV infections do not normally stimulate the immune system of a normal, healthy person because they’re above the basal layer of the epithelium. So the immune system does not actually come in contact with the HPV particle; these are inside the cell and they don’t replicate fast. Most people tend to think it’s a recurrence of the same viral type.

• #55 Patient education: Genital warts in women (Beyond the Basics) – UpToDate

  https://www.uptodate.com/contents/genital-warts-in-women-beyond-the-basics/print

  Warts may appear weeks to a year or more after being exposed to the virus; it is not usually possible to know when or how you became infected. […] Even with treatment, it is possible that the warts will come back within a few weeks or months. This is because treating the warts does not necessarily get rid of all of the virus (HPV) causing the warts. Some cells in the normal-appearing genital skin and vagina may remain infected with HPV. There is currently no treatment that will permanently get rid of HPV in all infected cells, but most people will clear the virus and the warts with their own immune systems within two years. […] Getting rid of warts does not necessarily mean that the virus causing the warts (HPV) is gone. If warts come back, they usually do so within three to six months of treatment. This problem is more common in people with a weakened immune system (such as diabetes, HIV, or certain medications).

• #56 Genital Warts | Craig Singer MD Dermatology

  https://singerderm.com/genital-warts/

  It is estimated that 30% of genital warts spontaneously regress within the first four months of infection. The long-term remission rates of genital warts are unknown. Many genital warts (20% to 50%) will recur despite appropriate treatment. Risk factors for long-term persistence of genital warts include a weakened immune system as well as high risk HPV types. […] There is no specific antiviral therapy available to cure HPV infection. In general, current treatments remove the warty growth rather than eliminate the viral infection. Recurrences after treatment are common. It is uncertain as to whether treatment of genital warts reduces the long-term risk of HPV induced cancer. […] Immunotherapy uses a persons own immune system to fight the human papilloma virus (HPV). Vaccination against HPV (during the young teenage years) prior to sexual exposure is the ideal way to prevent HPV and genital warts. Once HPV is acquired, immunity is often difficult to achieve. Methods to induce immunity involve the injection of an allergen directly into the wart, or possibly with a topically applied contact sensitizing agent.

• #57 Genital Warts | Craig Singer MD Dermatology

  https://singerderm.com/genital-warts/

  It is estimated that 30% of genital warts spontaneously regress within the first four months of infection. The long-term remission rates of genital warts are unknown. Many genital warts (20% to 50%) will recur despite appropriate treatment. Risk factors for long-term persistence of genital warts include a weakened immune system as well as high risk HPV types. […] There is no specific antiviral therapy available to cure HPV infection. In general, current treatments remove the warty growth rather than eliminate the viral infection. Recurrences after treatment are common. It is uncertain as to whether treatment of genital warts reduces the long-term risk of HPV induced cancer. […] Immunotherapy uses a persons own immune system to fight the human papilloma virus (HPV). Vaccination against HPV (during the young teenage years) prior to sexual exposure is the ideal way to prevent HPV and genital warts. Once HPV is acquired, immunity is often difficult to achieve. Methods to induce immunity involve the injection of an allergen directly into the wart, or possibly with a topically applied contact sensitizing agent.

• #58 Genital Warts (HPV) (for Teens) | Nemours KidsHealth

  https://kidshealth.org/en/teens/std-warts.html

  Genital warts and other types of HPV can be prevented by a vaccine. The HPV vaccine series is recommended for all kids when they’re 9-11 years old. Teens and adults (up to age 45) also can get the vaccine. Even if someone already has had one type of HPV infection, the HPV vaccine can protect against other types of HPV.

