This variability has resulted, in addition to quasi species in every infected subject, in seven viral genotypes (denoted 1 to 7) and more than 67 subtypes (denoted alphabetically a, b, c, etc.).4 The majority of infections are caused by genotypes 1a, 1b, 2, 3 (almost exclusively 3a) and 4, while infections with genotypes 5, 6 and 7 are less frequent or limited to specific geographic areas.1,5 The viral genotype has been determinant in the therapeutic guidelines of chronic HCV infection with pegylated-interferon plus ribavirin6 and with first-generation protease inhibitors.7,8 Although its usefulness has been greatly reduced by the introduction of new pangenotypic oral treatments,911 genotype determination remains crucial due to the marked geographical differences in the genotypic profiles which may be affected by migration trends and by changes in the routes of infection.1,5,1216 At the end of World War II there was an explosive spread of genotype 1b infections associated with the mass implementation of blood transfusions and unsafe health practices in Western countries.15 Almost simultaneously there were a significant spread of genotype 1a linked to unsafe health practices and the rapid expansion of intravenous drug use (IDU).15 These changes paralleled with a marked increase in genotype 3a infection from the Asian continent associated with the heroin trade and IDU16 and migratory movements of certain populations.17 The spread of genotype 4, endemic in the Middle East, Egypt and Central Africa, to Europe has had different epidemiological settings

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Normal Rates of Whole-Body Fat Oxidation and Gluconeogenesis after Overnight Fasting and Moderate-Intensity Exercise in Patients with Medium-Chain Acyl-CoA Dehydrogenase Deficiency. Journal of Inherited Metabolic Disease , vol
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