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Management of HBV/HIV Co-Infection

Review Article | DOI: https://doi.org/10.31579/2834-5029/016

Management of HBV/HIV Co-Infection

  • Rehan Haider *

Riggs pharmaceutical, Department of Pharmacy, University of Karachi, Pakistan.

*Corresponding Author: Rehan Haider, Riggs pharmaceutical, Department of Pharmacy, University of Karachi, Pakistan.

Citation: Haider R., (2023), Management of HBV/HIV Co-Infection, International Journal of Biomed Research, 2(2): DOI:10.31579/2834-5029/016

Copyright: © 2023, Rehan Haider, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: 15 March 2023 | Accepted: 28 March 2023 | Published: 04 April 2023

Keywords: liver/hepatitis; antiretroviral therapy; antiviral therapy; pathogenesis; reverse transcriptase inhibitors

Abstract

The prevalence and transmission routes of HBV co-infection in the HIV+ population vary substantially by geographic region. In the United States and Europe, the majority of HIV-positive gay men have evidence of past HBV infection, and 5–10% show persistence of HBs antigen, with or without replicative hepatitis B as defined by the presence of HBV DNA. Overall, rates of HBV/HIV co-infection are slightly lower among intravenous drug users compared to gay men and much lower among people infected through heterosexual contact. In endemic regions of Africa and Asia, the majority of HBV infections are transmitted vertically at birth or before the age of 5 through close contact within households, medical procedures, and traditional scarification. The prevalence among youth in most Asian countries has substantially decreased since the introduction of vaccination on a nationwide scale. In Europe, vaccination of children and members of risk groups is promoted and reimbursed by health care systems in most countries. The natural history of hepatitis B is altered by simultaneous infection with HIV. Immune control of HBV is negatively affected, leading to a reduction in HBs-antigen seroconversion. If HBV persists, the HBV DNA levels are generally higher in HIV-positive patients not on antiretroviral therapy. In addition, with the progression of cellular immune deficiency, reactivation of HBV replication despite previous HBs-antigen seroconversion may occur. However, after immune recovery due to antiretroviral therapy, He-antigen and HBs-antigen seroconversion occurs in a higher proportion of patients compared to HBV mono infected patients treated for chronic hepatitis B. In untreated HIV infection, faster progression to liver cirrhosis is reported for HBV/HIV-co-infected patients Moreover, hepatocellular carcinoma may develop at an earlier age and is more aggressive in this population.

Introduction

Being HBV-coinfected results in increased mortality for HIV-positive individuals, even after the introduction of effective antiretroviral therapy (ART), as demonstrated by an analysis of the Euro SIDA Study, which shows a 3.6-fold higher risk of liver-related deaths among HBsAg-positive patients compared to HBsAg negative individuals (Konopnicki 2005, Nikolopoulos 2009) [16] (Figure 1). In the Multicenter AIDS Cohort Study (MACS), an 8-fold increased risk of liver-related mortality was seen among HBV/HIV co-infected compared to HIV-mono infected individuals, particularly among subjects with low nadir CD4+ cell counts. Even at present, despite the widespread use of tenofovir, HBV/HIV coinfection is still associated with increased morbidity (Crowell 2014) [18], and liver-related deaths in HBV/HIV-infected patients still do occur (Rosenthal 2014) [19].The beneficial impact of treatment of HBV in HBV/HIV coinfection was first demonstrated by data from a large cohort showing a reduction in mortality with lamivudine treatment compared to untreated patients (Puoti 2004, Brau 2007)This result is even more remarkable because lamivudine is the least effective HBV polymerase inhibitor due to the rapid development of drug resistance. In general, because of its limited long-term efficacy, lamivudine monotherapy cannot be considered an appropriate therapy for either mono HBV infection or HBV/HIV coinfection.

Figure 1: Association of HBV/HIV coinfection and mortality (Konopnicki 2005). More than one cause of death allowed per patient; p-values from chi-squared tests.

In addition, two large cohort studies (EuroSIDA and MACS) plus data from HBV mono-infection studies showing a reduction in morbidity and mortality established the need to treat chronic hepatitis B in HBV/HIV-co-infected patients.

