HIV infected patients with chronic hepatitis B should be counseled for liver . countries) showed association between HBV co-infection and lower CD4 cell count. PDF | Introduction Human Immunodeficiency Virus (HIV) and Conclusion Hepatitis B virus infection is infrequent among PLWHIV in this setting. .. association between risk factors and HBV infection is shown in Table. 2. Impact of co infection on the natural history of HBV and HIV infection in homosexual men and its relation to prior human immunodeficiency.
Compensatory And Vaccine Escape Mutations Top of page The in vitro characterization of viral mutations has demonstrated the emergence of compensatory mutations that enhance the reduced viral replication of primary resistance mutations.
Compensatory mutations in regions distant from the HBV polymerase active site can result in conformational changes that can affect the cross-sensitivity profile of several antiviral agents and confer potential multidrug resistance Bartholomeusz, Due to the overlapping reading frames of the genes encoding HBV polymerase and HBsAg, mutations in one gene may affect the other.
The frequency of this mutation increases with duration of 3TC treatment. This and other mutations, known as vaccine escape mutations, create antigenically altered HBsAg proteins and demonstrate markedly reduced binding to anti-HBs Torresi, These mutations may also affect the ability of current assays to detect HBsAg and compromise the ability to diagnose HBV so-called diagnostic escape mutants.
This might be one underlying explanation of occult HBV infection. HBV infection is a dynamic disease and coinfection with HIV considerably complicates its diagnosis and management. Combination therapy should be used to avoid development of antiviral resistance. Continuous monitoring of HBV patients, regardless of need for treatment or history of seroconversion, is imperative to recognize reactivation and subsequent need for treatment, and to identify drug resistance and viral breakthrough early.
Prompt changes in therapy when resistance emerges will reduce the development of compensatory mutations that will affect our ability to use newer therapies and lead to transmission of drug-resistant viruses in vaccinated individuals.
In many respects, the treatment of HBV is a step behind HIV which has embraced combination therapy with a variety of drug targets. Unfortunately only nucleos t ide analogs are as yet available for HBV but much has been learned from the lessons of HIV treatment. The complexities of HBV-HIV coinfection highlight the importance of close working relationships between hepatologists, infectious disease specialists and primary-care providers in order to optimize patient outcomes.
Resistance to adefovir dipivoxil therapy associated with the selection of a novel mutation in the HBV polymerase. Mechanistic basis for hepatitis B virus resistance to acyclic nucleoside phosphonate analogues, adefovir and tenofovir [abstract]. Long-term incidence of hepatitis B virus resistance to lamivudine in human immunodeficiency virus-infected patients.
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Hepatitis B and HIV Coinfection
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Virology And Clinical Management of Hepatitis B And HIV Coinfection
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Management of antiviral resistance in patients with chronic hepatitis B.
Long-term safety of lamivudine treatment in patients with chronic hepatitis B. Most children infected at birth or during early childhood will be immune tolerant and remain in the immune tolerant phase for years or even decades; however, most eventually will progress to immune active disease. Given the lack of immune response to HBV, treatment is not recommended during this period, but individuals should be monitored for transition to immune active disease as well as for hepatic fibrosis and hepatocellular carcinoma HCC as they age.
Because of the high level of HBV viremia, this is a highly infectious phase. This phase is characterized by elevated liver enzymes and liver inflammation on biopsy. Despite the lower levels of HBV viremia, eAg-negative hepatitis can be difficult to treat, usually requiring indefinite treatment with nucleoside therapy, rarely transitions to inactive carrier phase, and is associated with a high risk of progression to fibrosis.
In addition, eAg-negative disease is characterized by ongoing liver inflammation and, in most cases, elevated transaminases. However, given the nature of the long-lived cccDNA that resides in hepatocytes during HBV infection, it may be more appropriate to think of these individuals as immunologically controlled because, in rare cases, HBV disease can reactivate in the setting of severe immunosuppression.
The interpretations of acute and chronic hepatitis serologies are summarized in Table 1. That indicates one of the following scenarios: However, as even low levels of HBV viremia may increase the risk of liver disease, 29 these individuals may be at higher risk of hepatic disease and many experts recommend managing these patients as chronically HBV infected.
Loss of sAb can occur over time, particularly with immunosuppressed patients. Individuals who do not respond to a booster of HBV vaccination may have a false-positive HBcAb result or may have an impaired antibody response to prior infection.
Vaccination with a full series is recommended. Sex partners, household members, children with close physical contact, and those who share injection drug equipment with the patient should be screened for HBV and vaccinated if they are not actively infected see " Immunization ," below.
As with HIV prevention, condom use with sex and avoidance of shared needles and other equipment for injection drug use are recommended measures for reducing the risk of HBV transmission. It is important to note that significant liver fibrosis may be present in persons with normal transaminases. Pegylated interferon IFN is an option in this scenario, but there are limited efficacy and safety data in HIV coinfection, and long-term treatment with IFN is not feasible because of toxicity and poor tolerability.
Once 3TC resistance has developed, HBV medications such as telbivudine will no longer have activity against HBV, and agents such as entecavir may be less efficacious and more prone to development of HBV resistance.