Whether hepatitis B (HBV) coinfection affects outcome in HIV-1-infected patients remains unclear.
To assess the prevalence of HBV (assessed as HBsAg) coinfection and its possible impact on progression to AIDS, all-cause deaths, liver-related deaths and response to highly active antiretroviral therapy (HAART) in the EuroSIDA cohort.
Data on 9802 patients in 72 European HIV centres were analysed. Incidence rates of AIDS, global mortality and liver-related mortality, time to 25% CD4 cell count increase and time to viral load < 400 copies/ml after starting HAART were calculated and compared between HBsAg-positive and HBsAg-negative patients.
HBsAg was found in 498 (8.7%) patients. The incidence of new AIDS diagnosis was similar in HBsAg-positive and HBsAg-negative patients (3.3 and 3.4/100 person-years, respectively) even after adjustment for potential confounders: the incidence rate ratio (IRR) was 0.94 [95% confidence interval (CI), 0.74-1.19; P = 0.61]. The incidences of all-cause and liver-related mortalities were significantly higher in HBsAg-positive subjects (3.7 and 0.7/100 person-years, respectively) compared with HBsAg-negative subjects (2.6 and 0.2/100 person-years, respectively). The adjusted IRR values were 1.53 for global (95% CI, 1.23-1.90; P = 0.0001) and 3.58 for liver-related (95% CI, 2.09-6.16; P < 0.0001) mortality. HBsAg status did not influence viral or immunological responses among the 1679 patients starting HAART.
The prevalence of HBV coinfection was 9% in the EuroSIDA cohort. Chronic HBV infection significantly increased liver-related mortality in HIV-1-infected patients but did not impact on progression to AIDS or on viral and immunological responses to HAART.
"Because Human Immunodeficiency Virus (HIV) and hepatitis B virus (HBV) share similar routes of transmission, HIV/HBV coinfection rate is considerable (6.3-9.7%). This coinfection is associated with higher HBV viremia, HBV reactivation, chronic HBV infection, cirrhosis and eight fold increase in liver-related mortality. "
[Show abstract][Hide abstract] ABSTRACT: Purpose:
Hepatitis B virus (HBV) vaccination is recommended for all human immunodeficiency virus (HIV)-infected patients without HBV immunity. However, serological response to standard HBV vaccination is frequently suboptimal in this population and the appropriate strategy for revaccination of HIV-infected nonresponders remained controversial. We aimed to determine the serological response to one booster dose of HBV vaccine given by intradermal (ID) or intramuscular (IM) route in HIV-positive nonresponders to standard HBV vaccination.
Materials and Methods:
In this study, 42 HIV-infected nonresponders were enrolled. We randomized them to receive either 10 μg (0.5 mL) for ID (20 cases) or 20 μg (1 mL) for IM (22 cases) administration of HBV vaccine as a one booster dose. After 1 month, anti-HBs titer was checked in all cases. A protective antibody response (seroconversion) defined as an anti-HBs titer ≥10 IU/L.
Seroconversion was observed in 47.6% of subjects after 1 ID dose. A total of 30% showed antibody titers above 100 IU/L. Except one case, all responders had CD4+ >200 cells/mm3. Mean anti-HBs titer was 146.5 ± 246 IU/L. After the one IM booster dose, seroconversion was observed in 50% of cases. A total of 36.3% of subjects had anti-HBs ≥100 IU/L. All responders had CD4+ >200 cells/mm3, except one case. Mean anti-HBs titer was 416.4 ± 765.6 IU/L. Responders showed significantly higher CD4+ cell counts, in comparison to nonresponders (P < 0.001).
One booster dose administered IM or ID to HIV-infected nonresponders resulted in similar rates of seroconversion, overall response rate 50%. However, higher anti-HBs titers observed more frequently in IM group.
