ABSTRACT
This study aimed to investigate relationship of the HCV genome structure and treatment with Pegylated Interferonα/Ribavirin (peg-IFNα/RBV) Egyptian patient. Mutations in two sites of HCV genome; the internal ribosome entry site(IRES) and the interferon sensitivity determining region (ISDR) of HCV genotype 4a were studied in details including DNAsequences and mutations detection in response to treatment. Ninety patients, responders and non-responders, to treatmentwith peg-IFN α /RBV were included in this study. IRES and ISDR regions were amplified by RT-PCR using specific designedprimers, and amplified regions were sequenced. The data obtained were aligned with published sequences in GenBank usingBLAST program. Results of this study have revealed that there are different mutations in the studied sequences in both ISDRand IRES regions. The predicted amino acids sequences in the ISDR region showed significant differences ranging from oneup to more than eight mutations in the HCV Genome sequences. Although there was a significant difference betweensequences of HCV RNA isolated from responders and non-responders, these data were not able to give an absolute answerwhether response to interferon therapy is directly/relates to the structure of the HCV genome
ABSTRACT
SEN virus [SENV] has been tentatively linked to transfusion-associated non A-E hepatitis. The aim of the present study was to determine the prevalence of SENV among Egyptian patients with HCV-related chronic liver disease [CLD] and haemodialysis [HD] patients and to assess the clinical effect of SENV infection on coexistent hepatitis C either in the severity or the probability of developing hepatocellular carcinoma [HCC]. Polymerase chain reaction [PCR] was used to detect SENV-D and SENV-H DNA in serum samples of 74 HCV-related CLD patients, 45 uraemic patients on maintenance HD and 28 healthy controls. SENV DNA was detected in 13.5%, 11.1%, and 7.1% of CLD, HD patients and healthy controls respectively with no significant differences between patients and control group. No statistically significant differences were demonstrated between SENV infected and non infected CLD or haemodialysis patients regarding the clinical and biochemical parameters. SENV infection was significantly higher in CLD patients with HCC [33.3%] than without [8.5%] [p<0.05]. In conclusion, SENV does not seem to be a common infection in Egyptian patients. It has no apparent influence on the severity of co-existent HCV related CLD but it could be a risk factor for developing HCC in these patients. Further studies are needed to define the aetiopathogenic role of SENV infection in HCC development