HIV Outcomes in HBV Coinfected Individuals on HAART
Hepatitis B virus (HBV) is more common in HIV-infected individuals than in the general population because of similar routes of transmission for viral acquisition. Current evidence suggests that HIV infection has an adverse impact on HBV-related liver disease progression, with an increase in HBV replication, reduction in the rate of clearance of serum hepatitis B e antigen, and increased risk of cirrhosis, liver-related mortality, and hepatocellular carcinoma at lower CD4 T-cell counts. Coinfection rates are estimated between 5% and 10%, with up to 40% of immunocompromised patients developing chronic infection.
Clinical studies before the general availability of highly active antiretroviral therapy (HAART) evaluating the impact of HB on HIV progression have been mixed. Some studies found no differences in HIV progression between those with and without chronic HB, whereas other studies have shown that chronic HB may negatively impact HIV progression with a significant increased risk of AIDS or death.
Studies evaluating the influence of HIV-HBV coinfection on HIV RNA suppression, immunologic CD4 cell count recovery, and clinical outcomes in individuals on HAART have been limited and conflicting, with several studies finding no difference. Several studies from HBV-endemic countries have also found no difference on HIV outcomes. Law et al showed a smaller early increase in CD4 response after HAART initiation (HI), however, this was not sustained. Hawkins et al showed that coinfected compared with monoinfected individuals had significantly lower CD4 counts throughout the period of recovery. Other studies have shown that coinfected individuals are less likely to achieve virologic suppression (VS) as compared with HIV-monoinfected individuals. Recent studies have for the most part failed to show a substantial impact of HBV coinfection on immunologic or HIV virologic responses to antiretroviral therapy (ART). Idoko et al, however, found a lower proportion of HBeAg-positive individuals achieving HIV VS at 24 weeks as compared with HBeAg-negative or HIV-monoinfected individuals, but the findings were not seen at 48 weeks. One recent study evaluating HIV outcomes during the first 3 years of ART found impaired CD4 cell recovery in hepatitis B surface antigen (HsAg)-positive and anti-HBc patients as compared with HBV-uninfected patients. Heterogeneity of available data warrants further evaluation of this key question.
Limitations and heterogeneity of results from other studies may be attributed to the small number of individuals analyzed, defining patients with chronic HB sometimes with only 1 positive test for HBsAg, or limited follow-up after HI. We sought to evaluate the impact of HBV infection in HIV-coinfected HAART recipients in a large cohort with known and limited duration of HIV infection, free access to health care, racial diversity, minimal injection drug use (IDU), and long-term follow-up.
Hepatitis B virus (HBV) is more common in HIV-infected individuals than in the general population because of similar routes of transmission for viral acquisition. Current evidence suggests that HIV infection has an adverse impact on HBV-related liver disease progression, with an increase in HBV replication, reduction in the rate of clearance of serum hepatitis B e antigen, and increased risk of cirrhosis, liver-related mortality, and hepatocellular carcinoma at lower CD4 T-cell counts. Coinfection rates are estimated between 5% and 10%, with up to 40% of immunocompromised patients developing chronic infection.
Clinical studies before the general availability of highly active antiretroviral therapy (HAART) evaluating the impact of HB on HIV progression have been mixed. Some studies found no differences in HIV progression between those with and without chronic HB, whereas other studies have shown that chronic HB may negatively impact HIV progression with a significant increased risk of AIDS or death.
Studies evaluating the influence of HIV-HBV coinfection on HIV RNA suppression, immunologic CD4 cell count recovery, and clinical outcomes in individuals on HAART have been limited and conflicting, with several studies finding no difference. Several studies from HBV-endemic countries have also found no difference on HIV outcomes. Law et al showed a smaller early increase in CD4 response after HAART initiation (HI), however, this was not sustained. Hawkins et al showed that coinfected compared with monoinfected individuals had significantly lower CD4 counts throughout the period of recovery. Other studies have shown that coinfected individuals are less likely to achieve virologic suppression (VS) as compared with HIV-monoinfected individuals. Recent studies have for the most part failed to show a substantial impact of HBV coinfection on immunologic or HIV virologic responses to antiretroviral therapy (ART). Idoko et al, however, found a lower proportion of HBeAg-positive individuals achieving HIV VS at 24 weeks as compared with HBeAg-negative or HIV-monoinfected individuals, but the findings were not seen at 48 weeks. One recent study evaluating HIV outcomes during the first 3 years of ART found impaired CD4 cell recovery in hepatitis B surface antigen (HsAg)-positive and anti-HBc patients as compared with HBV-uninfected patients. Heterogeneity of available data warrants further evaluation of this key question.
Limitations and heterogeneity of results from other studies may be attributed to the small number of individuals analyzed, defining patients with chronic HB sometimes with only 1 positive test for HBsAg, or limited follow-up after HI. We sought to evaluate the impact of HBV infection in HIV-coinfected HAART recipients in a large cohort with known and limited duration of HIV infection, free access to health care, racial diversity, minimal injection drug use (IDU), and long-term follow-up.
