Papillomaviruses may be classified into distinct groups based on the host that they infect.

Structure:

Papillomaviruses are small (50-60 nm), nonenveloped, icosahedral DNA viruses that encode for up to 80 early and 2 late genes. The open reading frames (ORFs) of the virus genomes are designated E1 to E7 and L1 and L2, where “E” denotes early and “L” denotes late. L1 and L2 code for virus capsid proteins. The early genes are associated with functions cuh as viral replication and cellular transformation. Cook (US 6,602,697)

Human papillomaviruses (HPV)

HPV belongs to the papovavirus family have naked icosahedral symmetry and a double stranded small circular DNA genome. HPVs are a family of small DNA viruses with a pronounced tropism for epithelial cells. HPV are further classified into more than 70 types based on DNA sequence homology. Papillomavirus types appear to be type specific immunogens in that a neutralizing immunity to infection to one type of papillomavirus does not confer immunity agaisnt anotehr type of papillomavirus. Cook (US 6,602,697)

Transmission: HPV is transmitted through close direct, often sexual contact and replicates in the epithelium/mucosa. Infection of cells induces cell proliferation and warts. Diagnosis is via papanicolaou (PAP) smears (hybridization with strain specific DNA probes). 

Disease mechanism/pathology: Infection with HPV usually causes papillomatous hyperplasia (warts) but lesions cause by a subset of these viruses (e.g., HPV-16, -18, -31, or -33) have a propensity for maligant progression. Warts which are caused by HPV can be surgically removed or spontaneously regress. Laryngeal papillomas require surgery. Currently in Phase II clinical trials are recombinant papillomavirus structural (capsid) protein vaccines which successfully prevent cervical cancer.

During malignant progression, the HPV genome frequently integrates into the host DNA resulting in the expression of only two viral proteins, E6 and E7. E6 and E7 are viral proteins that interfere with the normal regulation of the cell cycle and apoptosis. During a normal cell cycle, the retinoblastoma protein (pRb) controls the activity of a transcription factor called E2F. When pRb is bound to E2F, progress thorugh the cell cycle is prevented. When cellular conditions are right for cell growth and division, pRb releases E2F, which then promotes cell cycle progression.

The viral E7 prtein binds to Rb, releasing E2F regardless of whether cell division should occur. This forces cell division when an infected cell is receiving signals to not divde. Fortunately, a mechanism exists to prevent this aberrant cell division. If levels of E2F become abnromally high as they do when E7 forces release of E2F from Rb, a host cell protein called p53 triggers apoptosis. However, the virus can overcome this mechanisms when the viral E6 prtoein binds and inactivates p53.

Detection: HPV can be detected by PAP smear which takes only minutes to do. It is recommended that all women, especially those between 35 and 64 be tested. If negative, it is recommended to do another PAP every 3 years. 

Prevention & Treatment: There is currently no known treatment which exists that can cure the virus. However, there are 2 vaccines:

1) Cervarix: prevents infection against the the 2 types of HPV which cuase the majority of cases of utirine cancer.

2) Gardasil: prevents infection against the 16 and 18 types of virus and also the 6 and 11 types which cause genital warts.