[Relationship between the gene mutations of mannose binding protein and the progression of hepatitis B infection].

OBJECTIVE: To investigate the relationship between the gene mutations of mannose binding protein(MBP) and the progression of hepatitis B. METHODS: The MBP gene mutations in 52 patients with chronic hepatitis B and 62 patients with severe hepatitis B and 64 HBsAg-negative healthy controls were investigated. The mutations in MBP gene were analyzed by polymerase chain reaction (PCR) and direct DNA sequencing. RESULTS: A mutation of MBP gene codon 54 was found. The mutation frequency in the group of severe hepatitis B (35.5%, 22/62) was higher than those in the chronic hepatitis B group (15.4%, 8/52) and the HBsAg-negative healthy controls(14.1%, 9/64), respectively, and their difference was significant (chi-square was 7.79, P< 0.01; chi-square was 5.89,lzP<0.05). The difference between the chronic hepatitis B group and the HBsAg-negative healthy control group was not significant (P > 0.05). CONCLUSION: There is only mutation in codon 54 of the MBP gene in patients with hepatitis B infection in the area analyzed. Codon 54 mutation of MBP gene is not related to the persistence of hepatitis B, but it was associated with the progression of hepatitis B infection.

[Effect of interferon-alpha therapy on the capacity of antigen presenting of peripheral blood dendritic cells from patients with chronic hepatitis B].

OBJECTIVE: To study the effect of interferon -alpha therapy on the capacity of antigen presenting of peripheral blood dendritic cells from patients with chronic hepatitis B (CHB). METHODS: The peripheral blood samples were obtained from 23 patients who were given interferon-alpha therapy just before treatment and after treatment for 4 months, respectively. The peripheral blood mononuclear cells (PBMC) were isolated and cultured, and recombinant human IL-4 and GM-CSF were added to the cultures. After cultured for 7 days, dendritic cells (DC) were harvested and then incubated with HBsAg for 3 hours, then mixed with autogenous PBMC and cocultured for additional 72 hours. Before ending the culiration, 7.4 x 10(4) Bq (3)H-TDR was added to the culture for 12 hours, and then all cells were collected and detected for cpm values. Eight healthy individuals were used as controls. RESULTS: After treatment for 4 months with interferon-alpha, the proliferating level of DC markedly increased in posttreatent group when compared with that in the pretreatment group and the total number of DC proliferation averagely increased 2.8 times in the same culture condition. The capacity of antigen presenting of DC in the pretreatment group markedly decreased compared with that either in posttreatment group or in healthy group, respectively (P < 0.001), and there was no significant difference between the posttreatment group and the healthy group (P > 0.05). Both before and after treatment the capacities of DC antigen presenting in interferon-alpha complete responder group were significantly stronger than those in the nonresponder group (P < 0.01 and P < 0.001). There was no significant difference between the partial responder group and nonresponder one (P > 0.05). CONCLUSION: The results indicate the capacity of antigen presenting of peripheral blood DC from CHB patients is dysfunctional. Interferon-alpha therapy may markedly improve the capacity. The potential of antigen presenting of DC in CHB patients may be closely correlated with the response to interferon-alpha therapy.