This study investigates the dynamics of hepatitis B virus (HBV) infection using a mathematical model and lamivudine treatment. The research reveals that in patients with chronic HBV infection, the half-life of HBV particles in the plasma is approximately 1 day, indicating a 50% daily turnover of free virus. Total daily viral release is estimated at around 10¹¹ virus particles. The turnover rate of infected cells is estimated using two methods: comparing viral production before and after treatment, and analyzing the decline of hepatitis B antigen (HBeAg) during treatment. These methods show that the half-lives of virus-producing cells range from 10 to 100 days, reflecting differences in immune responses against infected cells. The study also compares HBV dynamics with those of human immunodeficiency virus (HIV). While HBV carriers produce more plasma virus than HIV patients, the half-life of virus-producing cells is much shorter in HIV. Notably, there is no evidence of drug resistance in HBV-infected patients treated for up to 24 weeks. The mathematical model used in the study includes uninfected cells (x), infected cells (y), and free virus (v), with differential equations describing their dynamics. The model shows that the decay of free virus follows an exponential pattern, with a half-life of 1 day. The total daily production of plasma virus is estimated to be around 1.3 × 10¹¹ particles, with a wide distribution among patients, likely reflecting differences in the number of infected cells. The study also finds that the initial decay of HBeAg reflects the decay of infected hepatocytes. The half-life of infected cells ranges from 10 to 100 days, with a strong correlation between the decay rate of infected cells and the levels of alanine aminotransferase (ALT), an indicator of liver cell damage. After 24 weeks of treatment, patients showed the ability to return to their pretreatment steady-state levels, indicating that the factors determining the initial virus levels have not changed over time. The study also highlights the importance of understanding HBV dynamics for optimal treatment strategies, including the timing of drug treatment and immunotherapy. The findings suggest that HBV infection involves a rapid turnover of infected cells and virus production, with significant implications for the development of hepatocellular carcinoma. The study provides a quantitative understanding of HBV replication dynamics, which can inform the design of individualized treatment strategies for chronic HBV infection.This study investigates the dynamics of hepatitis B virus (HBV) infection using a mathematical model and lamivudine treatment. The research reveals that in patients with chronic HBV infection, the half-life of HBV particles in the plasma is approximately 1 day, indicating a 50% daily turnover of free virus. Total daily viral release is estimated at around 10¹¹ virus particles. The turnover rate of infected cells is estimated using two methods: comparing viral production before and after treatment, and analyzing the decline of hepatitis B antigen (HBeAg) during treatment. These methods show that the half-lives of virus-producing cells range from 10 to 100 days, reflecting differences in immune responses against infected cells. The study also compares HBV dynamics with those of human immunodeficiency virus (HIV). While HBV carriers produce more plasma virus than HIV patients, the half-life of virus-producing cells is much shorter in HIV. Notably, there is no evidence of drug resistance in HBV-infected patients treated for up to 24 weeks. The mathematical model used in the study includes uninfected cells (x), infected cells (y), and free virus (v), with differential equations describing their dynamics. The model shows that the decay of free virus follows an exponential pattern, with a half-life of 1 day. The total daily production of plasma virus is estimated to be around 1.3 × 10¹¹ particles, with a wide distribution among patients, likely reflecting differences in the number of infected cells. The study also finds that the initial decay of HBeAg reflects the decay of infected hepatocytes. The half-life of infected cells ranges from 10 to 100 days, with a strong correlation between the decay rate of infected cells and the levels of alanine aminotransferase (ALT), an indicator of liver cell damage. After 24 weeks of treatment, patients showed the ability to return to their pretreatment steady-state levels, indicating that the factors determining the initial virus levels have not changed over time. The study also highlights the importance of understanding HBV dynamics for optimal treatment strategies, including the timing of drug treatment and immunotherapy. The findings suggest that HBV infection involves a rapid turnover of infected cells and virus production, with significant implications for the development of hepatocellular carcinoma. The study provides a quantitative understanding of HBV replication dynamics, which can inform the design of individualized treatment strategies for chronic HBV infection.