This report covers 7-year follow-up studies on 35 HBs Ag carriers whose anti-HBc titer levels were 10 (log 2) or more and who had normal liver functions at the start of the studies, when 9 of them (25.7%) were HBe Ag positive, 24 (68.6%) anti-HBe positive and 2 (5.7%) negative to both. 1. There was no significant difference in the incidence of abnormal SGPT levels as a whole between HBe Ag positives and anti-HBe positives. But abnormally high SGPT levels of 100 KU or more were observed at a higher percentage among HBe Ag positives (4/9. 44.4%) than among anti-HBe positives (1/24. 4.2%. p<0.02). 2. Based on the results of the 7-year studies, all cases were classified into six clinical stages. HBe Ag positives were divided into three groups by the stage with different SGPT levels : 5 cases (15.2%) whose SGPT levels never rose above 50 KU were classified as Stage 1; 3 cases with chronic active hepatitis (9.6%) whose highest SGPT levels were over 200 KU (2 new cases and 1 case with a relapse of chronic inactive hepatitis) as Stage 2 and 1 case (3.0%) seroconverted to anti-HBe positive following an acute relapse of chronic inactive hepatitis as Stage 3. Anti-HBe positives were divided into another three groups similarly according to their mean HBs Ag titer levels : 6 cases (18.2%) whose mean HBs Ag titer levels ranged from 10 to 13 (log 2) were classified as Stage 4; 13 cases (39.4%) whose mean HBs Ag titer levels ranged from 6 to 9 as Stage 5 and 5 cases (15.2%), including 2 cases turned negative to HBs Ag, whose mean HBs Ag titer levels were below 5 as Stage 6. The average age of each group increased with its clinical stage, namely, 32.6 in Stage 1, 34.3 in Stage 2, 33.0 in Stage 3, 34.5 in Stage 4 and 37.0 in Stage 5, but the average age in Stage 6 was 29.0. 3. All HBe Ag positives showed fluctuations in HBs Ag titer levels. The fluctuations were particularly noteworthy among cases with chronic active hepatitis in Stage 2 during an acute relapse. The HBs Ag titers rose just before the acute relapses in a case of chronic active hepatitis when SGPT levels went over 200 KU. This suggested a proliferation of the virus. On the other hand, in anti-HBe positives, a decrement of the virus was suggested by the fact that an increasing proportion of cases showed their HBs Ag titer levels to fluctuate or to become lower with the progress of stages (p<0.05) and two cases turned negative to HBs Ag as plotted in Stage 6. And the proportion of cases with abnormal SGPT levels decreased with the progress of stages (p<0.05). One case whose SGPT level was 125 KU, highest among anti-HBe positives, followed the clinical course of chronic inactive hepatitis and lowered in HBs Ag titer. 4. Between HBe Ag and anti-HBe cases, there were considerable differences in the occurrence of liver disturbances and their clinical courses. The fluctuations in HBs Ag titers seem to indicate that a difference in active virus replication is the primary factor causing the difference in the occurrence of liver disturbances and their clinical courses.