Treatment of chronic hepatitis B in HBV/HIV-co-infected patients on antiretroviral therapy

In the well-known, beginning hepatitis B therapy depends on the diploma of liver fibrosis and the HBV DNA level. however, as the artwork is now encouraged for all HIV sufferers unbiased of CD4-be counted to reduce HIV-associated morbidity and mortality and to prevent HIV transmission, all HBV/HIV-co-infected patients are considered eligible for art with the aid of cutting-edge hints (e.g., every 2016). The previous complicated recommendations for a way to deal with continual hepatitis B in patients without artwork are obsolete. As antiretroviral capsules which can be additionally lively towards HBV can commonly be used, interferon-based total treatment of HBV is now not often indicated. statistics within the literature for HIV-co-infected patients on interferon therapy for HBV infection are restrained and no longer very encouraging. In addition, intensified treatment research combining pegylated interferon with adefovir or intensifying TDF therapy with pegylated interferon for 12 months confirmed no boom in HBV seroconversion quotes (Ingiliz 2008. In widespread, tenofovir is the usual care for HBV in HIV-co-infected patients, because of its strong HBV polymerase hobby and antiretroviral efficacy. Tenofovir has been a protracted-acting and effective therapy in the giant majority of dealt with HBV/HIV-co-infected patients (van Bömmel 2004, Mathews 2009, Martin-Carbonero 2011, Thibaut, its antiviral efficacy isn’t impaired in HBV/HIV-coinfected as compared to HBV-mono infected sufferers. No conclusive pattern of resistance mutations has been recognized in research or cohorts (Snow-Lampart 2011). [28] These data are nonetheless legitimate at the cease of 2016. In idea, resistance might also arise in sufferers on lengthy-time period therapy, as with some other antivirals. For patients with HBV DNA <2000>

The potentially nephrotoxic effect of TDF is a concern. Although nephrotoxicity is rarely observed in HIV-negative patients treated with TDF monotherapy renal impairment has been more frequently reported in HIV-positive patients using TDF as a component in ART and may be associated in particular with the combined use of TDF and ritonavir-boosted HIV protease inhibitors (Mauss 2005, Fux 2007, Goicoechea 2008, In addition, the recently approved cytochrome P450 3A inhibitor cobicistat can also increase creatinine levels. Regular monitoring of renal function in HBV/HIV-co-infected patients, including estimated glomerular filtration rate (eGFR) and assessment of proteinuria, is necessary. In the case of a reduced eGFR, TDF should be substituted by TAF or should be dosed at a reduced frequency according to the label. In the case of significant proteinuria, TDF should also be replaced by TAF. Alternatively, in specific situations in the case of tenofovir-associated nephrotoxicity, tenofovir can also be replaced by entecavir.

Conclusion

The number of available HBV polymerase inhibitors for chronic hepatitis B has increased substantially over the last few years. In general, the choice is confined to two mostly non-cross-resistant classes, the nucleotide, and nucleoside compounds HBV/HIV co-infected patients, ART is indicated to treat both infections simultaneously. The HBV treatment of choice is tenofovir. Due to the rapid development of resistance when HBV is not fully suppressed HBV monotherapy with either lamivudine or emtricitabine should not generally be considered. A combination of tenofovir plus lamivudine or emtricitabine as a primary combination therapy has theoretical advantages over tenofovir alone, but studies supporting this concept have not been published to date. However, as tenofovir is combined with emtricitabine or lamivudine in most antiretroviral regimens today. This seems to be a more theoretical argument and not reflected by reality. In general, the treatment of HBV as a viral disease follows the same rules as HIV therapy, aiming at full suppression of the replication of the virus to avoid the development of resistance. Successful viral suppression of hepatitis B results in the inhibition of necro-inflammatory activity, reversion of fibrosis, and most importantly a decrease in the incidence of hepatic decompensation and hepatocellular carcinoma.

Acknowledgment

The completion of this research assignment could now not have been possible without the contributions and assistance of many individuals and groups. We're. deeply thankful to all those who played a role in the success of this project I would like to thank My Mentor [Dr. Naweed Imam Syed Prof branch of mobile Biology at the University of Calgary for their useful input and guidance for the duration of the research system. Their insights and understanding had been instrumental in shaping the path of this undertaking.

Authors' Contribution

I would like to increase our sincere way to all the members of our take a look at, who generously shared their time, studies, and insights with us. Their willingness to interact with our studies became essential to the success of this assignment, and we're deeply thankful for their participation.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Conflict of Interest

The authors declare no conflict-of-interest.

References

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