• #59 Genital and extragenital warts unresponsive to immunotherapy | IMCRJ

  https://www.dovepress.com/a-case-of-genital-and-extragenital-warts-unresponsive-to-immunotherapy-peer-reviewed-fulltext-article-IMCRJ

  Anogenital warts (AGWs) are globally recognized as the most common sexually transmitted infections (STIs) caused by the human papillomavirus (HPV), particularly types 6 and 11. […] Measles, mumps, and rubella (MMR) vaccine induce the production of various T helper 1 cytokines to elicit immune responses, resulting in the clearance of both treated and untreated warts. […] Based on the results, several factors must be considered to determine the best candidate for immunotherapy, particularly with MMR vaccine, to achieve an optimal outcome. These factors include the active state of diseases, duration of diseases, as well as a history of sensitization, and broad-spectrum antibiotics. […] The extensive lesions observed in some patients might explain the long duration of the disease and subsequent autoinoculation to extragenital areas.

• #60 Genital wart – Wikipedia

  https://en.wikipedia.org/wiki/Genital_wart

  The diagnosis of genital warts is most often made visually, but may require confirmation by biopsy in some cases. […] Because genital warts are caused by low-risk HPV types, DNA tests cannot be used for diagnosis of genital warts or other low-risk HPV infections. […] HPV vaccines have excellent safety profiles and are highly efficacious, or have met immunobridging standards. […] They prevent genital warts, with the quadrivalent and nonavalent vaccines providing virtually complete protection. […] Existing treatments are directed towards the removal of visible warts, but these may also regress on their own without any therapy. […] There is no evidence to suggest that removing visible warts reduces transmission of the underlying HPV infection.

• #61 Genital Warts | Craig Singer MD Dermatology

  https://singerderm.com/genital-warts/

  It is estimated that 30% of genital warts spontaneously regress within the first four months of infection. The long-term remission rates of genital warts are unknown. Many genital warts (20% to 50%) will recur despite appropriate treatment. Risk factors for long-term persistence of genital warts include a weakened immune system as well as high risk HPV types. […] There is no specific antiviral therapy available to cure HPV infection. In general, current treatments remove the warty growth rather than eliminate the viral infection. Recurrences after treatment are common. It is uncertain as to whether treatment of genital warts reduces the long-term risk of HPV induced cancer. […] Immunotherapy uses a persons own immune system to fight the human papilloma virus (HPV). Vaccination against HPV (during the young teenage years) prior to sexual exposure is the ideal way to prevent HPV and genital warts. Once HPV is acquired, immunity is often difficult to achieve. Methods to induce immunity involve the injection of an allergen directly into the wart, or possibly with a topically applied contact sensitizing agent.

• #62 Genital and extragenital warts unresponsive to immunotherapy | IMCRJ

  https://www.dovepress.com/a-case-of-genital-and-extragenital-warts-unresponsive-to-immunotherapy-peer-reviewed-fulltext-article-IMCRJ

  The outcome of MMR vaccine as immunotherapy for AGWs can be affected by several factors including the active state of diseases, duration, and the history of sensitization, which includes but is not limited to previous vaccination, and broad-spectrum antibiotics. […] In this study, the patient was administered an intralesional injection of 0.5 mL MMR vaccine into the largest warts every 3 weeks. This protocol was adapted from Sharma and Agarwal, due to the similarity in the type of warts treated and the highest efficacy reported in their study compared to others. […] Successful intralesional antigen immunotherapy usually requires a strong host CMI. […] Although the previous vaccination status was not confirmed, evidence showed that the patient was not previously sensitized to MMR.

• #63 Genital Warts in Pregnancy

  https://www.healthline.com/health/pregnancy/infections-prevention-genital-warts

  Genital warts are caused by certain strains of the human papillomavirus (HPV). HPV is the most common of all STIs. Not all HPV infections cause genital warts, though. Some strains cause warts, while others can cause cancer in both men and women. […] The strains of HPV that cause genital warts haven’t been shown to increase the risk of miscarriage or problems with delivery. […] There are now HPV vaccines available for most of the strains of HPV that cause genital warts and cancer. These vaccines are most effective when administered before a person becomes sexually active and are recommended for both boys and girls. […] Very rarely, genital warts may be passed on to your baby. In these cases, your infant will usually develop warts in their mouth or throat several weeks after birth.

