Despite the successful advent of prophylactic vaccines, Human Papilloma Virus (HPV) burden is still very high, accounting for more than 600,000 new cancer cases worldwide and about 900,000 new genital wart cases per year just in Europe.
HPVs are small, double-stranded DNA viruses which infect keratinocytes of the mucosal and cutaneous epithelia. Mucosal alpha-HPVs can be classified as low-risk (LR) and high-risk (HR) viruses on the basis of their tumorigenic potential. LR-HPVs, such as HPV-6 and -11, are associated with a spectrum of genital warts and oral papillomas that cause significant morbidity and difficulty in treatment. On the other end, infection with HR-HPVs is the primary cause of cervical cancer and recent evidence has now established a clear role for the virus also in oropharyngeal, anal, penile, vaginal, and vulvar cancers. In addition, epidemiological and biological data suggest that cutaneous beta-HPVs play a fundamental role in the initiation of UV-induced non-melanoma skin cancer.
HPV-mediated disease progression is driven by the ability of viral proteins to dysregulate a number of keratinocyte functions that finally enable persistent infection and pathological transformation of infected cells. Importantly, HPVs also influence host keratinocytes interaction and crosstalk with the surrounding microenvironment (including stroma, fibroblasts, and immune system), crucially reprogramming non-infected cells to phenotypes able to sustain the viral cycle. However, only a minority of HPV infections become persistent and lead to health problems, indicating that other, still not fully elucidated events, are needed. Hence, deeper comprehension of the host cellular and molecular mechanisms supporting HPV virulence is of paramount importance.
The aim of this Topic is therefore to collect relevant evidence that will improve our current understanding of how LR and HR-HPVs manipulate cellular pathways in host keratinocytes during each step of their viral cycle (infection, survival, persistence, malignant transformation) and their interaction with adjacent non-infected cells. To this end, we are looking for articles (Original Research, Reviews, Mini-Reviews, Perspectives, Brief Research Reports, oriented to basic and translational biology), covering various aspects in the cellular and molecular biology of HPV-related diseases that shed lights in potential pathobiological mechanisms.
Despite the successful advent of prophylactic vaccines, Human Papilloma Virus (HPV) burden is still very high, accounting for more than 600,000 new cancer cases worldwide and about 900,000 new genital wart cases per year just in Europe.
HPVs are small, double-stranded DNA viruses which infect keratinocytes of the mucosal and cutaneous epithelia. Mucosal alpha-HPVs can be classified as low-risk (LR) and high-risk (HR) viruses on the basis of their tumorigenic potential. LR-HPVs, such as HPV-6 and -11, are associated with a spectrum of genital warts and oral papillomas that cause significant morbidity and difficulty in treatment. On the other end, infection with HR-HPVs is the primary cause of cervical cancer and recent evidence has now established a clear role for the virus also in oropharyngeal, anal, penile, vaginal, and vulvar cancers. In addition, epidemiological and biological data suggest that cutaneous beta-HPVs play a fundamental role in the initiation of UV-induced non-melanoma skin cancer.
HPV-mediated disease progression is driven by the ability of viral proteins to dysregulate a number of keratinocyte functions that finally enable persistent infection and pathological transformation of infected cells. Importantly, HPVs also influence host keratinocytes interaction and crosstalk with the surrounding microenvironment (including stroma, fibroblasts, and immune system), crucially reprogramming non-infected cells to phenotypes able to sustain the viral cycle. However, only a minority of HPV infections become persistent and lead to health problems, indicating that other, still not fully elucidated events, are needed. Hence, deeper comprehension of the host cellular and molecular mechanisms supporting HPV virulence is of paramount importance.
The aim of this Topic is therefore to collect relevant evidence that will improve our current understanding of how LR and HR-HPVs manipulate cellular pathways in host keratinocytes during each step of their viral cycle (infection, survival, persistence, malignant transformation) and their interaction with adjacent non-infected cells. To this end, we are looking for articles (Original Research, Reviews, Mini-Reviews, Perspectives, Brief Research Reports, oriented to basic and translational biology), covering various aspects in the cellular and molecular biology of HPV-related diseases that shed lights in potential pathobiological mechanisms.
