What is the Difference Between HPV 16 and 18?

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HPV 16 and 18 are two high-risk types of human papillomavirus, which significantly increase the risk of cervical, vaginal, and vulvar cancer in women, as well as penile cancer in men. They are responsible for approximately 70% of all HPV-related cervical cancers and head and neck cancers. Some differences between HPV 16 and 18 include:

  1. Genome Integration: HPV 18 is more likely to integrate the viral genome into the host genome compared to HPV 16.
  2. Cancer Histological Types: Most HPV 16-positive cancers are squamous cell carcinomas, while around 50% of HPV 18-positive cancers are adenocarcinomas.
  3. Prevalence: HPV 16 is more prevalent than HPV 18, with a prevalence of 48% and 16% respectively in one study.
  4. Age Distribution: The age distribution of HPV 18-positive cases tends to be higher compared to HPV 16-positive cases.

Both HPV 16 and 18 are associated with the development of cervical intraepithelial neoplasia (CIN) and various types of cancer. The progression of HPV 16- or 18-infected cervical epithelium to CIN3 is much higher compared to other high-risk HPV types.

Comparative Table: HPV 16 vs 18

The main difference between HPV 16 and HPV 18 lies in their genotype and the type of cancer they are associated with. Here is a table comparing the two:

Feature HPV 16 HPV 18
Genotype α-9 α-7
Cancer Type High Grade Cervical Cancer Cervical Cancer
Replicative Activity High Lower
E2 Binding Sites Variation Found Found
Region of Interest Wide range Narrower range

Both HPV 16 and HPV 18 are associated with cervical cancer, but HPV 16 is more commonly found in high-grade cervical cancer, while HPV 18 is associated with the development of cytology grade. HPV 16 and its genus α-9 are known for their high replicative activity and are found in a wide range of cervical cancers. In contrast, HPV 18 and its genus α-7 usually show lower replicative activity and are associated with a narrower range of cytology grades.

One of the biggest differences between HPV 16 and HPV 18 might involve their integration into human cells. Variation in the E2 binding sites of HPV 16 and HPV 18 has been found, which may lead to a change in the replication process and the modulation of carcinogenicity. However, the specific difference in carcinogenicity modulation between these two types is not yet clear.