Perspectives in clinical research 07/2014; 5(3):134-8. DOI:10.4103/2229-3485.134318
"To our knowledge, the association between HBV infection and SCR has not been previously observed. Some studies have found no significant difference in the virologic and immunologic responses to HAART by hepatitis B co-infection status [1,13]. One study found that HIV and HBV co-infected patients had lower CD4 T cell count at ART initiation, and HBeAg positivity status decreased the likelihood of achieving undetectable HIV load after 24 weeks of ART . "
[Show abstract][Hide abstract] ABSTRACT: Background
A subset of HIV-1 infected patients starting highly active antiretroviral treatment (HAART) experience suboptimal CD4 response (SCR) despite virologic suppression. We studied the rate of and risk factors for SCR among women starting HAART in the ACTG A5208 study conducted in 7 African countries. 741 HAART-naive women with screening CD4 count <200 cells/μL were randomized to start HAART with Tenofovir/Emtricitabine plus either Nevirapine or Lopinavir/Ritonavir.
This analysis includes the 625 women who remained on-study through 48 weeks without experiencing protocol-defined virologic failure. We defined SCR as < 100 CD4 cells/μL increase from baseline and absolute CD4 cell count < 350 cells/μL, both at 48 weeks after HAART initiation.
The baseline characteristics for the 625 women prior to HAART initiation were: median age 33 years, screening CD4 count 134 cells/μL, and HIV-1 RNA 5.1 log10 copies/mL; 184 (29%) were WHO Stage 3 or 4.
Seventy one (11%) of these 625 women experienced SCR. Baseline factors independently associated with increased odds of SCR included older age, lower HIV-1 RNA, positive Hepatitis B surface antigen, and site location. At 96 weeks, only 6% of the SCR group had CD4 ≥ 350 cells/μL compared with 67% in the non SCR group.
After starting HAART, 11% of women with virologic suppression through 48 weeks experienced SCR. These patients were also less likely to achieve CD4 ≥ 350 cells/μL by 96 weeks. The underlying causes and long term clinical implications of SCR deserve further investigation.
Clinicaltrials.gov Identifier: NCT00089505
"Disease progression to cirrhosis in HIV positive patients is almost three-times faster as compared to HIV negative patients456. Most of the studies678 in HIV-HBV and HIV-HCV co-infected patients have been conducted among western patient populations. Understanding HBV and HCV co-infection with HIV is particularly important in Asian countries due to high background prevalence of HBV and HCV9. "
[Show abstract][Hide abstract] ABSTRACT: Background & objectives:
Co-infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) in human immunodeficiency virus (HIV) infected individuals results in increased hepatic complications. We undertook this study to evaluate the presence of HBV and HCV in HIV infected individuals attending a tertiary care centre in southern India.
A total of 120 cases with HIV infection and 120 healthy adult control subjects were included in the study. Samples were tested for hepatitis B surface antigen (HBsAg) and anti-HCV antibodies by enzyme linked immunosorbent assay (ELISA) method. HBsAg and anti-HCV positive serum samples were further tested for the presence of hepatitis B e antigen (HBeAg), anti-HBe antibodies, HBV-DNA and HCV-RNA.
The most common mode of transmission was sexual promiscuity (79%), followed by spouse positivity (15%) and history of blood transfusion (6%). HBsAg and anti-HCV were positive in 18 (15%) and 10 (8.3%) HIV infected patients; the corresponding figures in healthy controls being 2 (1.6%) 0 (0%) (P<0.0001). Among HIV infected patients, presence of HBeAg and anti-HBe antibodies was seen in 33.3 and 55.5 per cent, respectively; both HBeAg and anti-HBe antibodies were negative in 11.1 per cent. HBV DNA and HCV RNA were positive in 10 of 18 and in all anti-HCV positive samples. Triple infection with HBV, HCV and HIV was seen in three patients. CD4+ T-lymphocyte count less than 200/μl was seen in 22 of 28 co-infected cases.
Interpretation & conclusions:
The findings of our study showed presence of HBV (15%) and HCV (8.3%) co-infections in HIV positive patients which was higher than that seen in HIV negative controls. Co-infection with HBV and HCV is a common problem in HIV infected patients in India. Hence, all HIV patients need to be routinely tested for markers of HBV and HCV infection.
The Indian Journal of Medical Research 12/2013; 138(6):950-4. · 1.40 Impact Factor
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