OBJECTIVE: To identify the influence of transfusion transmitted virus (TTV) co-infection in other virus infected patients and its genotypes. METHODS: A conservative sequence of ORF1 in the TTV genome was selected as primers and TTV DNA was measured in students and other hepatitis patients by using microplate nucleic acid hybridization and ELISA. The results were statistically analyzed. Nucleotide sequence of divergence>50% was used as color probe for distinguishing TTV genotypes I or II. RESULTS: TTV DNA was detected in the sera from 2 (3.3%) of 60 students, 2 (14.3%) of 14 patients with non A-non E hepatitis, 6 (12%) of 50 patients with chronic hepatitis B, and 4 (16%) of 25 patients with liver cirrhosis, respectively. Statistical difference was observed between the patient group and the student group (P<0.05), but no significant difference in age, gender, serum ALT levels and TBiL between TTV DNA positive and negative patients (P>0.05). TTV genotype type I was by far the most frequent viral genotype (66.7%), followed by type II (25%), and mixed infection (8.3%). CONCLUSIONS: These results suggest that the routes of TTV infection may be similar to those of HBV and HCV, and concurrent infection with HBV, HCV are common. TTV co-infection could not affect the clinical features of patients with liver diseases and the pathological process. TTV is not a main causative factor for patients with non A-non E hepatitis. Further study is needed to clarify the role of TTV in patients with non A-non E hepatitis.
OBJECTIVE: To identify the influence of transfusion transmitted virus (TTV) co-infection in other virus infectedpatients and its genotypes. METHODS: A conservative sequence of ORF1 in the TTV genome was selected as primers and TTV DNA was measured in students and other hepatitispatients by using microplate nucleic acid hybridization and ELISA. The results were statistically analyzed. Nucleotide sequence of divergence>50% was used as color probe for distinguishing TTV genotypes I or II. RESULTS: TTV DNA was detected in the sera from 2 (3.3%) of 60 students, 2 (14.3%) of 14 patients with non A-non E hepatitis, 6 (12%) of 50 patients with chronic hepatitis B, and 4 (16%) of 25 patients with liver cirrhosis, respectively. Statistical difference was observed between the patient group and the student group (P<0.05), but no significant difference in age, gender, serum ALT levels and TBiL between TTV DNA positive and negative patients (P>0.05). TTV genotype type I was by far the most frequent viral genotype (66.7%), followed by type II (25%), and mixed infection (8.3%). CONCLUSIONS: These results suggest that the routes of TTV infection may be similar to those of HBV and HCV, and concurrent infection with HBV, HCV are common. TTV co-infection could not affect the clinical features of patients with liver diseases and the pathological process. TTV is not a main causative factor for patients with non A-non E hepatitis. Further study is needed to clarify the role of TTV in patients with non A-non E hepatitis.