Viral hepatitis and HIV co-infection

Soriano, Vincent; Vispo, Eugenia; Labarga, Pablo; Medrano, José; Barreiro, Pablo

doi:10.1016/j.antiviral.2009.10.021

Cited by 177 publications

(149 citation statements)

References 96 publications

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“…More than two billion people have been infected with HBV worldwide, and 350 to 400 million people are chronic carriers 1 . It is estimated that nearly 600,000 people die annually from complications related to hepatitis B 2 Coinfection with HBV and HIV is commonly observed because these viruses share common routes of transmission 5,6 . The prevalence of HBV/HIV coinfection refl ects geographical variations 7 , and the predominant routes of HBV transmission often correlate with the degree of endemicity.…”

mentioning

confidence: 99%

The prevalence of hepatitis B virus infection markers and socio-demographic risk factors in HIV-infected patients in Southern Brazil

Martins

Livramento

Andrigueti

et al. 2014

Rev. Soc. Bras. Med. Trop.

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confidence: 99%

The prevalence of hepatitis B virus infection markers and socio-demographic risk factors in HIV-infected patients in Southern Brazil

Martins

Livramento

Andrigueti

et al. 2014

Rev. Soc. Bras. Med. Trop.

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“…In addition, intravenous drug use (IVDU) also plays a significant role in transmission based on sharing of contaminated needles, and other injection paraphernalia [1] as well as risky sexual behavior [14]. Globally, based on the 35 million people infected with HIV-1, it is estimated that approximately 7 million people suffer from chronic HCV infection, which is about 20% of the HIV-1-infected population [15]. Alarmingly, HIV-1-infected individuals are at an increased risk of dying due to coinfection with chronic HCV in addition to other acquired immunodeficiency syndrome (AIDS)-related complications.…”

Section: Introductionmentioning

confidence: 99%

“…It has been shown that treatment of chronic HCV can lead to reduced hepatotoxicity [28] and regression of the drawbacks such as liver fibrosis [15,29,30]. While HCV genotype and viral load can influence the response to HCV therapy, extent of hepatic fibrosis and CD4 counts are most indicative of the individuals that should be receiving HCV therapy [15]. HCV therapy is usually initiated in individuals who have more than 200-350 CD4 + T cells/mm3.…”

Section: Introductionmentioning

confidence: 99%

“…HCV therapy is usually initiated in individuals who have more than 200-350 CD4 + T cells/mm3. However, in individuals who are on HAART and with CD4 + T-cell counts below 200 cells/mm3, treating HCV is a challenging task, since there are other factors such as, severity of liver disease, extent of HIV suppression and time since being termed as being HCV-positive, that have to be taken into consideration [15,31]. Thus, it is evident that within co-infected individuals, treatment options are varied as compared to individuals with HCV mono-infection.…”

Section: Introductionmentioning

confidence: 99%

“…It is crucial to treat chronic HCV in HIV-1 and HCV coinfected individuals, due to the rapid progression to end-stage liver disease within these individuals [15,26]and reduced tolerance of antiretroviral agents which is associated with greater hepatotoxicity [1,27]. It has been shown that treatment of chronic HCV can lead to reduced hepatotoxicity [28] and regression of the drawbacks such as liver fibrosis [15,29,30].…”

Section: Introductionmentioning

confidence: 99%

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Coinfection with Hepatitis C Virus among HIV-1-Infected Individuals Increases Proinflammatory Cytokines and HIV-1 Disease Severity

Wigdahl¹

2016

MOJI

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Submit Manuscript | http://medcraveonline.com infection that is spontaneously cleared [3].However, in cases of HIV-1 and HCV coinfection, the number of chronic HCV infections rises to 90% [4]. The result of any viral infection depends on the interplay between the activation of host cellular factors to the infection and the viral mechanisms that counteract them [5]. HCV is responsible for activating antiviral interferon (IFN)-α/β expression, but irrespective of the expression of these cytokines, HCV can still replicate within the liver [6]. This could be due to the fact that the nonstructural proteins, nonstructural protein (NS)3 and NS5A, and the structural protein E2 can block the expression as well as transcription of IFN-α/β genes. Also, the NS5A protein induces expression of interleukin (IL)-8, associated with IFN-α inhibition [7] HCV can also block the antiviral action of natural killer (NK) and NKT cells thus hindering the expression of IFN-γ (an antiviral cytokine) due to the interaction between E2 and NK-cell CD81 molecule [8]. The production of cytokines by dendritic cells (DCs) is particularly affected by chronic HCV infection and there are contradictory reports concerning the expression of Th1 cytokines, with some studies suggesting that a Th1 response is suppressed [9] and some studies suggesting a progressive liver injury during chronic HCV has been associated with an increase in the Th1 responseassociated cytokines [10]. In this regard, HCV CD4 + T cells also play an important role in providing an adaptive response by activating cytotoxic and humoral responses. This can involve the secretion AbstractHIV-1, along with hepatitis B and C viruses (HBV and HCV), are known to share similar routes of transmission, including intravenous drug use, blood transfusions, sexual intercourse, and perinatal exposure. Thus, coinfection with HIV-1 and HBV or HCV is common. HIV-1 impacts the natural course of HBV and HCV infection by accelerating the progression of HBV/HCV-associated liver disease toward endstage cirrhosis and quantitative depletion of the CD4+ T-cell compartment. HBV or HCV coinfection with HIV-1 has also been associated with increased mortality when compared to either infection alone. In particular, we focus on the impact of coinfection with HCV on the HIV-1 pathogenic process in patients in the Drexel Medicine CNS AIDS Research and Eradication Study (CARES) Cohort. Comparing HIV-1 mono-infection with HIV-1/HCV coinfection allows defining the detrimental effect of HCV coinfection as it relates to viral pathogenesis, disease progression, and the associated immune response during the course of this complex interplay, in the background of drug abuse, which is an important risk factor to both HIV-1 and HCV infection and on HIV-1 disease severity. The uniqueness of this study includes the fact that the patients are part of a cohort of HIV-1-infected individuals whose drug histories have been recorded longitudinally.

