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  • Furthermore the absolute lack of E allele expression in both


    Furthermore, the absolute lack of E2 allele expression in both chronic and SVR cases, supports the protective role of the E2 allele against HCV infection at a time of exposure. However this hypothesis could not be entirely proved by this study due to lack of healthy individuals participation. Similarly, Price et al., 2006 found a lack of E2/E2 genotype among patients who are HCV antibody positive, assuming that the E2/E2 genotype may grant a relative resistance for stabilizing HCV infection in exposed individuals [22]. Sheridan et al., 2009, also hypothesize that the E2 allele may protect against viral infection by means of defective engagement of HCV to the cellular receptors such as LDL receptors [25]. In Dp44mT to these findings, no differences in apoE allele frequencies between the HCV RNA-positive group and the HCV RNA-negative individuals while studying the impact of apoE genotype on the outcome of HCV infection among both HCV patients with chronic infection or cleared infection by Wozniak et al., 2002 [26]. Nevertheless, the same study revealed significantly lower E4 allele frequencies in patients with severe versus mild inflammation when they examined the apoE genotype impact on the severity of HCV-induced liver damage [26]. Interactions between chronic hepatitis C virus infection and lipid metabolism have been described in some studies. A higher prevalence of hypocholesterolemia and low LDL levels in HCV-infected patients was reported in many studies [27], [28]. This study revealed that patients with chronic HCV had significantly lower total cholesterol and LDL serum levels compared to the group with SVR (P-value < .001, for both). The intrahepatic cholesterol synthesis might be impaired due to HCV replication through two possible pathways; first, decreasing the availability of a substantial intermediate (geranylpyrophosphate) for synthesis of cholesterol, Second, cholesterol could be utilized for intracellular membranes synthesis during viral replication. Both mechanisms results in a negative feedback on the amount of cholesterol available for physiologic intracellular processes and for peripheral delivery via VLDL, consequently serum cholesterol levels will be decreased. Also, the decrease of serum LDL levels in HCV infection might occur due to reduction of available intracellular cholesterol that may also increase LDL receptors resulting in increased intrahepatic LDL with subsequent reduction of serum LDL level [29]. Although no statistically significant difference could be elucidated between the Apo E genotypes concerning cholesterol and LDL serum levels, yet their levels was lower in E3 allele carriers the which confreres chronicity. Similar results were also obtained by Marzouk et al., 2007, Corey et al., 2009 and Nashaat et al., 2010 [29], [30], [31]. Also, no statistically significant differences between the two groups as regards HDL, VLDL and triglyceride levels could be demonstrated which agree with Corey et al., 2009 [30], but disagree with Marzouk et al., 2007 & Perlemuter et al., 2002 who found a drop in these levels among chronic HCV infected patients [29], [32]. These results shed new light on the exploitation of the functional major role of ApoE in the production of LVP, presumably by direct interaction with viral envelope glycoproteins. Lee et al., 2014 suggested that ApoE acts at a belated step of assembly, such as particle maturation and infectivity, where ApoE depletion affected neither the formation of nucleocapsids nor their envelopment [33]. Further characterization of the LVP have shown that HCV-LVP binding, hepatocyte cell lines entry and upregulation of the LDL receptors with consequent increases their internalization could be blocked by anti-apolipoprotein E [34].
    Acknowledgment The fund of this study was offered by the Science and Technology Development Fund (STDF), Egypt, Grant No. 1530.
    Background Chronic hepatitis C virus (HCV) infection is a significant threat to global public health. Worldwide, 71 million people are estimated to be affected [1], and the progressive liver damage that can ensue has severe consequences including cirrhosis, liver failure and hepatocellular carcinoma [2,3]. The landscape of chronic hepatitis C changed dramatically with the introduction of oral, direct acting antiviral (DAA) drugs. These regimens are well tolerated, can be administered for short duration, and are highly effective, producing cure (sustained virologic response, “SVR”) in >95% of treated individuals, across almost all HCV genotypes [[4], [5], [6]]. DAA’s have provided the medical rationale for the implementation of expanded, birth cohort-based HCV screening recommendations, because chronically infected individuals can now be effectively treated with relative ease.