Effect Of HCV Mono-infection And HCV/HIV Co-infection On HCV-specific Antibody And Serum Zinc And Iron

BackgroundAcute hepatitis C virus (HCV) infection is primarily followed by chronichepatitis C infection (CHC) and spontaneous recovery of HCV infection (SR-HCV)occurs in a minority of infected population. HCV is also found as a commonco-infecting pathogen in HIV/AIDS patients as these two viruses share similar riskfactors for transmission. Identification of SR-HCV clinically depends on twocombined experimental indicators, persistent undetectable peripheral HCV RNA andreactive result of anti-HCV assay. However, the characteristics of dynamic variationof plasma anti-HCV antibodies in SR-HCV, especially in those patients coinfectedwith HIV, are still undefined. Despite the belief that HCV infection can be cured byconsistent optimization of therapeutic regimens containing PEG-IFN/Ribavirin,Thismay be due to different genotypes,older ages and single-nucleotide polymorphisms(SNPs) in the IL28B genes; however, dysregulated iron and Zn homeostasis may beanother reason. Few study examined the status of trace elements in the patients withHCV/HIV coinfection, it is important to clarify the distribution characteristics of traceelements.ObjectiveHere we investigated the variation of characteristics of anti-HCV in hepatitis Cpatients with or without HIV infection.And analyze the characteristics of serumzinc,iron and iron-related indictor in different infection of HCV.MethodThis study followed a cohort containing both HCV and HCV/HIV individualsmainly infected through unsanitary commercial blood collection practices. Thecharacteristics of anti-HCV decay in SR-HCV were analyzed. Additionally, theoverall time of anti-HCV from starting point of resolving the infection to undetectablelevels were predicted in SR-HCV individuals with or without HIV infection.Indicators of zinc and iron status were analyzed and compared across the threegroups.Results1.The annual decreasing rate of anti-HCV is gradually accelerating in SR-HCV subjects. The decay of anti-HCV was accelerated by HIV-related impairment ofimmune function. However, the variation in decline of anti-HCV presented a slowlyaccelerated process within the early decrease stage and a gradually deceleratedprocess within the latter decrease stage. We deduced it expended approximately20years from natural HCV recovery to undetectable anti-HCV antibodies in HCVresolvers, while this time was significantly shortened by HIV coinfection。2.The results showed that serum levels of iron and ferritin and the Tfs weresignificantly higher in HCV-monoinfected patients than in the healthy controls;however, there were no differences in iron levels and Tfs between HCV/HIVcoinfected patients and healthy controls. Additionally, although serum hepcidin levelsin HCV-monoinfected and HCV/HIV-1-coinfected patients were lower than those inhealth controls, the levels in coinfected patients were higher than those inHCV-monoinfected patients. Serum iron and ferritin levels in HCV-monoinfectedpatients were positively correlated with serum ALT/AST. serum transferrin levelswere negatively correlated with ALT/AST levels but not with serum hepcidin levels.The levels of iron in the serum of coinfected patients with a CD4+T-cell count<500/μl were lower than those in patients with a CD4+T-cell count≥500/μl, whereasserum hepcidin levels showed the opposite trend.Conclusions1.HIV coinfection accelerates decay of humoral responses in spontaneousresolvers of HCV infection. The prevalence of HCV infection may be severelyunderestimated in the large-scale retrospective epidemiologic investigation inHIV-infected population.2. HCV infection induce deficiency of serum zinc and HCV/HIV co-infectionaggravates the decrease of serum zinc concentration. Significant correlation wasfound between the levels of zinc and albumin in HCV mono-infected patients. Inaddition, the deficiency of serum zinc is associated with the immunocompromisedcondition in HCV/HIV coinfection. These data indicate that HIV coinfection canalleviates the iron accumulation caused by persistent HCV infection to some extent.