What are the implications of low anti-HBe (Hepatitis B e-antibody) levels?

From the Guidelines

Low anti-HBe antibody levels indicate a specific stage in hepatitis B virus (HBV) infection, suggesting chronic hepatitis B with active viral replication, and patients should undergo further testing, including HBV DNA quantification, liver function tests, and possibly liver imaging or biopsy to assess disease activity and liver damage. Treatment may be necessary if there is evidence of active liver disease or high viral load, typically with antiviral medications such as entecavir (0.5mg daily) or tenofovir (300mg daily), which suppress viral replication 1. These medications often require long-term or indefinite use. Regular monitoring every 3-6 months is essential to track viral load, liver function, and treatment response. Low anti-HBe antibody levels can sometimes represent a transitional phase in chronic HBV infection, where the virus is shifting from an active to an inactive state, or it may indicate viral mutations that affect HBe antigen expression. Some key points to consider in the management of patients with low anti-HBe antibody levels include:

• The level of HBV replication represents the strongest single predictive biomarker associated with disease progression and the long-term outcome of chronic HBV infection 1.
• The inhibition of viral replication by antiviral treatment has been shown to achieve the elimination of chronic HBV-induced necroinflammatory activity and progressive fibrotic liver processes in the vast majority of patients, in turn reducing the risk of HCC 1.
• Treatment-induced HBeAg loss and seroconversion to anti-HBe characterizes the induction of a partial immune control often leading to a low replicative phase of the chronic HBV infection 1.
• Suppression of HBV DNA to undetectable levels is normally associated with normalization of ALT levels 1.
• Persistence of elevated ALT levels in patients with complete suppression of viral replication is associated with a lower chance of fibrosis regression and can be a reason for histologic disease progression 1. Consultation with a hepatologist or infectious disease specialist is recommended for proper interpretation and management. The goal of therapy for CHB is to eliminate or significantly suppress HBV replication and thus prevent progression of liver disease to cirrhosis, liver failure, or HCC 1. The primary aim of treatment should be to reduce and maintain serum HBV DNA at the lowest possible levels (ie, achieve durable HBV DNA suppression) 1. Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance and can be confidently used as first-line monotherapies 1. The other three NAs may only be used in the treatment of CHB if more potent drugs with high barrier to resistance are not available 1. Treatment strategies include treatment of finite duration with (PEG-)IFN or a NA and long-term treatment with NA(s) 1. Finite-duration treatment with (PEG-)IFN is mainly recommended for HBeAg-positive patients with the best chance of anti-HBe seroconversion 1. Long-term therapy with entecavir or tenofovir can lead to regression of fibrosis and frequently even reversal of cirrhosis and thus change the course of CHB-related liver disease 1. The loss of HBsAg is regarded as the optimal treatment endpoint, termed ‘functional cure’, but it is only rarely achieved with our current antiviral armamentarium 1. HBsAg loss is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. The clinical relevance of occult HBV infection (detectable HBV DNA in the liver with low-level [<200 IU/ml] HBV DNA in blood) is unclear 1. Immunosuppression may lead to HBV reactivation in these patients 1. In the “HBsAg-negative phase” after HBsAg loss, low-level HBV replication may persist with detectable HBV DNA in the liver 1. Generally, HBV DNA is not detectable in the serum, while anti-HBc antibodies with or without anti-HBs are detectable 1. HBsAg loss before the onset of cirrhosis is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. Spontaneous HBsAg seroreversion with reactivation of the inflammatory liver process after HBsAg loss is rare and may occur in patients with a significant impairment of their immune function 1. The main advantage of HBsAg loss is that it allows a safe discontinuation of antiviral therapy 1. As chronic HBV infection cannot be completely eradicated due to the persistence of cccDNA and integrated HBV DNA, it remains unclear whether HBsAg loss adds to the prevention of the long-term complications of chronic HBV infection beyond what can be achieved by the suppression of HBV DNA replication