Virion morphology and genetic organization
Members of the Papillomaviridae family are non-enveloped viruses. This means they completely lack an outer lipid envelope (supercapsid). The virion is 52–55 nm in size and 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 (ring) DNA molecule. It does not exist independently, but is bound to cellular histone proteins, forming a dense nucleoprotein complex.
The genetic apparatus of the virus is divided into two groups:
- Late genes (late, L1 and L2): responsible exclusively for the synthesis of capsid structural elements.
- Early genes (early, E1–E8): control replication. A special place among them is occupied by E6 and E7 genes. These are key markers of oncogenicity, which are always detected in cells that have undergone tumor transformation induced by the virus.
Life cycle and cell differentiation dependence
Infection occurs via contact through microtraumas (upon contact with the basal layers of the epithelium), sexual contact, and also intranatally (vertical transmission to the newborn during childbirth).
HPV reproduction has a unique feature: it is impossible in standard cell cultures because it is strictly linked to epithelial differentiation processes.
Replication stages:
- Adsorption and penetration occur in the basal layer of the epithelium. Here the virus sheds its coat (uncoats) 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 suprabasal (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 destruction and cell lysis.
Important nuance: during malignant transformation (malignancy), the viral genome loses its plasmid form and irreversibly integrates into the host cell chromosomes.
Type classification and clinical manifestations
The highest incidence is recorded in the 18–30 age group. Papillomavirus infection is often combined with other STIs (chlamydia, genital herpes, gonorrhea, syphilis). Viruses are conventionally divided into mucosal and cutaneous types.
According to the degree of malignancy risk, genital strains are classified into:
- Low-oncogenic (types 6, 11): cause anogenital warts (condylomata acuminata) as moist growths resembling cauliflower.
- High-oncogenic (key types 16, 18, as well as 31, 33, 35, 45, 51, 52, 58): capable of inducing epithelial proliferation and cervical cancer.
Skin lesions include common warts (types 1, 2, 4, 7 on the 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, and types 5, 8, and 16 are most frequently detected in foci of squamous cell carcinoma.
A separate threat is recurrent respiratory papillomatosis, in which benign tumor-like papillomas grow from the nose to the lungs, creating a risk of obstruction.
Principles of diagnostics and prevention
Keratinized cells of papillomas serve as the material for microbiological study. The virological method is not used, and serology is uninformative due to low antibody titers. PCR and molecular DNA hybridization are the leading methods.
No specific antiviral drugs have been developed. Treatment is reduced to removing papillomas by physical or chemical methods (cryodestruction, laser, keratolytics) and prescribing immunomodulators (interferons, imiquimod). Most common, plane, and genital warts are capable of 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 (without viral DNA) and is intended for children aged 9–17, as well as young women aged 18–26 to protect against cervical cancer.
Briefly: answers to topical questions
What is the molecular mechanism of the oncogenic action of viral proteins E6 and E7?
The molecular mechanism of the oncogenic action of viral proteins E6 and E7 lies in the inactivation of cellular tumor suppressor proteins.
- p53 protein — normally stops the cell cycle for DNA repair upon damage or initiates apoptosis. Viral proteins block it, permitting the division of cells with a damaged genome.
- Rb protein (retinoblastoma) — controls cellular proliferation; its normal function is also disrupted by viral proteins.
Which human papillomavirus types cause recurrent respiratory papillomatosis?
Recurrent respiratory papillomatosis is caused by low-oncogenic-risk human papillomaviruses, which include types 6 and 11.
This disease is a benign tumor-like proliferation of papillomas in the respiratory tract (from the nasal cavity to the larynx and lungs), creating a risk of obstruction. The infection is usually transmitted from an infected mother during birth.
To remember the classification of genital HPV risk: lower-numbered types (6 and 11) cause only benign warts, while higher-numbered types (16 and 18) carry a high oncogenic risk.
Class and exam questions
Why is it impossible to culture HPV in laboratory conditions for diagnostics?
The virus does not replicate in standard cell cultures, as its replicative cycle strictly depends on the stages of natural maturation and differentiation of skin or mucosal epithelium.
In what form is the viral material located inside the host cell?
In the cells of the basal layer, the virus persists latently as an extrachromosomal plasmid. However, during the development of a malignant process (malignancy), the viral DNA integrates directly into the cell genome.
Which viral proteins are evidence of tumor transformation?
The products of early genes E6 and E7, which are constantly detected in transformed cells, serve as markers of oncogenicity.
What else to study on this topic
- Mechanisms of viral DNA integration into host cell chromosomes
- Molecular functions of E6 and E7 proteins in the process of malignancy
- Features of the comorbid course of HPV and other STIs (syphilis, chlamydia)
- Pathogenesis and complications of recurrent respiratory papillomatosis
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