• #64 Genital Warts (HPV) (for Teens) | Nemours KidsHealth

  https://kidshealth.org/en/teens/std-warts.html

  Genital warts and other types of HPV can be prevented by a vaccine. The HPV vaccine series is recommended for all kids when they’re 9-11 years old. Teens and adults (up to age 45) also can get the vaccine. Even if someone already has had one type of HPV infection, the HPV vaccine can protect against other types of HPV.

• #65 The Effectiveness of Genital Wart Treatments – Journal of Urological Surgery

  https://jurolsurgery.org/articles/the-effectiveness-of-genital-wart-treatments/doi/jus.galenos.2023.2023-6-8

  Podophyllotoxin inhibits the proliferation of human skin keratinocytes by its antimitotic effect and cures genital HPV by inhibiting the proliferation of HPV-infected cells and destroying infected tissue. […] Imiquimod induces several proinflammatory cytokines including interferon alpha, interleukin 1,6,8,12, tumor necrosis factor alpha, and other cellular proteins. It also induces the production of monocytes and macrophages. Imiquimod has antiviral and antitumor effects by enhancing the immune system without tissue destruction. […] Ingenol tebutate stimulates the inflammatory response and neutrophil infiltration and by this way stimulates cell death in proliferating keratinocytes. […] Retinoids have effects on epithelial differentiation and proliferation and may also have an immunomodulatory inhibitory effect on HPV replication.

• #66 The Effectiveness of Genital Wart Treatments – Journal of Urological Surgery

  https://jurolsurgery.org/articles/the-effectiveness-of-genital-wart-treatments/doi/jus.galenos.2023.2023-6-8

  Podophyllotoxin inhibits the proliferation of human skin keratinocytes by its antimitotic effect and cures genital HPV by inhibiting the proliferation of HPV-infected cells and destroying infected tissue. […] Imiquimod induces several proinflammatory cytokines including interferon alpha, interleukin 1,6,8,12, tumor necrosis factor alpha, and other cellular proteins. It also induces the production of monocytes and macrophages. Imiquimod has antiviral and antitumor effects by enhancing the immune system without tissue destruction. […] Ingenol tebutate stimulates the inflammatory response and neutrophil infiltration and by this way stimulates cell death in proliferating keratinocytes. […] Retinoids have effects on epithelial differentiation and proliferation and may also have an immunomodulatory inhibitory effect on HPV replication.

• #67 Approaches to Treatment: External Genital Warts (Slide with Transcript)

  https://www.medscape.org/viewarticle/567995

  The 2 most common provider-applied are the trichloroacetic acid (TCA) and cryosurgery. Those are both 60% to 70% effective in eliminating the lesion(s) treated. But unfortunately recurrence rates can be anywhere from 20% to 40%. […] It can be. Imiquimod — trade name Aldara — is an immune-enhancer. It’s a 5% cream that’s applied at bedtime, generally 3 times a week. It actually allows chemical signals to be sent from the cells alerting the body’s immune system. […] These chemical signals basically alert the immune system so that the monocytes and the macrophages actually build up immunity to the HPV types, even though they have not come in contact with them. […] The study found clearly that the best benefit in terms of cost and reduced office visits for recurrent patients was to go right to [imiquimod], with the hope that it would enhance immunogenicity for the patient’s immune system to clear the lesions.

• #68 Human Papillomavirus Infection: Management and Treatment | IntechOpen

  https://www.intechopen.com/chapters/72773

  The intact immune system plays the most important role for preventing HPV infection. This can be seen in patients with primary immunodeficiency or in immunosuppressed patients. […] HPV-induced warts are the most common skin disorder in organ transplant recipients. […] The goals of wart treatment are to resolve all or a maximum number of warts, make it painless, need only one or a part of a wart treated, only need minimum number of treatments, leave no scar, offer lifetime HPV immunity and be easily available for all patients. […] Cryotherapy may have an effect on wart clearance either by simple necrotic destruction of HPV-infected keratinocytes or possibly by inducing local inflammation conducive to the development of an effective cell-mediated response. […] Liquid nitrogen can easily be stored and used by simple equipment in clinic-based practice.

