Introduction

Epstein–Barr virus, hepatitis B and C viruses, human papillomavirus, human T-cell lymphotropic virus, Kaposi's associated sarcoma virus, and Merkel cell polyomavirus are all examples of human oncogenic viruses. HPVs infect the skin and mucosa, taking advantage of the highly organized process of tissue renewal in stratified squamous epithelia. Through a micro-abrasion, the virus infects cells in the lower, basal layer of the epithelium and establishes a long-term; Papillomaviruses are non-enveloped viruses with 55-nm icosahedral capsids and 8,000-bp double-stranded DNA genomes. They are found all over the animal kingdom, specifically infecting squamous epithelia and causing wart formation. Warts had an infectious etiology for a long time, which was eventually proven in the nineteenth century." After a short time, a wart appeared on the injured area, which was repeatedly destroyed but reappeared until the nail on the injured thumb was removed." Ullmann also observed a similar unintentional transmission of laryngeal papillomas and performed self-inoculation experiments with laryngeal papilloma extracts applied to scarified sites on his forearm, yielding warts after a 9-month latency period. Similar inoculation experiments with extracts derived from common hand warts, as well as serial inoculation experiments with human subjects, were carried out.

Description

For a long time, genital warts and cervical cancer were thought to be manifestations of then-common venereal diseases like syphilis and gonorrhea. This theory was challenged in a heinous paper published in 1917. To inoculate places on the author's body, extracts from a penile condyloma were taken from a young medical student who had no other overt indications of sexual illness and his assistant's forearms, as well as the genital mucosa of a "virgo intacta." After 2.5 months, the unfortunate female subject developed genital condyloma, and two male probands developed flat warts on their forearms. These and other studies revealed that genital warts are distinct disease entities caused by a communicable agent. Approximately 200 different HPVs have now been identified, and new types are being added to the list on a regular basis. These viruses are divided into two types: mucosal and cutaneous HPVs. Individual viruses within each of these HPV groups are classified as high risk or low risk based on their proclivity for malignant progression of the lesions they cause. Most HPVs are low risk and cause localized benign warts that do not progress to malignancy if left untreated.

Conclusion

The HPV replication cycle takes at least three weeks because the keratinocyte must go through the entire differentiation cycle. Infection with high-risk human papillomaviruses can cause pathological changes in infected tissues, such as the induction of cervical carcinoma. HPV infects dividing basal epithelial cells and inserts its dsDNA episomal genome into nuclei. An infected daughter cell begins the process of keratinocyte differentiation after basal cell division, triggering a tightly orchestrated pattern of viral gene expression to achieve a productive infection.