Serological Marker Profiles of Chronic Hepatitis B Virus Infection among HBsAg-Positive Patients Seeking Medical Care in the North Rift Region of Kenya

Background: Serological marker and viral load testing in hepatitis B virus (HBV) infection is essential for accurate diagnosis, interpretation of serological profiles and infectivity, guiding treatment, and monitoring patient progress. In Baringo County, Kenya, the HBV prevalence of 10.8%, exceeds the national average of 3%, indicating a hyperendemic focus. Despite the adoption of World Health Organization (WHO) HBV treatment guidelines at Moi Teaching and Referral Hospital and Marigat Sub-County Hospital in 2017, routine use of serological markers and viral load testing remains limited in clinical practice. Methods: This cross-sectional study included 65 chronic HBV patients receiving treatment at Moi Teaching and Referral Hospital and Marigat Sub-County Hospital. Plasma samples were analyzed for HBsAg, HBsAb, HBeAg, HBeAb and HBcAb-IgM using the Quick Profile^TM HBV-5 panel Test. HBV DNA viral load was quantified by quantitative real-time polymerase chain reaction (qPCR). Descriptive statistics were used to summarize the distribution of serological markers, while viral load results were expressed as medians with interquartile ranges (IQR). The Chi-square test was used to assess categorical distributions. Results: All 65 (100%) subjects were found to have HBsAg, confirming chronic HBV infection. The most frequent pattern was HBsAg (+), HBsAb (–), HBeAg (–), HBeAb (–), HBcAb-IgM (–) and was seen in 31 patients (47.7%). This profile was typical of chronic Hepatitis B infection with no evidence of acute activity or HBeAg seroconversion in the last several months. HBV DNA levels were relatively low in this group with a median of 509 copies/mL (IQR: 28.7 - 14,231) with some variation in viral load seen in many individuals, mostly low-replicative. Twenty-three-point one percent (23.1%) of patients were HBcAb-IgM positive, which is an active immune response and suggests viral reactivation. HBeAb positivity without HbcAb-IgM was detected in 21.5%, which is in line with HBeAg-negative serological profile with persistent viral replication. 7.7% of participants were co-positive for HBsAb and HBsAg, indicating partial immune control. The median viral loads were significantly different between serological profile: lowest for HBcAb-IgM positive patients, 162 copies/mL (IQR: 28 - 1,500,000); highest for HBeAb positive without HBcAb-IgM, 17,589 copies/mL (IQR: 118 - 27,353,162); and intermediate for those with both HBsAb and HBsAg positivity, (1642 copies/mL IQR: 567 - 11,466). Conclusion: The serological and viral load profile