The main viruses, the human papillomavirus (HPV), that cause cervical cancer evades its hosts' immune systems by using a protein that it produces.
Around 1,550 women are diagnosed with high-grade pre-malignant cervical cancer in New Zealand, and globally around half a million women are diagnosed with cervical cancer each year. In countries without organized screening programs, cervical cancer is a leading cause of cancer mortality in women.
‘Identifying the mechanisms behind the failure of T-cells to be activated to attack the virus may allow new therapies that enable the body to fight off a persistent HPV infection.’
While most people with an HPV infection will clear the virus from their bodies within two years, 10-20% of those infected will fail to do so and become at much higher risk of developing cervical cancer.
The findings, which are published in the international journal Scientific Reports
, suggest that a protein known as E7, produced by a high-risk type of human papillomavirus (HPV16), may be the key player in suppressing the body's immune response to the virus.
Study lead author Associate Professor Merilyn Hibma from University of Otago, New Zeland, says that exactly how HPV16 suppresses the body's immune responses has remained a matter of debate.
"Our new findings show that E7, in the absence of other HPV16 proteins, is sufficient enough to cause a range of effects on specialized cells normally involved in priming the body's T-cells to combat viral infection," Associate Professor Hibma says.
Further teasing out the mechanisms behind the failure of T-cells to be primed to attack the virus may allow new therapies that enable the body to fight off a persistent HPV infection, she says.
"This knowledge also helps us to understand how cancer cells avoid being detected by the immune system as E7 is also produced by cervical cancer cells. From this we may be able to identify new ways to block cancer suppression of the immune response. This approach is similar to 'checkpoint inhibitors' such as Keytruda and Opdiva."