Here, our main focus was the effect of HCV/HIV-1 coinfection on iron status. We found that coinfected patients had significantly lower levels of serum iron and a lower Tfs than HCVmonoinfected patients; however, there were no differences between HCV/HIV-1-coinfected patients and healthy individuals. Even though the levels of serum hepcidin were lower in HCVmonoinfected and HCV/HIV-1-coinfected patients than in healthy individuals, the levels were higher in HCV/HIV-1coinfected patients than in HCV-monoinfected patients. HIV infects CD4+ helper T-cells, macrophages, and dendritic cells, all of which play vital roles in the immune response. Macrophages also play an important role in iron homeostasis by recycling around 30 mg of iron per day, which is 20�C30-fold greater than the amount absorbed from food. If macrophages are compromised by HIV, much of the iron may accumulate within the cells and is not released into the serum, resulting in reduced serum iron levels in infected patients. This is consistent with our data showing that the RBC was lower in coinfected patients than in monoinfected patients. The reason for this reduction in the RBC is complicated, and may involve the drugs taken by HIV-infected patients. For example, it is known that for infants, anemia prevalence and serum ferritin level decrease after HAART Cinoxacin without routine iron supplementation. All of HIV-infected patients in our study had received zidovudine-containing HAART treatment, either regularly or intermittently. The decreased iron load in HIVinfected patients may be caused by both of 
HIV per se and HAART therapy. Despite the belief that HCV infection can be cured by consistent optimization of therapeutic regimens containing PEG-IFN/ Ribavirin, a certain proportion of chronically-infected patients do not respond to treatment. This may be due to different genotypes and single-nucleotide polymorphismsin the IL28B genes; however, dysregulated iron homeostasis may be another reason. Evidence suggests that excess iron exerts toxic and fibrogenic effects via pathways involving the production of oxyradicals and oxidative stress; indeed, several studies show that removing excess iron through therapeutic phlebotomy reduces the severity of hepatic inflammation associated with Riociguat BAY 63-2521 chronic HCV infection. Accordingly, determining the status of serum iron and other iron-associated parameters, will be helpful to understand the complexity of alternations in iron distribution in HCVinfected patients, particularly those coinfected with HIV-1. In the last decade it has become possible to annotate a greater number of lncRNA transcripts. Consequently the study of them has gained much significance as many of them have been linked with epigenetic, transcriptional and post-transcriptional regulation of gene expression. Despite having generally a lower level of concentration than protein coding transcripts, lncRNAs exhibit more tissue specific expressions. A vast set of lncRNA transcripts are differentially expressed during development where many of them play critical roles. LncRNAs are now known to have a major involvement in cancer. Though, till now, a majority of the lncRNAs have been linked with epigenetic modulation of gene expressions, they can also regulate gene expression by transcriptional or post transcriptional modes. LncRNAs can influence post-transcriptional regulation by interfering with the miRNA pathways, by acting as competing endogenous RNAs.