Virion Morphology and Genetic Organization
Members of the Papillomaviridae family are non-enveloped viruses, meaning they completely lack an outer lipid envelope (supercapsid). The virion is 52–55 nm in size and is protected by an icosahedral capsid. This protein shell consists of 72 pentamers formed by two capsid proteins encoded by late genes—L1 and L2.
Inside the capsid lies the genetic material: a double-stranded circular DNA molecule. It is associated with cellular histone proteins, forming a dense nucleoprotein complex.
The viral genome is divided into two groups:
- Late genes (late, L1 and L2): responsible exclusively for the synthesis of structural capsid elements.
- Early genes (early, E1–E8): control replication. A special place among them is occupied by the E6 and E7 genes. These are key markers of oncogenicity that are consistently found in cells that have undergone tumor transformation induced by the virus.
Life Cycle and Dependence on Cell Differentiation
Infection occurs via contact through microtraumas (contact with the basal layers of the epithelium), sexual intercourse, and intranatally (vertical transmission to the newborn during delivery).
HPV replication has a unique feature: it is impossible in standard cell cultures because it is strictly dependent on the processes of epithelial differentiation.
Stages of Replication:
- Adsorption and penetration occur in the basal layer of the epithelium. Here, the virus sheds its coat (uncoating) and remains in a latent state as an extrachromosomal plasmid. Transcription of early genes and DNA replication begin.
- As the infected cell moves into the parabasal (differentiating) layers, intensive viral multiplication is triggered.
- When the cell reaches the superficial squamous layer, new virions assemble in its nucleus. They leave the host upon nuclear breakdown and cell lysis.
Important nuance: during malignant transformation (malignization), the viral genome loses its plasmid form and irreversibly integrates into the host cell chromosomes.
Classification of Types and Clinical Manifestations
The highest incidence is recorded in the 18–30 age group. Papillomavirus infection is often coinfected with other STIs (chlamydia, genital herpes, gonorrhea, syphilis). Viruses are conventionally divided into mucosal and cutaneous types.
Based on the degree of malignant risk, genital strains are classified into:
- Low-risk (types 6, 11): cause anogenital warts (condylomata acuminata) appearing as cauliflower-like moist growths.
- High-risk (key types 16, 18, as well as 31, 33, 35, 45, 51, 52, 58): capable of inducing epithelial proliferation and cervical cancer.
Cutaneous lesions include common warts (types 1, 2, 4, 7 on extremities), plane warts (types 3, 10 in children on the face and hands), and painful, inward-growing plantar warts. Non-melanoma skin cancer is associated with types 5 and 8, while foci of squamous cell carcinoma most frequently harbor types 5, 8, and 16.
A separate threat is recurrent respiratory papillomatosis, in which benign tumor-like papillomas proliferate from the nose to the lungs, creating a risk of airway obstruction.
Principles of Diagnosis and Prevention
The material for microbiological study consists of keratinized cells from papillomas. Virological culture is not used, and serology is uninformative due to low antibody titers. The leading diagnostic methods are PCR and DNA molecular hybridization.
Specific antiviral drugs have not been developed. Treatment relies on physical or chemical removal of papillomas (cryodestruction, laser therapy, keratolytics) and administration of immunomodulators (interferons, imiquimod). Most common, flat, and genital warts undergo spontaneous regression without treatment within two years.
Reliable protection against oncogenic strains is vaccination. The vaccine consists of a mixture of structural proteins of types 6, 11, 16, and 18 (lacking viral DNA) and is intended for children aged 9–17, as well as young women aged 18–26 to protect against cervical cancer.