• #69 Destructive therapies for cutaneous warts: A review of the evidence

  https://www1.racgp.org.au/ajgp/2022/october/destructive-therapies-for-cutaneous-warts

  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.

• #70 Human Papillomavirus Infection: Management and Treatment | IntechOpen

  https://www.intechopen.com/chapters/72773

  The overall cure rate for warts with radiosurgery ranges between 33 and 80% depending on the number of sittings and the type of warts. […] Interferon has been shown to be active against HPV both in vitro and in vivo, to protect murine cells against infection with bovine papillomaviruses and to eliminate extrachromosomal viral DNA from infected cells.

• #71 The Effectiveness of Genital Wart Treatments – Journal of Urological Surgery

  https://jurolsurgery.org/articles/the-effectiveness-of-genital-wart-treatments/doi/jus.galenos.2023.2023-6-8

  Podophyllotoxin inhibits the proliferation of human skin keratinocytes by its antimitotic effect and cures genital HPV by inhibiting the proliferation of HPV-infected cells and destroying infected tissue. […] Imiquimod induces several proinflammatory cytokines including interferon alpha, interleukin 1,6,8,12, tumor necrosis factor alpha, and other cellular proteins. It also induces the production of monocytes and macrophages. Imiquimod has antiviral and antitumor effects by enhancing the immune system without tissue destruction. […] Ingenol tebutate stimulates the inflammatory response and neutrophil infiltration and by this way stimulates cell death in proliferating keratinocytes. […] Retinoids have effects on epithelial differentiation and proliferation and may also have an immunomodulatory inhibitory effect on HPV replication.

• #72 The Effectiveness of Genital Wart Treatments – Journal of Urological Surgery

  https://jurolsurgery.org/articles/the-effectiveness-of-genital-wart-treatments/doi/jus.galenos.2023.2023-6-8

  Podophyllotoxin inhibits the proliferation of human skin keratinocytes by its antimitotic effect and cures genital HPV by inhibiting the proliferation of HPV-infected cells and destroying infected tissue. […] Imiquimod induces several proinflammatory cytokines including interferon alpha, interleukin 1,6,8,12, tumor necrosis factor alpha, and other cellular proteins. It also induces the production of monocytes and macrophages. Imiquimod has antiviral and antitumor effects by enhancing the immune system without tissue destruction. […] Ingenol tebutate stimulates the inflammatory response and neutrophil infiltration and by this way stimulates cell death in proliferating keratinocytes. […] Retinoids have effects on epithelial differentiation and proliferation and may also have an immunomodulatory inhibitory effect on HPV replication.

• #73 The Effectiveness of Genital Wart Treatments – Journal of Urological Surgery

  https://jurolsurgery.org/articles/the-effectiveness-of-genital-wart-treatments/doi/jus.galenos.2023.2023-6-8

  Human papillomaviruses (HPV) are a family of DNA viruses that infect the epithelium. They cause benign proliferative lesions called anogenital warts. HPV infection is common in men and women and is the most common sexually transmitted infection. HPV infection can cause cervical, penile, anal, vaginal, vulvar and oropharyngeal cancers. Genital warts adversely affect the quality of life. It may cause anxiety, guilt, anger, and loss of self-esteem and may cause anxiety about the cancer risk. […] The most common HPV types seen in angenital verruca are HPV types 6 and 11. After HPV transmission, clinical presentation of symptoms is nearly 11-12 months among males and 5-6 months among females. HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59 are carcinogenic. […] Genital wart treatments are generally painful, prolonged, hard for the patient to apply, and unfortunately often recurrence of the lesions seen after treatment. Treatments generally depend on the physical destruction of the lesion because this recurrence can be easily seen. A treatment that has antiviral effects on human papillomavirus would give more success and lower recurrence rates.

