Background Schistosomiasis, a parasitic helminth infection, affects over 250 million people
worldwide. The blood-borne S. mansoni eggs either penetrate the gut lumen, or become
trapped in the liver sinusoids.
Hepatitis B virus (HBV) is a DNA virus, causing hepatic inflammation and necrosis
and ultimately hepatocellular carcinoma (HCC).
Coinfections of S. mansoni and HBV occur disproportionally often in endemic areas.
This project aimed to investigate their combined effects on hepatic carcinogenesis
and metabolism.
Methods Transgenic (tg) mice expressing the large form of the HBV surface proteins (collectively
called HBsAg) were infected with S. mansoni at the age of 43 weeks. After nine weeks
of infection, the animals were sacrificed. Liver-to-body weight ratios, ALT, glucose,
and albumin levels, hepatic tumor numbers and sizes were determined and compared to
infected wt-mice, as well as non-infected wt- and tg-control animals.
Results S. mansoni-infected mice showed a larger liver-to-bodyweight ratio than non-infected
animals, while also exhibiting higher serum ALT levels. Glucose levels of infected
tg-mice were significantly lower compared to both infected wt- and non-infected tg-animals.
Infected tg-mice show lower albumin levels than wt- and tg-mice. Furthermore, infected
tg-animals presented larger tumors and increased numbers of atypical nucleoli.
Conclusion The observed increase in liver-to-bodyweight ratios and ALT levels suggest an additive
effect on hepatocellular damage in S. mansoni infected, HBsAg-tg-mice compared to
the individual disease models. Furthermore, decreases in serum glucose and albumin
levels indicate hepatic decompensation. Tumor size and atypical nucleoli strongly
suggest enhanced carcinogenesis in this co-infection model.
