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Review
. 2022 Feb 3:12:780887.
doi: 10.3389/fmicb.2021.780887. eCollection 2021.

Insights Into the Coinfections of Human Immunodeficiency Virus-Hepatitis B Virus, Human Immunodeficiency Virus-Hepatitis C Virus, and Hepatitis B Virus-Hepatitis C Virus: Prevalence, Risk Factors, Pathogenesis, Diagnosis, and Treatment

Affiliations
Review

Insights Into the Coinfections of Human Immunodeficiency Virus-Hepatitis B Virus, Human Immunodeficiency Virus-Hepatitis C Virus, and Hepatitis B Virus-Hepatitis C Virus: Prevalence, Risk Factors, Pathogenesis, Diagnosis, and Treatment

Sagarika Shahriar et al. Front Microbiol. .

Erratum in

Abstract

Human immunodeficiency virus, hepatitis B virus, and hepatitis C virus are three blood-borne viruses that can cause major global health issues by increasing severe morbidity. There is a high risk of coinfection with these viruses in individuals because of their same transmission routes through blood using shared needles, syringes, other injection equipment, sexual transmission, or even vertical transmission. Coinfection can cause various liver-related illnesses, non-hepatic organ dysfunction, followed by death compared to any of these single infections. The treatment of coinfected patients is complicated due to the side effects of antiviral medication, resulting in drug resistance, hepatotoxicity, and a lack of required responses. On the other hand, coinfected individuals must be treated with multiple drugs simultaneously, such as for HIV either along with HBV or HCV and HBV and HCV. Therefore, diagnosing, treating, and controlling dual infections with HIV, HBV, or HCV is complicated and needs further investigation. This review focuses on the current prevalence, risk factors, and pathogenesis of dual infections with HIV, HBV, and HCV. We also briefly overviewed the diagnosis and treatment of coinfections of these three blood-borne viruses.

Keywords: HBV; HCV; HIV; coinfection; pathogenesis; prevalence; risk factors.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
After HIV GP120 binds with the receptors on the CD4 cell surface, the viral particle fuses with the membrane and enters the cell. The HIV genome ssRNA is reverse transcribed into the dsDNA using reverse transcriptase. The viral DNA is then integrated with the host cell DNA using integrase. The various structural and non-structural proteins are produced from the integrated DNA, and then viral particles are assembled and released from the cell.
FIGURE 2
FIGURE 2
Hepatitis B virus particle binds with the NTCP receptor, fuses with the membrane, and enters the host cell. The rcDNA is converted into cccDNA, transcribed into pgRNA, and finally packaged into the capsid. The capsid is enveloped by the ER-Golgi/MVB and released into the extracellular space.
FIGURE 3
FIGURE 3
Hepatitis C virus particle binds with the CD81 receptor, fuses with the membrane, and enters the host cell. Upon entering, the ssRNA(+) is translated by ribosomal machinery and produces both structural and non-structural proteins, which assemble and mature in the Golgi body and are then released into extracellular space.
FIGURE 4
FIGURE 4
Major risk factors and consequences of HIV, HBV, and HCV coinfection.

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