Approximately half of the patients with type C hepatitis do not have a history of parenteral exposure. The route of nonparenteral infection remains unknown. To evaluate the possible role of body fluids, the existence of hepatitis C virus (HCV) RNA in saliva, urine, seminal fluid, and ascites was examined by "nested" polymerase chain reaction (PCR). Amplification of the HCV 5' noncoding sequences was carried out. The amplified product was confirmed by Southern blot hybridization and restriction endonuclease digestion. Among 34 patients with chronic liver disease who were positive for anti-HCV and serum HCV RNA, the prevalence of HCV RNA in body fluids was 100% (7/7) in ascites, 48% (15/31) in saliva, 24% (4/17) in seminal fluid, and 7% (2/29) in urine. The body fluids collected from 3 healthy subjects and 5 patients with chronic liver disease who were positive for anti-HCV but negative for serum HCV RNA were all negative for HCV RNA. Hence, the potential infectivity of body fluids in patients testing negative for serum HCV RNA can probably be discounted. Conversely, the presence of HCV RNA in saliva and seminal fluid of patients positive for serum HCV RNA suggests sexual and household contact as likely modes of nonparenteral transmission of type C hepatitis. Furthermore, the high prevalence of HCV RNA in ascites and saliva may have important implications in medical and dental practice.

The nested polymerase chain reaction (PCR) technique was applied to investigate hepatitis C virus (HCV) RNA in the peripheral blood mononuclear cells (PBMCs), saliva, and serum of patients with chronic type C hepatitis. The specificity of the amplified products was analyzed and confirmed by agarose gel electrophoresis, Southern blot hybridization, and restriction endonuclease pattern analysis. HCV RNA was detectable in the PBMCs of 24% (12/50) of the patients. The HCV RNA detected in PBMCs was not due to the contamination from plasma, since no viral sequences could be detected in the third washing of PBMCs. Of the 12 patients with HCV RNA in PBMCs, five were negative for HCV RNA sequences in the serum. Thus the presence of HCV RNA in PBMCs was not strictly correlated to the results for sera. Among 25 patients with HCV RNA in their saliva, 18 were negative for PBMCs. Among 25 patients without HCV RNA in their saliva, five had HCV RNA in PBMCs. In conclusion, PBMCs are an extrahepatic target for chronic HCV infection. However, we do not suggest that PBMCs act as a vehicle for carrying HCV to saliva, since the presence of HCV RNA in PBMCs and in saliva was not closely correlated.

To evaluate the intrafamilial transmission of hepatitis C virus (HCV) 104 index patients with type C chronic liver disease and their 307 family contacts were interviewed. After a questionnaire on the risk factors of parenteral exposure, blood samples were obtained and tested for liver biochemistry and anti-HCV antibody by enzyme-linked immunosorbent assay (Abbott II). Overall, 52 family contacts (17%) were positive for anti-HCV, indicating a higher anti-HCV prevalence among family contacts than among the general population in Taiwan. The anti-HCV prevalences in parents, spouses, children, and other contacts of the patients were 54% (14/26), 28% (25/91), 6.9% (10/143), and 6.4% (3/47), respectively. The contacts of index patients had increasingly greater risk of HCV infection when they became older and had lived longer with index patients. All family contacts were divided into two groups categorized by whether the index patients had or did not have a history of parenteral exposure. Among 126 family contacts of the 42 patients without parenteral exposure, blood transfusion and surgery were the factors significantly associated with HCV infection in these family contacts (odds ratio = 7.26, 95% confidence interval = 2.32-32.67; odds ratio = 3.95, 95% CI = 1.29-12.11, respectively). Risk factors were not significantly associated with HCV infection among 181 family contacts of the 62 index patients with parenteral exposure. It is concluded that the index patients without parenteral exposure appeared to have acquired the disease from HCV-infected family members with risk factors. Most of the index patients had a history of parenteral exposure and in turn served as the source of the disease for family members.