Abstract:We assessed the effect of co-infection by hepatitis C virus (HCV) on immunological and virological response at 48 weeks from initiation of antiretroviral therapy (ART).We included patients from the Cohort of Spanish HIV Research Network (CoRIS) starting ART between January 2004 and November 2014, had at least 1 CD4 T-cell count and viral load measurements both in the previous 6 months and at 48 (±12) weeks from ART initiation, and HCV serology before ART initiation. We used linear regression for mean differenc… Show more
“…As estimated, up to 25% of HIV- infected population in the United States are also co-infected with HCV[8]. Co-infection with HCV and HIV has been associated with a faster progression of hepatitis and a higher liver-related mortality even in the era of antiretroviral therapy (ART)[9,10]. The exact role of HCV-infection in the natural history of HIV-infection is not clear.…”
“…As reported, while HCV infection is not associated with an increase in AIDS-related events or deaths, co-infected individuals may have lower CD4 + T cell counts as compared to HIV-mono-infected patients[11,12]. In contrast, HIV co-infection produces numerous adverse effects by increasing replication of HCV[13], slowing down the HCV clearance, enhancing fibrogenesis[14] and decreasing the response to direct acting antiviral (DAA) treatment[10], ultimately increasing liver dysfunction and incidence of death. Eyster et al[15] compared the levels of HCV RNA before and after HIV-seroconversion in HCV-infected patients and reported that HCV RNA levels were enhanced 8-fold in patients co-infected with HIV compared to HCV mono-infected.…”
Hepatotropic viruses induced hepatitis progresses much faster and causes more liver- related health problems in people co-infected with human immunodeficiency virus (HIV). Although treatment with antiretroviral therapy has extended the life expectancy of people with HIV, liver disease induced by hepatitis B virus (HBV) and hepatitis C virus (HCV) causes significant numbers of non-acquired immune deficiency syndrome (AIDS)-related deaths in co-infected patients. In recent years, new insights into the mechanisms of accelerated fibrosis and liver disease progression in HIV/HCV and HIV/HBV co-infections have been reported. In this paper, we review recent studies examining the natural history and pathogenesis of liver disease in HIV-HCV/HBV co-infection in the era of direct acting antivirals (DAA) and antiretroviral therapy (ART). We also review the novel therapeutics for management of HIV/HCV and HIV/HBV co-infected individuals.
“…As estimated, up to 25% of HIV- infected population in the United States are also co-infected with HCV[8]. Co-infection with HCV and HIV has been associated with a faster progression of hepatitis and a higher liver-related mortality even in the era of antiretroviral therapy (ART)[9,10]. The exact role of HCV-infection in the natural history of HIV-infection is not clear.…”
“…As reported, while HCV infection is not associated with an increase in AIDS-related events or deaths, co-infected individuals may have lower CD4 + T cell counts as compared to HIV-mono-infected patients[11,12]. In contrast, HIV co-infection produces numerous adverse effects by increasing replication of HCV[13], slowing down the HCV clearance, enhancing fibrogenesis[14] and decreasing the response to direct acting antiviral (DAA) treatment[10], ultimately increasing liver dysfunction and incidence of death. Eyster et al[15] compared the levels of HCV RNA before and after HIV-seroconversion in HCV-infected patients and reported that HCV RNA levels were enhanced 8-fold in patients co-infected with HIV compared to HCV mono-infected.…”
Hepatotropic viruses induced hepatitis progresses much faster and causes more liver- related health problems in people co-infected with human immunodeficiency virus (HIV). Although treatment with antiretroviral therapy has extended the life expectancy of people with HIV, liver disease induced by hepatitis B virus (HBV) and hepatitis C virus (HCV) causes significant numbers of non-acquired immune deficiency syndrome (AIDS)-related deaths in co-infected patients. In recent years, new insights into the mechanisms of accelerated fibrosis and liver disease progression in HIV/HCV and HIV/HBV co-infections have been reported. In this paper, we review recent studies examining the natural history and pathogenesis of liver disease in HIV-HCV/HBV co-infection in the era of direct acting antivirals (DAA) and antiretroviral therapy (ART). We also review the novel therapeutics for management of HIV/HCV and HIV/HBV co-infected individuals.
“…In addition, HCV treatment in PLWH is less effective [23,39]. The role of HCV as a co-factor in HIV disease progression remains controversial, but some studies have found lower absolute CD4+ cell counts and reduced immunological and virological responses after ART initiation [32,40,41].…”
Background Coinfections of HIV patients with hepatitis B virus (HBV) and hepatitis C virus (HCV) are mayor public health problems, contributing to the emerging burden of HIV-associated hepatic mortality. Coinfection rates vary geographically, depending on various factors such as predominant transmission modes, HBV vaccination rates, and prevalence of HBV and HCV in the general population. In South America, the epidemiology of coinfections is uncertain, since systematic studies are scarce. Our study aimed to analyze rates of HBV and HCV infection in people living with HIV attending centers of the public and private health system in Chile. Methods We performed a cross-sectional study including a public university hospital and a private health center in Santiago, Metropolitan Region in Chile. Serum samples were used to determine serological markers of hepatitis B (HBsAg, anti-HBs, anti-HBc total, HBeAg, anti-HBe) and anti-HCV. Demographic, clinical and laboratory data were obtained from medical records. Results 399 patients were included (353 from public, 46 from private health center). Most (92.8%) were male, with a median age of 38.3 years; 99.4% acquired HIV through sexual contact
“…With the extended life expectancy offered by combined antiretroviral therapy, this patient subpopulation is at increased risk of long-term complications from HCV-associated chronic liver disease, including cirrhosis and hepatocellular carcinoma. The development of direct-acting antiviral agents (DAAs) has dramatically improved the treatment options for HCV, and a sustained virological response (SVR) in HIV/HCV coinfected patients is achieved at rates similar to those of HCV monoinfected patients [ 3 , 4 , 5 ]. However, outside of clinical trials, the population of HIV/HCV coinfected patients may have risk factors that, by themselves or in combination, may lead to lower SVR [ 6 ].…”
Resistance-associated substitutions (RASs) may exist prior to treatment and contribute to the failure of treatment with direct-acting antivirals (DAAs). As the major site of HCV replication, naturally occurring variants with RASs may segregate into the liver. In the present study, we performed viral population sequencing to retrospectively investigate the NS3 and NS5A RAS profiles in 34 HIV/HCV coinfected patients naïve to anti-HCV treatment who underwent diagnostic liver biopsy between 2000 and 2006 and had liver and plasma samples available. Sixteen were infected by HCV genotype (GT) 1a, 11 by GT3a, and 7 by GT4d. The analysis of the NS3 domain in GT1a showed a difference in strain between the liver and plasma in three cases, with a preponderance of specific RASs in the liver compartment. In GT4d samples, 6/7 coupled liver and plasma samples were concordant with no RASs. Sequence analysis of the NS5A domain showed the presence of RASs in the livers of 2/16 patients harboring GT1a but not in the corresponding plasma. In GT4d, NS5A RASs were detected in 7/7 liver tissues and 5/7 plasma samples. NS3 domain and NS5A domain were found to be conserved in plasma and livers of patients infected with GT3a. Thus, RASs within GT1a and GT4d more likely segregate into the liver and may explain the emergence of resistant strains during DAA treatment.
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