• #74 HPV and Genital Warts

  https://practicaldermatology.com/topics/general-topics/hpv-and-genital-warts/20756/

  Human papillomavirus (HPV) is the most common sexually transmitted disease (STD) worldwide. […] There are approximately 100 types of HPV, about 40 of which affect the anogenital area, causing conditions such as genital warts. […] The fluidity of HPVs natural history ranges from successful elimination by the bodys own immune system, to invisible and asymptomatic infection, to infection that becomes symptomatic weeks or even years after initial infection. […] The mechanism of action is not entirely understood, but it may relate to induction of infected cellular apoptosis, immune upregulation and/or a direct antiviral effect. […] SB206 is an investigational topical gel that uses a nitric oxide mechanism of action inside a carrier molecule, releasing the gas and destroying the wart, presumably by damaging or killing the causative virus.

• #75 Condyloma Acuminatum (Genital Warts): Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/781735-overview

  Condyloma acuminatum (also known as genital warts or anogenital warts) refers to an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 180 types of double-stranded HPV papovavirus have been isolated to date. Many of these have been related directly to an increased neoplastic risk in men and women. […] Approximately 90% of condylomata acuminata are related to HPV types 6 and 11. These 2 types are the least likely to have a neoplastic potential. Risk for neoplastic conversion has been determined to be moderate (types 33, 35, 39, 40, 43, 45, 51-56, 58) or high (types 16, 18), with many other isolated types. […] Cells of the basal layer of the epidermis are invaded by human papillomavirus (HPV). These penetrate through skin and cause mucosal microabrasions. A latent viral phase begins with no signs or symptoms and can last from a month to several years. Following latency, production of viral DNA, capsids, and particles begins. Host cells become infected and develop the morphologic atypical koilocytosis of condyloma acuminatum. […] Multiple simultaneous lesions are common and may involve subclinical states as well-differentiated anatomic sites. Subclinical infections have been established to carry both an infectious and oncogenic potential.

• #76 Core Concepts – Human Papillomavirus Infection – Self-Study Lessons – National STD Curriculum

  https://www.std.uw.edu/go/comprehensive-study/hpv

  Transmission of genital HPV is predominantly associated with sexual activity that results in friction-induced microabrasions during skin-to-skin contact. The transmission rate of HPV between sex partners is high, and transmission often occurs from persons with HPV who are asymptomatic or have subclinical infection. Consistent and correct use of condoms reduces the risk of genital HPV acquisition or transmission, thereby reducing the risk for HPV-associated diseases. Condom use, however, does not entirely prevent transmission of HPV, since exposure to HPV can occur in areas that are not fully covered or protected by a condom. Treatment of warts or cervical cellular abnormalities will reduce, but not eliminate, the risk of transmission. […] Available data, primarily from cervical HPV natural history, suggest that more than 90% of individuals with genital HPV infections are asymptomatic and clear the infection within 3 years. The viral clearance can entail complete elimination of HPV from the tissues or cell-mediated immune suppression of the HPV to such a low level that HPV DNA levels are undetectable using sensitive HPV DNA tests (referred to as viral latency).

• #77 How Long Do Genital Warts Last?

  https://www.healthline.com/health/healthy-sex/how-long-do-genital-warts-last

  Genital warts are cauliflower-like growths caused by certain types of the human papillomavirus (HPV). They may clear away on their own or with treatment. But, HPV isn’t always curable, so warts may reappear. […] Genital warts are caused by certain types of the human papillomavirus (HPV), which is the most common viral sexually transmitted disease in the United States. […] That’s because genital warts are only a symptom of HPV, which may become a chronic, lifelong infection for some. […] Some strains are high risk and associated with later formation of squamous cell carcinoma (cancer), and you may not even know if you have a high-risk HPV strain until precancerous or cancerous lesions form. […] HPV symptoms take a while to show, so warts may not appear until weeks or months after infection. In some cases, genital warts can take years to develop.