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Sofosbuvir and Ribavirin for Hepatitis C in Patients With HIV Coinfection

Sulkowski

Naggie

Lalezari

et al. 2014

JAMA

245

180

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Importance Treatment of hepatitis C virus (HCV) infection in HIV-1 co-infected patients has been limited due to the use of interferon and drug interactions with antiretroviral therapies (ART). Objective To determine the rates of HCV eradication (sustained virologic response, SVR) and adverse events in HCV/HIV-1 co-infected patients receiving sofosbuvir and ribavirin treatment. Design Multicenter, open-label, non-randomized, uncontrolled phase 3 trial (PHOTON-1) conducted in the United States and Puerto Rico from August 2012 until November 2013 evaluating treatment with sofosbuvir and ribavirin. Setting Thirty-four academic, private practice, and community health centers with a median of 6 patients (range 1–17) enrolled at each site. Participants Patients with HCV genotypes 1, 2, or 3 and concurrent HIV-1 were eligible. Patients were required to be receiving antiretroviral treatment with an HIV-1 RNA <50 copies/mL and a CD4 T-cell count of >200 cells/mm3 or have untreated HIV-1infection with a CD4 T-cell count of >500 cells/mm3. In total, 223 participants (114 treatment-naïve participants with HCV genotype 1, 68 treatment-naïve participants with HCV genotype 2 or 3, and 41 peginterferon/ribavirin treatment-experienced participants with HCV genotype 2 or 3) were enrolled. Interventions Participants received sofosbuvir (400 mg) and weight-based ribavirin for 12 weeks (for treatment-naïve patients with HCV genotype 2 or 3) or for 24 weeks (for treatment-naïve patients with HCV genotype 1 or treatment-experienced patients with HCV genotype 2 or 3). Main Outcome and Measure The primary study outcome was proportion of patients with SVR (serum HCV <25 copies/mL) 12 weeks after cessation of HCV therapy (SVR12). Results Among treatment-naïve participants, SVR12 rates were 76% (95% confidence interval [CI], 67–84) for genotype 1 infection, 88% (95% CI, 70–98) for genotype 2 infection, and 67% (95% CI, 51–80) for genotype 3 infection. Among treatment-experienced participants, SVR12 was 92% (95% CI, 73–99) for genotype 2 infection and 94% (95% CI, 71–100) for genotype 3 infection. The most common adverse events were fatigue, insomnia, headache, and nausea. Seven patients (3%) discontinued HCV treatment due to adverse events. No adverse effect on HIV disease or its treatment was observed. Conclusions and Relevance In this open-label, nonrandomized, uncontrolled phase 3 study, HIV-1-infected patients coinfected with HCV genotype 1, 2, or 3 who received the oral, interferon-free combination of sofosbuvir and ribavirin for 12 or 24 weeks had high rates of sustained virologic response 12 weeks after cessation of therapy. Further studies of this oral regimen in diverse populations of coinfected patients are warranted. Trial Registration clinicaltrials.gov Identifier: NCT01667731

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Viral hepatitis and HIV co-infection

Cited by 177 publications

References 96 publications

The prevalence of hepatitis B virus infection markers and socio-demographic risk factors in HIV-infected patients in Southern Brazil

The prevalence of hepatitis B virus infection markers and socio-demographic risk factors in HIV-infected patients in Southern Brazil

Coinfection with Hepatitis C Virus among HIV-1-Infected Individuals Increases Proinflammatory Cytokines and HIV-1 Disease Severity

Sofosbuvir and Ribavirin for Hepatitis C in Patients With HIV Coinfection

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