Background: Hepatitis C is one of the common types of viral hepatitis that threatens human life worldwide. Hepatitis C virus (HCV) is a single-strand RNA virus that has the ability to be transmitted by contaminated blood products and intravenous drug use. HCV is characterized by its ability to have a high genetic diversity, which eventually results in different HCV genotypes and numerous subtypes; however, this genetic variety is a core reason for the lack of a successful vaccine for these types of viruses. Methods: HCV nucleic acid was isolated from 597 patients diagnosed with chronic hepatitis C in Security Forces Hospital (SFHR) in Riyadh. HCV nucleic acid was extracted to make the target accessible for amplification and genotype detection. The process of nucleic acid extraction and amplification was accomplished with the Abbott Molecular Systems m2000sp and m2000rt using the Abbott RealTime HCV Genotype II. Results: The findings in this study illustrated a major prevalence of genotype 4 (60% of cases). The study also showed a large number of patients (27%) identified as HCV genotype 1. Furthermore, the HCV genotype 1 testing detected subtypes 1a and 1b in a number of patients. It was also demonstrated that a limited number of hepatitis C patients had mixed genotypes and undermined genotypes. Conclusion: The study has confirmed that HCV genotype 4 has a high prevalence when compared to the rest of the identified genotypes. Furthermore, the majority of identified genotypes and subtypes were found to be linked with age more than 50 years, which might indicate an association of HCV genotype detection with age.

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Chronic myeloid leukemia (CML) is considered a common blood cancers and accounts for approximately 15–20% of the total cases of leukemia. Recent studies indicated that above 95% of patients suffering of CML have been found with a distinctive Philadelphia chromosome that originates from a mutual translocation between both arms of chromosomes 9 and 22. During this mutation the translocation of the ABL gene located on chromosome 9 get transferred to the breakpoint cluster region (BCR) of chromosome 22 as an effect of a joined BCR-ABL gene. Furthermore, BCR-ABL oncogene is characteristically found in CML, causing cells to divide uncontrollably and inducing severe consequences among CML patients. In line with this, applying quantification technique of the BCR-ABL gene using molecular approaches is crucial for patient controlling, initiation of the proper treatment, measurement of response to therapy, and prediction of relapse. Of greater significance, molecular assay and monitoring of the BCR-ABL gene in CML using quantitative RT-PCR provides physicians with essential diagnostic and prognostic information.

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