• #78 Genital Warts – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK441884/

  Genital warts (condyloma acuminatum) are a sexually transmitted infection caused by the human papillomavirus (HPV) types 6 and 11. These are spread by skin-to-skin contact, usually during sex. […] HPV is transmitted primarily through penetrative sex. While HPV also can be transmitted via non-penetrative sexual activity, it is less common. […] HPV infection appears to be the cause of most cases of anal cancer (about 90%) and virtually all cases of cervical cancer in women, with HPV type 16 accounting for about 50% of these. […] Although treatments can remove warts, they do not remove HPV. Warts may sometimes spontaneously regress. Traditional theories postulate that the virus remains in the body for a lifetime. However, it is now believed that the virus may be either cleared or suppressed to levels below what polymerase chain reaction (PCR) tests can measure.

• #79 Patient education: Genital warts in women (Beyond the Basics) – UpToDate

  https://www.uptodate.com/contents/genital-warts-in-women-beyond-the-basics/print

  Warts may appear weeks to a year or more after being exposed to the virus; it is not usually possible to know when or how you became infected. […] Even with treatment, it is possible that the warts will come back within a few weeks or months. This is because treating the warts does not necessarily get rid of all of the virus (HPV) causing the warts. Some cells in the normal-appearing genital skin and vagina may remain infected with HPV. There is currently no treatment that will permanently get rid of HPV in all infected cells, but most people will clear the virus and the warts with their own immune systems within two years. […] Getting rid of warts does not necessarily mean that the virus causing the warts (HPV) is gone. If warts come back, they usually do so within three to six months of treatment. This problem is more common in people with a weakened immune system (such as diabetes, HIV, or certain medications).

• #80 Genital Warts (HPV) (for Teens) | Nemours KidsHealth

  https://kidshealth.org/en/teens/std-warts.html

  Genital warts and other types of HPV can be prevented by a vaccine. The HPV vaccine series is recommended for all kids when they’re 9-11 years old. Teens and adults (up to age 45) also can get the vaccine. Even if someone already has had one type of HPV infection, the HPV vaccine can protect against other types of HPV.

• #81 The Effectiveness of Genital Wart Treatments – Journal of Urological Surgery

  https://jurolsurgery.org/articles/the-effectiveness-of-genital-wart-treatments/doi/jus.galenos.2023.2023-6-8

  Human papillomaviruses (HPV) are a family of DNA viruses that infect the epithelium. They cause benign proliferative lesions called anogenital warts. HPV infection is common in men and women and is the most common sexually transmitted infection. HPV infection can cause cervical, penile, anal, vaginal, vulvar and oropharyngeal cancers. Genital warts adversely affect the quality of life. It may cause anxiety, guilt, anger, and loss of self-esteem and may cause anxiety about the cancer risk. […] The most common HPV types seen in angenital verruca are HPV types 6 and 11. After HPV transmission, clinical presentation of symptoms is nearly 11-12 months among males and 5-6 months among females. HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59 are carcinogenic. […] Genital wart treatments are generally painful, prolonged, hard for the patient to apply, and unfortunately often recurrence of the lesions seen after treatment. Treatments generally depend on the physical destruction of the lesion because this recurrence can be easily seen. A treatment that has antiviral effects on human papillomavirus would give more success and lower recurrence rates.

• #82 HPV and Genital Warts

  https://practicaldermatology.com/topics/general-topics/hpv-and-genital-warts/20756/

  Human papillomavirus (HPV) is the most common sexually transmitted disease (STD) worldwide. […] There are approximately 100 types of HPV, about 40 of which affect the anogenital area, causing conditions such as genital warts. […] The fluidity of HPVs natural history ranges from successful elimination by the bodys own immune system, to invisible and asymptomatic infection, to infection that becomes symptomatic weeks or even years after initial infection. […] The mechanism of action is not entirely understood, but it may relate to induction of infected cellular apoptosis, immune upregulation and/or a direct antiviral effect. […] SB206 is an investigational topical gel that uses a nitric oxide mechanism of action inside a carrier molecule, releasing the gas and destroying the wart, presumably by damaging or killing the causative virus.

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