P31: Sero‐prevalance of HBV among university students in Sargodha, Pakistan

Abstract

reflect different magnitude of HBV-specific immune response. Characterization of T cell profiles is relevant to the improved understanding of chronic HBV infection and the design of antiviral therapy. The aim of the present study is to determine the absolute CD4 counts in different phases of CHB infection. METHODS: 106 hepatitis B patients were included in the study. All CHB patients fulfilled the following criteria: positive HBsAg for at least 6 months, no other concomitant causes of liver disease (hepatitis A, E and C, HIV infection and alcohol consumption of more than 60 g/day, autoimmune hepatitis and metabolic liver disease). None of the patients were drug user or exposed to hepatotoxins. Liver function tests, blood urea and creatinine, Haemoglobin%, total leucocyte and lymphocyte counts, platelet count and INR were measured for all patients. CD4 counts were determined by flow cytometry. HIV antibody and HBV markers (HBsAg, HBsAb, HBeAg, HBeAb, HBcAb, and anti-HBcAb IgM) were detected by enzyme-linked immunosorbent assay. Serum HBV DNA load was assessed by quantitative real-time polymerase chain reaction. RESULTS: Absolute CD4 count and CD4% were normal in acute hepatitis B and 'immune tolerant' CHB. But CD4 declines from 'immune reactive' to 'HBeAg-negative' CHB. Average CD4 counts were below 500/lL in these two phases -351.12 + 33.23 and 237.0 + 118.27 respectively. CD4 counts were below 350/lL in 72.72% and below 200/lL in 27.27% in these two phases. Such low levels of CD4 count are not proportionate to the total lymphocyte counts in these two phases. Absolute CD4 count rises to moderate level in 'inactive HBV carrier state' (754.4 + 174.87) and 'treatment-experienced' patients (734.5 + 204.57). Similarly CD4% were low in 'immune reactive' to 'HBeAg-negative' (<25%) in contrast to 'immune tolerant' and 'inactive HBV carrier state' (>35%) CHB. CONCLUSIONS: CD4 count gradually declines with progressive liver damage in 'immune reactive' and 'HBeAg-negative' CHB and it may be implicated in the design of the antiviral therapy. Interferon may be unsuitable for CHB with very low CD4 counts (<250/lL). Sequential therapy comprising oral anti viral followed by Peg-Interferon might be theoretically appropriate approach in this group of patients. On the other hand, those with higher CD4 are appropriate for Peg-Interferon first followed by oral anti viral.