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Active replication of hepatitis B virus (HBV) in HIV type 1 and in HIV type 2 infected patients
M F Barros1, J Piedade, G Nunes
1Serviço de Imunologia, Faculdade de Ciências Médicas, Universidade Nova de Lisboa (UNL), Portugal.
Insights
Concurrent human immunodeficiency virus (HIV) infection does not correlate with hepatitis B virus (HBV) active replication. HIV-infected individuals may maintain sufficient immunity to prevent HBV reactivation or reinfection.
Area of Science:
- Virology
- Immunology
- Public Health
Background:
- Concurrent infections with human immunodeficiency virus (HIV) and hepatitis B virus (HBV) are common globally.
- Understanding the impact of HIV on HBV status is crucial for managing co-infected individuals and informing public health strategies.
Purpose of the Study:
- To evaluate the effect of concurrent HIV infection on HBV infection and immunity.
- To assess the prevalence of HBV active replication in HIV-positive individuals compared to HIV-negative controls.
Main Methods:
- Serological markers of HBV infection and HBV DNA in serum were monitored in 66 HIV-1 positive Caucasian patients and 38 HIV-2 positive asymptomatic African individuals.
- HIV-positive groups were compared with age, sex, and ethnologically matched seronegative controls.
- HBV DNA presence in serum was used as an indicator of active hepatitis B virus replication.
Main Results:
- No significant correlation was found between HIV infection and HBV active replication.
- HBV DNA was detected in 7.6% of HIV-1+ Caucasian patients and 3.2% of seronegative controls.
- In African HIV-2+ individuals, 2.6% were HBV DNA positive, similar to HIV-2 seronegative controls (2.9%).
Conclusions:
- HIV infection does not appear to increase the risk of HBV active replication.
- The immune system, even in symptomatic HIV infection, may retain sufficient function to prevent HBV reactivation or reinfection.
- Findings are relevant for developing preventive strategies in populations at risk for both HIV and HBV.
Abstract:
To evaluate the effect of concurrent infection by HIV on HBV infection or immunity, we have studied a group of 66 HIV1+ symptomatic Caucasian patients and another of 38 African HIV2+ asymptomatic individuals, concerning their HBV status: serological markers of infection and presence of HBV-DNA in serum, the last taken as sign of hepatitis B virus active replication, were monitored. HIV+ groups were compared with seronegative controls, adequately matched for age, sex and ethnological background. HBV DNA was found in 7.6% of HIV1+ Caucasian patients and 3.2% of seronegative controls; in African HIV2+ individuals 2.6% were also HBV DNA+, a percentage close to that found in HIV2 seronegative controls (2.9%). No correlation was found between HIV infection and HBV active replication. Immunodepression that follows HIV infection over time may be compatible with a degree of T cell function capable of avoiding reinfection with or reactivation of HBV, even in symptomatic stages of acquired immunodeficiency syndrome. Our findings are relevant to the choice of preventive strategies in populations at risk for HIV and HBV infection.