How does HPV cause cervical cancer?
The human papillomavirus (HPV) is the main cause of cervical cancer worldwide, killing hundreds of thousands of people every year. Here’s how the virus triggers cancer.
- 7 February 2024
- 3 min read
- by Priya Joi
The human papillomavirus (HPV) is one of the most common sexually transmitted infections (STIs) globally. By the age of 45, around four in five men and women will have had at least one HPV infection. In nine out of ten people the body naturally clears the virus, but for some people, HPV can cause cancers such as cervical cancer.
When HPV hasn't been cleared by the immune system, it infects the skin cells in the cervix, causing them to become abnormal: a process called cervical dysplasia. These changes in cervical skin cells are what health professionals look for when they do a smear test, where cells are scraped from the cervix and studied.
When HPV hasn't been cleared by the immune system, it infects the skin cells in the cervix, causing them to become abnormal: a process called cervical dysplasia.
If they look abnormal, the severity is graded starting at CIN1 (also called mild dysplasia), in which not much of the tissue looks abnormal. Most often these cells will change back to normal cells. In CIN2 or CIN3 (also called moderate/severe dysplasia) more of the tissue looks abnormal. In this case, there is higher risk that the cells can become cancerous and therefore they will need to be watched closely or removed.
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So how does HPV cause cancer? It starts by disrupting the way healthy cells function. In our bodies, human cells eventually self-destruct, which is a crucial process in normal cell turnover, physical development and functioning of the immune system. This is called apoptosis (from the Greek, meaning "to fall away") and is a tidying process in which the cell self-destructs and is cleared away by the immune system. For a cell to become cancerous, it has to ignore the signals telling it to self-destruct – effectively they become immortal, and never stop replicating.
HPV does this by integrating its genetic code, or genome, into the genome of cervical cells. The cervix is a cylinder that connects the uterus to the vagina. The ectocervix is the outer part of the cervix that can be seen during a gynaecologic exam. The ectocervix is covered with thin, flat cells called squamous cells. The endocervix is the inner part of the cervix, covered with glandular cells. These two types of cells meet at a place called the transformation zone, which is where cervical cancer tends to start.
Next it sets about making these cells cancerous.
Two HPV proteins, E6 and E7, are the main drivers of cervical cancer development. The first of these, the E6 protein, binds to a protein in our cervical cells that is responsible for flagging which cell proteins should be destroyed. Together they then bind to another protein that stops cancerous tumours from forming. This means that when the body decides to destroy the invasive HPV protein, it takes this crucial tumour suppressing protein with it, making it far more likely that cancer can develop.
Meanwhile, HPV's E7 protein interacts with a different tumour-suppressing protein to inhibit its activity, again increasing the chances of cells becoming cancerous.
The good news is that there is an HPV vaccine that is 97% effective, which is being rolled out across the world. The key now is getting the vaccine to everyone who needs it.
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