alone 1. HCC may still develop even after spontaneous HBsAg loss (annual rate approximately 0.55%) 1. The risk, however, is lower if HBsAg loss is achieved at a younger age and/or in the absence of significant fibrosis 1. In an Asian cohort followed for 287 patient-years after NA treatment-induced HBsAg seroclearance, only two patients with baseline cirrhosis developed HCC or died (0.7% annual risk), which was a significantly lower rate compared with propensity score-matched patients without HBsAg seroclearance (HR 0.09, p < 0.01) 1. The level of HBV DNA suppression that should be attained in order to achieve these benefits is not well defined, but inferred that the lower, the better 1. The goal of therapy for CHB is to eliminate or significantly suppress HBV replication and thus prevent progression of liver disease to cirrhosis, liver failure, or HCC 1. The primary aim of treatment should be to reduce and maintain serum HBV DNA at the lowest possible levels (ie, achieve durable HBV DNA suppression) 1. Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance and can be confidently used as first-line monotherapies 1. The other three NAs may only be used in the treatment of CHB if more potent drugs with high barrier to resistance are not available 1. Treatment strategies include treatment of finite duration with (PEG-)IFN or a NA and long-term treatment with NA(s) 1. Finite-duration treatment with (PEG-)IFN is mainly recommended for HBeAg-positive patients with the best chance of anti-HBe seroconversion 1. Long-term therapy with entecavir or tenofovir can lead to regression of fibrosis and frequently even reversal of cirrhosis and thus change the course of CHB-related liver disease 1. The loss of HBsAg is regarded as the optimal treatment endpoint, termed ‘functional cure’, but it is only rarely achieved with our current antiviral armamentarium 1. HBsAg loss is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. The clinical relevance of occult HBV infection (detectable HBV DNA in the liver with low-level [<200 IU/ml] HBV DNA in blood) is unclear 1. Immunosuppression may lead to HBV reactivation in these patients 1. In the “HBsAg-negative phase” after HBsAg loss, low-level HBV replication may persist with detectable HBV DNA in the liver 1. Generally, HBV DNA is not detectable in the serum, while anti-HBc antibodies with or without anti-HBs are detectable 1. HBsAg loss before the onset of cirrhosis is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. Spontaneous HBsAg seroreversion with reactivation of the inflammatory liver process after HBsAg loss is rare and may occur in patients with a significant impairment of their immune function 1. The main advantage of HBsAg loss is that it allows a safe discontinuation of antiviral therapy 1. As chronic HBV infection cannot be completely eradicated due to the persistence of cccDNA and integrated HBV DNA, it remains unclear whether HBsAg loss adds to the prevention of the long-term complications of chronic HBV infection beyond what can be achieved by the suppression of HBV DNA replication alone 1. HCC may still develop even after spontaneous HBsAg loss (annual rate approximately 0.55%) 1. The risk, however, is lower if HBsAg loss is achieved at a younger age and/or in the absence of significant fibrosis 1. In an Asian cohort followed for 287 patient-years after NA treatment-induced HBsAg seroclearance, only two patients with baseline cirrhosis developed HCC or died (0.7% annual risk), which was a significantly lower rate compared with propensity score-matched patients without HBsAg seroclearance (HR 0.09, p < 0.01) 1. The level of HBV DNA suppression that should be attained in order to achieve these benefits is not well defined, but inferred that the lower, the better 1. Some key points to consider in the management of patients with low anti-HBe antibody levels include:
• The level of HBV replication represents the strongest single predictive biomarker associated with disease progression and the long-term outcome of chronic HBV infection 1.
• The inhibition of viral replication by antiviral treatment has been shown to achieve the elimination of chronic HBV-induced necroinflammatory activity and progressive fibrotic liver processes in the vast majority of patients, in turn reducing the risk of HCC 1.
• Treatment-induced HBeAg loss and seroconversion to anti-HBe characterizes the induction of a partial immune control often leading to a low replicative phase of the chronic HBV infection 1.
• Suppression of HBV DNA to undetectable levels is normally associated with normalization of ALT levels 1.
