This study examined 522 children born to hepatitis B surface antigen (HBsAg)-positive mothers from 1985 through 1994 and evaluated the protection provided by anti-hepatitis B virus (HBV) immunization at birth. Babies were given hepatitis B immunoglobulin and hepatitis B vaccine at birth. At 5-14 years after immunization, 17 children (3.3%) were anti-HB core antigen positive, and 3 also were HBsAg positive. One carrier child had a double mutation, with substitution of proline-->serine at codons 120 (P120S) and 127 (P127S) within the a determinant of HBsAg. Of the 522 children, 400 (79.2%) of 505 still had protective anti-HBsAg titers > or =10 mIU/mL. Thus, HBV vaccination of children born to HBsAg-positive mothers is effective and confers long-term immunity. There is no evidence that the emergence of HBV escape mutants secondary to the immune pressure against wild-type HBV is of concern.

The polymerase chain reaction (PCR) was used to investigate the presence of positive and negative hepatitis C virus (HCV) RNA strands in serum and peripheral blood mononuclear cells (PBMC) of 20 patients with histologically proven HCV-related chronic liver disease. All patients completed a course of interferon (IFN) treatment (6 MU of IFN-alpha 2b three times a week for 24 weeks) and were followed-up for 12 months after treatment was discontinued. Pre-treatment, end-treatment and 6-month follow-up serum and PBMC samples were examined. At enrollment, the positive strand of HCV-RNA was detected in serum of 18 patients (90%), the negative strand in none. Positive-stranded HCV-RNA was detected in PBMC of 15 patients (75%), 13 of whom also had detectable levels of negative-stranded HCV-RNA in PBMC. By the end of the treatment, 12 patients (60%) were responders. The pre-treatment HCV infection of PBMC, indicated by the presence of both RNA strands, was found in 8 (66.7%) responders compared to 5 (62.5%) non-responders (P = n.s.). End-treatment loss of PBMC HCV-RNA correlated significantly with the response since it occurred in all responders compared to 2 non-responders (P = 0.02). However, end-treatment-negative serum and PBMC HCV-RNA did not predict the occurrence of a sustained response, which was observed at month 12 in 5 of 12 responders (P = n.s.). On the other hand, the persistent absence of HCV RNA in serum and PBMC at the end of the 6-month follow-up was significantly associated with the occurrence of a sustained response (P < 0.0001).

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Anti-HCV positivity and viremia were frequently observed. The significant correlation between the detection of HCV RNA, the elevation of ALT, and positivity for anti-HCV suggests HCV infection. Exclusion of anti-HCV-positive donors and of anti-HCV-positive IVIG lots should improve the safety of IVIG.

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Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) have been examined in 38 patients with chronic hepatitis C liver disease treated with interferon. The sICAM-1 values were found to correlate significantly with the ALT values. Pre-treatment sICAM-1 values of responder and nonresponder patients were not significantly different while, by the end of the treatment, the values of responders were significantly lower compared to those of nonresponders. However, no difference could be found between sustained and relapse responders. Of the 21 patients examined for PBMC HCV-RNA, 15 (71.4%) were found to be positive. Neither the rate of responsivity to interferon treatment, nor the mean sICAM-1 values correlated with the positivity of PBMC HCV-RNA. However, the clearance of serum and PBMC HCV-RNA was associated to a significant decrease of sICAM-1 and ALT levels. In conclusion, sICAM-1 values were found to correlate with ongoing viral replication and liver cytonecrosis, but were not influenced by the concomitant HCV infection of PBMC.

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