In both phases strong, polyclonal, multi-specific CD8 T cells appear to be the primary component, although CD4 T cells serve a critical role in supporting such responses. Therefore, interventions to improve HBV Scutellarin-methylester serologic outcomes may target one or both phases of this response. The importance of cellular immune function in determining the serologic outcome from HBV infection is supported by several observations from our study including an increased risk of CHBV in those with HBV infection after HIV diagnosis and those with lower CD4 cell counts at the time of HBV diagnosis, as well as an increased Kaempferitrin likelihood of RHBV in those with higher CD4 cell counts, and improvements in HBV outcome for those infected with HBV while receiving HAART. The central importance of cellular immune function in determining HBV serologic status is also supported by a smaller previous study which similarly found those with CHBV had lower mean CD4 cell counts, and the proportion of CHBV infections in those with HBV after HIV was high, approximately 20%. Our findings also demonstrate the complex relationship between HBV serologic outcomes and the degree of immunologic function during either phase of the immune response to HBV. While CD4 cell count at the time of HBV diagnosis was inversely related to the risk of CHBV, such risk was also altered by whether or not HBV infection occurred after HIV diagnosis. In other words, an individual infected with HBV prior to HIV whose CD4 count later declined had lower risk of CHBV than an individual infected with HBV after HIV diagnosis with a similar CD4 cell count. Therefore, our study suggests a significant portion of HBV serologic outcome is determined by an individual��s ability to mount an effective immune response at the time of HBV exposure, regardless of future alterations in immune status. HBV serologies have been reported to fluctuate over time in HIV-infected individuals which could potentially limit conclusions from our study in this regard. However, even though we did not specifically evaluate longitudinal changes in HBV serologies, 91% of individuals we classified as having CHBV were persistently reactive for HBsAg from the date of HBV diagnosis further suggesting that CHBV is established early in the course of HBV infection.