• Persistence of elevated ALT levels in patients with complete suppression of viral replication is associated with a lower chance of fibrosis regression and can be a reason for histologic disease progression 1. Consultation with a hepatologist or infectious disease specialist is recommended for proper interpretation and management. The goal of therapy for CHB is to eliminate or significantly suppress HBV replication and thus prevent progression of liver disease to cirrhosis, liver failure, or HCC 1. The primary aim of treatment should be to reduce and maintain serum HBV DNA at the lowest possible levels (ie, achieve durable HBV DNA suppression) 1. Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance and can be confidently used as first-line monotherapies 1. The other three NAs may only be used in the treatment of CHB if more potent drugs with high barrier to resistance are not available 1. Treatment strategies include treatment of finite duration with (PEG-)IFN or a NA and long-term treatment with NA(s) 1. Finite-duration treatment with (PEG-)IFN is mainly recommended for HBeAg-positive patients with the best chance of anti-HBe seroconversion 1. Long-term therapy with entecavir or tenofovir can lead to regression of fibrosis and frequently even reversal of cirrhosis and thus change the course of CHB-related liver disease 1. The loss of HBsAg is regarded as the optimal treatment endpoint, termed ‘functional cure’, but it is only rarely achieved with our current antiviral armamentarium 1. HBsAg loss is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. The clinical relevance of occult HBV infection (detectable HBV DNA in the liver with low-level [<200 IU/ml] HBV DNA in blood) is unclear 1. Immunosuppression may lead to HBV reactivation in these patients 1. In the “HBsAg-negative phase” after HBsAg loss, low-level HBV replication may persist with detectable HBV DNA in the liver 1. Generally, HBV DNA is not detectable in the serum, while anti-HBc antibodies with or without anti-HBs are detectable 1. HBsAg loss before the onset of cirrhosis is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. Spontaneous HBsAg seroreversion with reactivation of the inflammatory liver process after HBsAg loss is rare and may occur in patients with a significant impairment of their immune function 1. The main advantage of HBsAg loss is that it allows a safe discontinuation of antiviral therapy 1. As chronic HBV infection cannot be completely eradicated due to the persistence of cccDNA and integrated HBV DNA, it remains unclear whether HBsAg loss adds to the prevention of the long-term complications of chronic HBV infection beyond what can be achieved by the suppression of HBV DNA replication alone 1. HCC may still develop even after spontaneous HBsAg loss (annual rate approximately 0.55%) 1. The risk, however, is lower if HBsAg loss is achieved at a younger age and/or in the absence of significant fibrosis 1. In an Asian cohort followed for 287 patient-years after NA treatment-induced HBsAg seroclearance, only two patients with baseline cirrhosis developed HCC or died (0.7% annual risk), which was a significantly lower rate compared with propensity score-matched patients without HBsAg seroclearance (HR 0.09, p < 0.01) 1. The level of HBV DNA suppression that should be attained in order to achieve these benefits is not well defined, but inferred that the lower, the better 1. Some key points to consider in the management of patients with low anti-HBe antibody levels include:
• The level of HBV replication represents the strongest single predictive biomarker associated with disease progression and the long-term outcome of chronic HBV infection 1.
• The inhibition of viral replication by antiviral treatment has been shown to achieve the elimination of chronic HBV-induced necroinflammatory activity and progressive fibrotic liver processes in the vast majority of patients, in turn reducing the risk of HCC 1.
• Treatment-induced HBeAg loss and seroconversion to anti-HBe characterizes the induction of a partial immune control often leading to a low replicative phase of the chronic HBV infection 1.
• Suppression of HBV DNA to undetectable levels is normally associated with normalization of ALT levels 1.
