🦠 Cervical Dysplasia-to-Cancer Prevention Timeline Simulator

HPV Infection & Spontaneous Clearance

Nearly every sexually active adult acquires HPV at some point.

• ~80%: Lifetime HPV exposure (of sexually active adults)
• ~70%: Cleared within 1 year (by host immune response)
• ~90%: Cleared within 2 years (cumulative clearance rate)
• ~14: High-risk HPV types (linked to cervical cancer)

How HPV enters the epithelium

HPV infects basal cells through microabrasions in tissue.

The immune response

T-cells and local immunity clear most infections silently.

Roughly 9 in 10 HPV infections clear without ever causing dysplasia.

Why some infections persist

Viral immune-evasion proteins can suppress local clearance.

Persistent Infection Beyond Two Years

Persistence, not exposure, is the real driver of cancer risk.

• ~10%: Persist beyond 2 years (of initial infections)
• ~24: Median time to persistence (months post-infection)
• HPV-16: Dominant persistent type (highest oncogenic risk)
• 2×: Smoking risk multiplier (higher persistence odds)

Viral integration into the genome

HPV DNA can integrate into host chromosomes over time.

Oncoprotein expression

E6 and E7 proteins disable key tumor-suppressor pathways.

E6 degrades p53; E7 inactivates Rb — both drive unchecked cell division.

Cofactors that favor persistence

Smoking, immunosuppression, and coinfections raise risk.

CIN1–2 — Cervical Intraepithelial Neoplasia

Persistent HPV begins reshaping the cervical epithelium.

• ~60%: CIN1 spontaneous regression (resolve without treatment)
• ~40%: CIN2 spontaneous regression (within 2 years)
• ~11%: CIN1→CIN3 progression (over 2–4 years)
• Pap/HPV: Typical detection method (cytology screening)

CIN1 — mild dysplasia

Abnormal cells confined to the lower third of epithelium.

CIN2 — moderate dysplasia

Atypia extends into the lower two-thirds of tissue.

Many CIN1–2 lesions still regress on their own without treatment.

Why screening matters here

Routine cytology catches change before cancer develops.

CIN3 — Severe Dysplasia

CIN3 is the last reversible step before invasive disease.

• ~30%: CIN3 untreated → cancer (over 20–30 years)
• ~30%: CIN3 spontaneous regression (lower than CIN1–2)
• >90%: Treatment cure rate (with LEEP excision)
• 25–35: Median age at diagnosis (years)

Full-thickness atypia

Abnormal cells now span the entire epithelial layer.

The membrane still holds

Cells have not yet crossed the basement membrane.

CIN3 is highly treatable — this is the critical intervention window.

Why treatment is offered now

Excision at CIN3 prevents almost all future cancers.

Invasive Cervical Cancer

Without vaccination, screening, or treatment, cancer can follow.

• ~660K: Global cases per year (new diagnoses)
• 10–15: Typical latency from CIN3 (years untreated)
• >90%: 5-year survival, early stage (when caught early)
• ~90%: Deaths preventable by vaccine (of HPV-driven cases)

Basement membrane breach

Cells invade the stroma and gain access to vasculature.

Local and distant spread

Angiogenesis and lymphatic invasion enable metastasis.

This entire pathway is preventable — vaccination stops it at step one.

The prevention window

Vaccination plus screening can make this stage rare.