Hepatitis C virus (HCV) isHepatitis C virus (HCV) is a leading cause of chronic liver disease, which affects around 170 million people worldwide. Infections are initially acute, and in many cases the symptoms are mild. However, around 80% of patients eventually develop a persistent chronic infection which can result in steatosis, fibrosis, cirrhosis, liver failure, and, in some cases, hepatocellular carcinoma. The main treatments currently available for chronically infected patients use a combination of pegylated alpha interferon and ribavirin, but these still result in a sustained antiviral response in only about 50% of genotype 1 infections (4). Consequently, more effective antivirals that target either the virus proteins directly or the host cell proteins required during HCV replication are currently being developed. In order to ensure that successful antivirals are generated, it is important that all aspects of the HCV life cycle and HCV-associated pathology are well understood.One way in which the different host processes that are an essential part of the HCV replication cycle can be studied is to investigate the effect that HCV infection has on cellular gene expression. RNA microarray hybridization is routinely used to investigate host gene expression and allows the entire transcriptomic profile of the cell to be characterized. Microarray analysis of HCV-infected cells can provide an insight into the genes involved in host cell antiviral responses, genes that are essential for the HCV replication cycle, and genes that contribute to HCV-associated liver pathology. Microarray expression profiling has already been used to study host gene expression in cells transfected with RNA encoding either individual HCV genes, HCV subgenomic replicons, or the full-length HCV genome. These studies have demonstrated that the replication of the HCV genome results in the regulation of a small number of host genes involved in lipid metabolism, cellular immunity, proliferation, apoptosis, and molecular transport (2,5,15,32). These studies have provided interesting insights into the HCV replication cycle. However, the biological significance of gene expression patterns identified is less clear, since the full virus replication cycle, including the processes of viral entry, assembly, and exit, does not take place.The recent discovery of JFH-1, a genotype 2a HCV clone that can undergo a complete infection cycle in cell culture, provides the opportunity to characterize the true effect of HCV infection on host gene expression (51). A recent study investigated the effects that a J6/JFH-1 chimera had on the gene expression profile of Huh7.5 cells during a time course infection with time points of 24, 48, 72, 96, and 120 h (53). The number of host genes regulated during infection was much higher than that previously observed for cells permitting only genome replication, indicating that the full replication cycle has additional effects on host gene expression.In this study, we present the results from an investigation
BackgroundChronic renal failure (CRF) leads in the majority of instances to end stage renal disease (ESRD) requiring renal replacement therapy. Our interest was to evaluate the possible associations of HLA class I and class II antigens with ESRD independent of other factors, in Saudi Arabia population.MethodologyA retrospective study to determine the HLA class I and class II polymorphisms and their association with ESRD, was performed on 350 patients with ESRD, and 105 healthy unrelated control. Patients and control groups were typed by SSOP lumenix techniques. The alleles positively associated to the ESRD were: HLA-B*15, B*18, B*49 - DRB1*03, negatively associated alleles were A*26, HLA-B*39, B*50. The haplotypes positively associated with ESRD were: HLA-A*01-DRB1*13 and HLA-A*30-DRBI*03. The negatively associated haplotypes were: HLA-A*02-B*39, A*02-B*50, A*24-B*35, A*24-B*58, A*24-DRB1*16, A*68-DRB1*04, A*02-DQB1*03, A*29-DQB1*02, A*29-DOB1*05 and B*27-DRB1*07 and the last one is the most significant protective haplotypes.ConclusionThe high Relative Risk (RR) observed and its statistical correlation reflect the strength of the described association between HLA antigens and ESRD.
There is an affiliation missing for the first author. Nuha Mahmoud Hamdi should also be affiliated with:
This study aimed to determine the persistence of induced immunity against hepatitis B virus (HBV) among adults routinely vaccinated during their infancy and correlate the level of induced immunity with participant characteristics. MethodologyThis was a cross-sectional study conducted among visitors to primary care centers of the Ministry of Health (MOH) in Riyadh, the Kingdom of Saudi Arabia (KSA) during the period from August 2020 to January 2021. The study population included healthy adults of both genders who had received full doses of the HBV vaccine in infancy. Data related to participant characteristics were collected using a self-administered questionnaire. A blood sample was then taken from each participant to measure the serum level of hepatitis B surface antigen (HBsAg), antibodies against HBsAg (anti-HBs), and antibodies against hepatitis B core antigen (ani-HBc). ResultsA total of 400 subjects participated in the study; the mean age of the cohort was 25 years. Almost all of them were Saudis (99.30%), and more than half (57.50%) were males. Only 24.30% had an anti-HBs antibodies level of ≥10 IU/L, and all respondents were negative for HBs antigen. No significant association between participant characteristics and anti-HBs antibody levels was found. ConclusionA decline in immunity many years after HBV vaccinations taken in infancy has been well-documented. However, for low-risk populations, the boosting of HBV vaccines is probably unnecessary since the immune memory provides sufficient protection despite low or undetectable anti-HBs antibodies.
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