• Persistence of elevated ALT levels in patients with complete suppression of viral replication is associated with a lower chance of fibrosis regression and can be a reason for histologic disease progression 1. Consultation with a hepatologist or infectious disease specialist is recommended for proper interpretation and management. The goal of therapy for CHB is to eliminate or significantly suppress HBV replication and thus prevent progression of liver disease to cirrhosis, liver failure, or HCC 1. The primary aim of treatment should be to reduce and maintain serum HBV DNA at the lowest possible levels (ie, achieve durable HBV DNA suppression) 1. Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance and can be confidently used as first-line monotherapies 1. The other three NAs may only be used in the treatment of CHB if more potent drugs with high barrier to resistance are not available 1. Treatment strategies include treatment of finite duration with (PEG-)IFN or a NA and long-term treatment with NA(s) 1. Finite-duration treatment with (PEG-)IFN is mainly recommended for HBeAg-positive patients with the best chance of anti-HBe seroconversion 1. Long-term therapy with entecavir or tenofovir can lead to regression of fibrosis and frequently even reversal of cirrhosis and thus change the course of CHB-related liver disease 1. The loss of HBsAg is regarded as the optimal treatment endpoint, termed ‘functional cure’, but it is only rarely achieved with our current antiviral armamentarium 1. HBsAg loss is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. The clinical relevance of occult HBV infection (detectable HBV DNA in the liver with low-level [<200 IU/ml] HBV DNA in blood) is unclear 1. Immunosuppression may lead to HBV reactivation in these patients 1. In the “HBsAg-negative phase” after HBsAg loss, low-level HBV replication may persist with detectable HBV DNA in the liver 1. Generally, HBV DNA is not detectable in the serum, while anti-HBc antibodies with or without anti-HBs are detectable 1. HBsAg loss before the onset of cirrhosis is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. Spontaneous HBsAg seroreversion with reactivation of the inflammatory liver process after HBsAg loss is rare and may occur in patients with a significant impairment of their immune function 1. The main advantage of HBsAg loss is that it allows a safe discontinuation of antiviral therapy 1. As chronic HBV infection cannot be completely eradicated due to the persistence of cccDNA and integrated HBV DNA, it remains unclear whether HBsAg loss adds to the prevention of the long-term complications of chronic HBV infection beyond what can be achieved by the suppression of HBV DNA replication alone 1. HCC may still develop even after spontaneous HBsAg loss (annual rate approximately 0.55%) 1. The risk, however, is lower if HBsAg loss is achieved at a younger age and/or in the absence of significant fibrosis 1. In an Asian cohort followed for 287 patient-years after NA treatment-induced HBsAg seroclearance, only two patients with baseline cirrhosis developed HCC or died (0.7% annual risk), which was a significantly lower rate compared with propensity score-matched patients without HBsAg seroclearance (HR 0.09, p < 0.01) 1. The level of HBV DNA suppression that should be attained in order to achieve these benefits is not well defined, but inferred that the lower, the better 1. Some key points to consider in the management of patients with low anti-HBe antibody levels include:
• The level of HBV replication represents the strongest single predictive biomarker associated with disease progression and the long-term outcome of chronic HBV infection 1.
• The inhibition of viral replication by antiviral treatment has been shown to achieve the elimination of chronic HBV-induced necroinflammatory activity and progressive fibrotic liver processes in the vast majority of patients, in turn reducing the risk of HCC 1.
• Treatment-induced HBeAg loss and seroconversion to anti-HBe characterizes the induction of a partial immune control often leading to a low replicative phase of the chronic HBV infection 1.
• Suppression of HBV DNA to undetectable levels is normally associated with normalization of ALT levels 1.
• Persistence of elevated ALT levels in patients with complete suppression of viral replication is associated with a lower chance of fibrosis regression and can be a reason for histologic disease progression 1. Consultation with a hepatologist or infectious disease specialist is recommended for proper interpretation and management. The goal of therapy for CHB is to eliminate or significantly suppress HBV replication and thus prevent progression of liver disease to cirrhosis, liver failure, or HCC 1. The primary aim of treatment should be to reduce and maintain serum HBV DNA at the lowest possible levels (ie, achieve durable HBV DNA suppression) 1. Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance and can be confidently used as first-line monotherapies 1. The other three NAs may only be used in the treatment of CHB if more potent drugs with high barrier to resistance are not available 1. Treatment strategies include treatment of finite duration with (PEG-)IFN or a NA and long-term treatment with NA(s) 1. Finite-duration treatment with (PEG-)IFN is mainly recommended for HBeAg-positive patients with the best chance of anti-HBe seroconversion 1. Long-term therapy with entecavir or tenofovir can lead to regression of fibrosis and frequently even reversal of cirrhosis and thus change the course of CHB-related liver disease 1. The loss of HBsAg is regarded as the optimal treatment endpoint, termed ‘functional cure’, but it is only rarely achieved with our current antiviral armamentarium 1. HBsAg loss is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. The clinical relevance of occult HBV infection (detectable HBV DNA in the liver with low-level [<200 IU/ml] HBV DNA in blood) is unclear 1. Immunosuppression may lead to HBV reactivation in these patients 1. In the “HBsAg-negative phase” after HBsAg loss, low-level HBV replication may persist with detectable HBV DNA in the liver 1. Generally, HBV DNA is not detectable in the serum, while anti-HBc antibodies with or without anti-HBs are detectable 1. HBsAg loss before the onset of cirrhosis is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. Spontaneous HBsAg seroreversion with reactivation of the inflammatory liver process after HBsAg loss is rare and may occur in patients with a significant impairment of their immune function 1. The main advantage of HBsAg loss is that it allows a safe discontinuation of antiviral therapy 1. As chronic HBV infection cannot be completely eradicated due to the persistence of cccDNA and integrated HBV DNA, it remains unclear whether HBsAg loss adds to the prevention of the long-term complications of chronic HBV infection beyond what can be achieved by the suppression of HBV DNA replication alone 1. HCC may still develop even after spontaneous HBsAg loss (annual rate approximately 0.55%) 1. The risk, however, is lower if HBsAg loss is achieved at a younger age and/or in the absence of significant fibrosis 1. In an Asian cohort followed for 287 patient-years after NA treatment-induced HBsAg seroclearance, only two patients with baseline cirrhosis developed HCC or died (0.7% annual risk), which was a significantly lower rate compared with propensity score-matched patients without HBsAg seroclearance (HR 0.09, p < 0.01) 1. The level of HBV DNA suppression that should be attained in order to achieve these benefits is not well defined, but inferred that the lower, the better 1. Some key points to consider in the management of patients with low anti-HBe antibody levels include:
• The level of HBV replication represents the strongest single predictive biomarker associated with disease progression and the long-term outcome of chronic HBV infection 1.
