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Oral feeding of hepatitis B proteins a promising treatment for chronic infection
  NEW YORK (Reuters Health) - In patients with chronic hepatitis B virus (HBV) infection, oral administration of HBV envelope proteins augments the anti-HBV immune response and alleviates immune-mediated liver damage, results of a new study indicate. There was a significant decrease in viral load and an improvement in the histological necroinflammatory score.
Building on earlier research showing that antiviral immunity could be modulated through oral feeding of viral proteins, Dr. Yaron Ilan from Hadassah-Hebrew University Medical Center in Jerusalem and colleagues treated 42 chronic HBV patients with HBV envelope proteins (HBsAg+preS1+preS2) three times per week for 20 to 30 weeks.
They followed the subjects for another 20 weeks after the end of the treatment period. Writing in the December issue of The American Journal of Gastroenterology, the team reports that the treatment was well tolerated and that 80% of those with elevated liver enzymes showed a favorable biochemical response.
Treatment led to a significant decrease in viral load in 15 patients (35.7%), an improvement in HBsAg and HBeAg scores on liver biopsy in 41% and 57%, respectively, and in the histological necroinflammatory score in 30%.
Five of 19 HBeAg positive patients (26.3%) became HBeAg negative.
Oral immune regulation toward HBV envelope proteins also significantly increased HBV-specific T cell proliferation and favorably altered the Th1/Th2 immune balance by increasing IFN-gamma T cell clones and decreasing IL-10 T cell clones.
An increase in peripheral blood levels of natural killer T (NKT) lymphocytes was also noted in all patients.
These results show that "HBV-specific T cell immune modulation can be elicited through p.o. administration of HBV envelope proteins to chronically infected individuals," Dr. Ilan and colleagues write. This approach "alleviated the disease, while leaving the general immunological defense of the recipient intact."
However, when treatment was halted, HBV DNA levels rebounded in roughly half of the responders and the antiviral T cell response was lost in 30% to 70% of responders although IL10 levels remained low.
"It is possible that correction of the anti-HBV immunological imbalance was partial, leading to an enhanced effect on part of T cell subtypes rather than a clearance or irreversible suppression of 'unwanted' T cells," they write.
Am J Gastroenterol 2003;98:2505-2515.
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