Introduction
Human papillomavirus (HPV) is a non-enveloped double-stranded circular DNA virus in the
Papillomaviridae family. There are over 150 types of HPV, 40 of which affect the anogenital
area and 15 of which are oncogenic.1
Important low-risk types include HPV-6 and HPV-11, which cause genital warts, the most
common viral sexually transmitted infection (STI).1
Worldwide, high-risk HPV causes around 5% of cancers, affecting the cervix, vulva, vagina,
anus, penis, head, and neck.2
This article will focus on the mechanism of HPV infection, and the pathophysiology, clinical
features, and management of genital warts. For more information on the closely linked cervical
cancer and anal cancer, please read their respective articles.
Epidemiology
HPV is extremely prevalent. Nearly all sexually active men and women acquire HPV infection
during their lifetime, and almost 40% of women are infected with HPV within the first two years
of sexual activity.3,4
All HPV types can cause proliferative lesions, however, the most prevalent types are classified
as high-risk if they can cause malignant neoplasms, and low risk if they can cause benign
lesions, such as genital warts.
Low-risk HPV-6 and HPV-11 are the most common causes of genital warts, which is the most
common viral STI diagnosed in sexual health clinics in the UK and worldwide. In 2019, there
were 50,700 diagnoses of the first episode of genital warts. This was almost halved to 27, 473 in
2020; this decline is thought to be related to the expanded HPV vaccine programme and the
reduction in face-to-face consultations owing to the COVID-19 pandemic.5
High-risk HPV causes around 5% of cancers worldwide and the prevalence of high-risk HPV in
the UK is 16%, including the most common type- HPV-16 (12%).6 Through the mechanisms
described below, HPV can cause cancer of the cervix, vulva, vagina, anus, penis, head, and
neck (Figure 1).
, Figure 1. Number of new diagnoses (blue) and
mortality (red) for HPV-related cancers for men (right) and women (left). Based upon data
collected in the United Kingdom and Northern Ireland in 2019.2
You might also be interested in our medical flashcard collection which contains over 1000
flashcards that cover key medical topics.
Aetiology
HPV belongs to the Papillomaviridae family and includes over 200 different types which are
grouped according to their genome. Although all HPV types can cause proliferative lesions,
the most prevalent types are classified as high-risk or low-risk according to their risk of causing
malignant neoplasms or benign lesions, such as genital warts.
Important high-risk types include HPV-16 and HPV-18, which contribute to over 70% of cervical
cancer, and 31, 33, 35, 45, 52 and 58, which account for an additional 20% of cervical cancers.
Low-risk HPV capable of causing genital warts include HPV-6 and HPV-11.1
HPV life cycle
Microtrauma to the epithelial cells of the skin, oral and genital mucosa provides the virus access
to basal keratinocytes. HPV uses its L1 and L2 capsid proteins to bind and enter the cell via
endocytosis.1
The undifferentiated basal layer acts as a reservoir, proliferating symmetrically to form more
basal cells, wherein HPV establishes a persistent infection, or asymmetrically, whereby one
daughter cell moves up through epithelium. As these infected basal cells differentiate into
epithelial cells, the virus begins expressing its early (E) genes, allowing it to replicate and
produce new virions to be released from the differentiated epithelial cell surface. 7
The majority (70-90%) of HPV infections are asymptomatic and are cleared within 12-14
months by the immune system via a Th1 pro-inflammatory and cell-mediated response.1
Human papillomavirus (HPV) is a non-enveloped double-stranded circular DNA virus in the
Papillomaviridae family. There are over 150 types of HPV, 40 of which affect the anogenital
area and 15 of which are oncogenic.1
Important low-risk types include HPV-6 and HPV-11, which cause genital warts, the most
common viral sexually transmitted infection (STI).1
Worldwide, high-risk HPV causes around 5% of cancers, affecting the cervix, vulva, vagina,
anus, penis, head, and neck.2
This article will focus on the mechanism of HPV infection, and the pathophysiology, clinical
features, and management of genital warts. For more information on the closely linked cervical
cancer and anal cancer, please read their respective articles.
Epidemiology
HPV is extremely prevalent. Nearly all sexually active men and women acquire HPV infection
during their lifetime, and almost 40% of women are infected with HPV within the first two years
of sexual activity.3,4
All HPV types can cause proliferative lesions, however, the most prevalent types are classified
as high-risk if they can cause malignant neoplasms, and low risk if they can cause benign
lesions, such as genital warts.
Low-risk HPV-6 and HPV-11 are the most common causes of genital warts, which is the most
common viral STI diagnosed in sexual health clinics in the UK and worldwide. In 2019, there
were 50,700 diagnoses of the first episode of genital warts. This was almost halved to 27, 473 in
2020; this decline is thought to be related to the expanded HPV vaccine programme and the
reduction in face-to-face consultations owing to the COVID-19 pandemic.5
High-risk HPV causes around 5% of cancers worldwide and the prevalence of high-risk HPV in
the UK is 16%, including the most common type- HPV-16 (12%).6 Through the mechanisms
described below, HPV can cause cancer of the cervix, vulva, vagina, anus, penis, head, and
neck (Figure 1).
, Figure 1. Number of new diagnoses (blue) and
mortality (red) for HPV-related cancers for men (right) and women (left). Based upon data
collected in the United Kingdom and Northern Ireland in 2019.2
You might also be interested in our medical flashcard collection which contains over 1000
flashcards that cover key medical topics.
Aetiology
HPV belongs to the Papillomaviridae family and includes over 200 different types which are
grouped according to their genome. Although all HPV types can cause proliferative lesions,
the most prevalent types are classified as high-risk or low-risk according to their risk of causing
malignant neoplasms or benign lesions, such as genital warts.
Important high-risk types include HPV-16 and HPV-18, which contribute to over 70% of cervical
cancer, and 31, 33, 35, 45, 52 and 58, which account for an additional 20% of cervical cancers.
Low-risk HPV capable of causing genital warts include HPV-6 and HPV-11.1
HPV life cycle
Microtrauma to the epithelial cells of the skin, oral and genital mucosa provides the virus access
to basal keratinocytes. HPV uses its L1 and L2 capsid proteins to bind and enter the cell via
endocytosis.1
The undifferentiated basal layer acts as a reservoir, proliferating symmetrically to form more
basal cells, wherein HPV establishes a persistent infection, or asymmetrically, whereby one
daughter cell moves up through epithelium. As these infected basal cells differentiate into
epithelial cells, the virus begins expressing its early (E) genes, allowing it to replicate and
produce new virions to be released from the differentiated epithelial cell surface. 7
The majority (70-90%) of HPV infections are asymptomatic and are cleared within 12-14
months by the immune system via a Th1 pro-inflammatory and cell-mediated response.1