• The inhibition of viral replication by antiviral treatment has been shown to achieve the elimination of chronic HBV-induced necroinflammatory activity and progressive fibrotic liver processes in the vast majority of patients, in turn reducing the risk of HCC 1.
• Treatment-induced HBeAg loss and seroconversion to anti-HBe characterizes the induction of a partial immune control often leading to a low replicative phase of the chronic HBV infection 1.
• Suppression of HBV DNA to undetectable levels is normally associated with normalization of ALT levels 1.
• Persistence of elevated ALT levels in patients with complete suppression of viral replication is associated with a lower chance of fibrosis regression and can be a reason for histologic disease progression 1. Consultation with a hepatologist or infectious disease specialist is recommended for proper interpretation and management. The goal of therapy for CHB is to eliminate or significantly suppress HBV replication and thus prevent progression of liver disease to cirrhosis, liver failure, or HCC 1. The primary aim of treatment should be to reduce and maintain serum HBV DNA at the lowest possible levels (ie, achieve durable HBV DNA suppression) 1. Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance and can be confidently used as first-line monotherapies 1. The other three NAs may only be used in the treatment of CHB if more potent drugs with high barrier to resistance are not available 1. Treatment strategies include treatment of finite duration with (PEG-)IFN or a NA and long-term treatment with NA(s) 1. Finite-duration treatment with (PEG-)IFN is mainly recommended for HBeAg-positive patients with the best chance of anti-HBe seroconversion 1. Long-term therapy with entecavir or tenofovir can lead to regression of fibrosis and frequently even reversal of cirrhosis and thus change the course of CHB-related liver disease 1. The loss of HBsAg is regarded as the optimal treatment endpoint, termed ‘functional cure’, but it is only rarely achieved with our current antiviral armamentarium 1. HBsAg loss is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. The clinical relevance of occult HBV infection (detectable HBV DNA in the liver with low-level [<200 IU/ml] HBV DNA in blood) is unclear 1. Immunosuppression may lead to HBV reactivation in these patients 1. In the “HBsAg-negative phase” after HBsAg loss, low-level HBV replication may persist with detectable HBV DNA in the liver 1. Generally, HBV DNA is not detectable in the serum, while anti-HBc antibodies with or without anti-HBs are detectable 1. HBsAg loss before the onset of cirrhosis is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. Spontaneous HBsAg seroreversion with reactivation of the inflammatory liver process after HBsAg loss is rare and may occur in patients with a significant impairment of their immune function 1. The main advantage of HBsAg loss is that it allows a safe discontinuation of antiviral therapy 1. As chronic HBV infection cannot be completely eradicated due to the persistence of cccDNA and integrated HBV DNA, it remains unclear whether HBsAg loss adds to the prevention of the long-term complications of chronic HBV infection beyond what can be achieved by the suppression of HBV DNA replication alone 1. HCC may still develop even after spontaneous HBsAg loss (annual rate approximately 0.55%) 1. The risk, however, is lower if HBsAg loss is achieved at a younger age and/or in the absence of significant fibrosis 1. In an Asian cohort followed for 287 patient-years after NA treatment-induced HBsAg seroclearance, only two patients with baseline cirrhosis developed HCC or died (0.7% annual risk), which was a significantly lower rate compared with propensity score-matched patients without HBsAg seroclearance (HR 0.09, p < 0.01) 1. The level of HBV DNA suppression that should be attained in order to achieve these benefits is not well defined, but inferred that the lower, the better 1. Some key points to consider in the management of patients with low anti-HBe antibody levels include:
• The level of HBV replication represents the strongest single predictive biomarker associated with disease progression and the long-term outcome of chronic HBV infection 1.
