Hepatitis B and hepatitis C viruses are causes of liver cancer. The former appears to act directly by damaging cells and their DNA. The latter shows an indirect effect, mediated by cirrhosis. For both, there is potential for nutrition status to have an effect at several stages: susceptibility to and duration of infection, liver damage, DNA damage, and cancer progression (Refer Figure 2 in Nutrition and Cancer ).
Around 7-8 per cent of the world’s population is estimated to be infected with hepatitis B virus. It is mostly spread by blood and sexual transmission. In endemic areas, the carrier rate may be 10-20 per cent. It is often acquired at birth or in childhood, and is endemic in areas of Africa and Asia. Chronic hepatitis B virus carriers have a 100-fold greater chance of developing liver cancer than non-carriers. Those infected in adulthood have a lower risk of this cancer than those infected in childhood because there is less time for virus to cause inflammation. Vaccination against hepatitis B virus has been shown to reduce the prevalence of liver cancer by 60 per cent.
Liver cancer in hepatitis B virus carriers is not necessarily connected with cirrhosis: up to 40 per cent of associated liver cancer cases are non-cirrhotic. Hepatitis B virus carries its genetic code as DNA rather than RNA. Viral DNA can insert itself into liver cells and alter their DNA.
Around 3 per cent of the world’s population is estimated to be infected with hepatitis C virus. It is more prevalent in high income countries. Approximately 80 per cent of these infections become chronic, of which 15-20 per cent develops into cirrhosis. Of those, 1-4 per cent develops into liver cancer each year. Interruption of the sequence of chronic hepatitis developing into cirrhosis prevents liver cancer. Also, there is an interaction between hepatitis C virus infection, liver cancer risk, and consumption of alcoholic drinks. There is no vaccine against hepatitis C. It is mostly spread by blood.
- aadautech, a cancer drug discovery and therapeutics blog.