Abstract and Introduction
Introduction
Hepatitis B virus (HBV) is more common in HIV-infected individuals than in the general population because of similar routes of transmission for viral acquisition. Current evidence suggests that HIV infection has an adverse impact on HBV-related liver disease progression, with an increase in HBV replication, reduction in the rate of clearance of serum hepatitis B e antigen, and increased risk of cirrhosis, liver-related mortality, and hepatocellular carcinoma at lower CD4 T-cell counts. Coinfection rates are estimated between 5% and 10%, with up to 40% of immunocompromised patients developing chronic infection.
Clinical studies before the general availability of highly active antiretroviral therapy (HAART) evaluating the impact of HB on HIV progression have been mixed. Some studies found no differences in HIV progression between those with and without chronic HB, whereas other studies have shown that chronic HB may negatively impact HIV progression with a significant increased risk of AIDS or death.
Studies evaluating the influence of HIV-HBV coinfection on HIV RNA suppression, immunologic CD4 cell count recovery, and clinical outcomes in individuals on HAART have been limited and conflicting, with several studies finding no difference. Several studies from HBV-endemic countries have also found no difference on HIV outcomes. Law et al showed a smaller early increase in CD4 response after HAART initiation (HI), however, this was not sustained. Hawkins et al showed that coinfected compared with monoinfected individuals had significantly lower CD4 counts throughout the period of recovery. Other studies have shown that coinfected individuals are less likely to achieve virologic suppression (VS) as compared with HIV-monoinfected individuals. Recent studies have for the most part failed to show a substantial impact of HBV coinfection on immunologic or HIV virologic responses to antiretroviral therapy (ART). Idoko et al, however, found a lower proportion of HBeAg-positive individuals achieving HIV VS at 24 weeks as compared with HBeAg-negative or HIV-monoinfected individuals, but the findings were not seen at 48 weeks. One recent study evaluating HIV outcomes during the first 3 years of ART found impaired CD4 cell recovery in hepatitis B surface antigen (HsAg)-positive and anti-HBc patients as compared with HBV-uninfected patients. Heterogeneity of available data warrants further evaluation of this key question.
Limitations and heterogeneity of results from other studies may be attributed to the small number of individuals analyzed, defining patients with chronic HB sometimes with only 1 positive test for HBsAg, or limited follow-up after HI. We sought to evaluate the impact of HBV infection in HIV-coinfected HAART recipients in a large cohort with known and limited duration of HIV infection, free access to health care, racial diversity, minimal injection drug use (IDU), and long-term follow-up.
Introduction
Hepatitis B virus (HBV) is more common in HIV-infected individuals than in the general population because of similar routes of transmission for viral acquisition. Current evidence suggests that HIV infection has an adverse impact on HBV-related liver disease progression, with an increase in HBV replication, reduction in the rate of clearance of serum hepatitis B e antigen, and increased risk of cirrhosis, liver-related mortality, and hepatocellular carcinoma at lower CD4 T-cell counts. Coinfection rates are estimated between 5% and 10%, with up to 40% of immunocompromised patients developing chronic infection.
Clinical studies before the general availability of highly active antiretroviral therapy (HAART) evaluating the impact of HB on HIV progression have been mixed. Some studies found no differences in HIV progression between those with and without chronic HB, whereas other studies have shown that chronic HB may negatively impact HIV progression with a significant increased risk of AIDS or death.
Studies evaluating the influence of HIV-HBV coinfection on HIV RNA suppression, immunologic CD4 cell count recovery, and clinical outcomes in individuals on HAART have been limited and conflicting, with several studies finding no difference. Several studies from HBV-endemic countries have also found no difference on HIV outcomes. Law et al showed a smaller early increase in CD4 response after HAART initiation (HI), however, this was not sustained. Hawkins et al showed that coinfected compared with monoinfected individuals had significantly lower CD4 counts throughout the period of recovery. Other studies have shown that coinfected individuals are less likely to achieve virologic suppression (VS) as compared with HIV-monoinfected individuals. Recent studies have for the most part failed to show a substantial impact of HBV coinfection on immunologic or HIV virologic responses to antiretroviral therapy (ART). Idoko et al, however, found a lower proportion of HBeAg-positive individuals achieving HIV VS at 24 weeks as compared with HBeAg-negative or HIV-monoinfected individuals, but the findings were not seen at 48 weeks. One recent study evaluating HIV outcomes during the first 3 years of ART found impaired CD4 cell recovery in hepatitis B surface antigen (HsAg)-positive and anti-HBc patients as compared with HBV-uninfected patients. Heterogeneity of available data warrants further evaluation of this key question.
Limitations and heterogeneity of results from other studies may be attributed to the small number of individuals analyzed, defining patients with chronic HB sometimes with only 1 positive test for HBsAg, or limited follow-up after HI. We sought to evaluate the impact of HBV infection in HIV-coinfected HAART recipients in a large cohort with known and limited duration of HIV infection, free access to health care, racial diversity, minimal injection drug use (IDU), and long-term follow-up.
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