• The inhibition of viral replication by antiviral treatment has been shown to achieve the elimination of chronic HBV-induced necroinflammatory activity and progressive fibrotic liver processes in the vast majority of patients, in turn reducing the risk of HCC 1.
• Treatment-induced HBeAg loss and seroconversion to anti-HBe characterizes the induction of a partial immune control often leading to a low replicative phase of the chronic HBV infection 1.
• Suppression of HBV DNA to undetectable levels is normally associated with normalization of ALT levels 1.
• Persistence of elevated ALT levels in patients with complete suppression of viral replication is associated with a lower chance of fibrosis regression and can be a reason for histologic disease progression 1. Consultation with a hepatologist or infectious disease specialist is recommended for proper interpretation and management. The goal of therapy for CHB is to eliminate or significantly suppress HBV replication and thus prevent progression of liver disease to cirrhosis, liver failure, or HCC 1. The primary aim of treatment should be to reduce and maintain serum HBV DNA at the lowest possible levels (ie, achieve durable HBV DNA suppression) 1. Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance and can be confidently used as first-line monotherapies 1. The other three NAs may only be used in the treatment of CHB if more potent drugs with high barrier to resistance are not available 1. Treatment strategies include treatment of finite duration with (PEG-)IFN or a NA and long-term treatment with NA(s) 1. Finite-duration treatment with (PEG-)IFN is mainly recommended for HBeAg-positive patients with the best chance of anti-HBe seroconversion 1. Long-term therapy with entecavir or tenofovir can lead to regression of fibrosis and frequently even reversal of cirrhosis and thus change the course of CHB-related liver disease 1. The loss of HBsAg is regarded as the optimal treatment endpoint, termed ‘functional cure’, but it is only rarely achieved with our current antiviral armamentarium 1. HBsAg loss is associated with improvement of the outcome with reduced risk of cirrhosis, decompensation, and HCC 1. The clinical relevance of occult HBV infection (detectable HBV DNA in the liver with low-level [<200 IU/ml] HBV DNA in blood) is unclear 1. Immunosuppression may lead to HBV reactivation in these patients 1. In the “HBsAg

From the Research

Low Anti-HBe Antibody

• Low levels of anti-HBe antibody may be associated with a lower likelihood of HBeAg seroconversion in patients with HBeAg-positive chronic hepatitis B after antiviral treatment 2, 3.
• Studies have shown that baseline serum anti-HBc level is a promising indicator for predicting HBeAg seroconversion in HBeAg-positive CHB patients after antiviral treatment 2.
• Patients with HBeAg seroconversion were associated with a higher level of HBcAb at baseline, compared with those without HBeAg seroconversion 3.
• The area under the receiver operating characteristic curve of baseline HBcAb for HBeAg seroconversion was 0.71, indicating a significant predictive value 3.

Association with Liver Inflammation

• Serum anti-HBc levels are associated with liver inflammation in chronic hepatitis B patients, and high serum anti-HBc is an independent risk factor of significant liver inflammation 4.
• The area under the receiver operating characteristic curve of serum anti-HBc in predicting significant liver inflammation was 0.769, with an optimal cut-off value of 10.87 S/CO 4.

Antibody Responses

• Antibody responses during hepatitis B viral infection play a crucial role in determining whether the infection is cleared or becomes chronic 5.
• High anti-HBV antibody levels, as in vaccinated individuals, can achieve viral clearance when the rate of synthesis of hepatitis B subviral particles is slow or when anti-HBV antibody production is fast 5.
• Anti-HBs responses are present and fluctuate over time in patients with HBeAg+ chronic hepatitis B, and key anti-HBs profiles associated with either functional cure or failure to achieve functional cure have been identified 6.