%0 Journal Article
%T Quantitative analysis of interferon alpha receptor subunit 1 and suppressor of cytokine signaling 1 gene transcription in blood cells of patients with chronic hepatitis C
%A Virginia Sede£¿o-Monge
%A Gerardo Santos-L¨®pez
%A Rosa C Rocha-Gracia
%A Daniel Mel¨¦ndez-Mena
%A Alberto Ram¨ªrez-Mata
%A Ver¨®nica Vallejo-Ruiz
%A Julio Reyes-Leyva
%J Virology Journal
%D 2010
%I BioMed Central
%R 10.1186/1743-422x-7-243
%X Ifnar1 transcription increased significantly in HCV-infected patients either untreated (3.26 ¡À 0.31), responders (3.1 ¡À 0.23) and non-responders (2.18 ¡À 0.23) with respect to non-infected individuals (1 ¡À 0.34; P = 0.005). Ifnar1 transcription increased significantly (P = 0.003) in patients infected with HCV genotypes 1a (4.74 ¡À 0.25) and 1b (2.81 ¡À 0.25) but not in 1a1b (1.58 ¡À 0.21). No association was found of Ifnar1 transcription with disease progress, initial viral load or other clinical factors. With respect to socs1 transcription, values were similar for non-infected individuals (1 ¡À 0.28) and untreated patients (0.99 ¡À 0.41) but increased in responders (2.81 ¡À 0.17) and non-responder patients (1.67 ¡À 0.41). Difference between responder and non-responder patients was not statistically significant. Socs1 transcription increased in patients infected with HCV genotypes 1a and 1b (2.87 ¡À 0.45 and 2.22 ¡À 0.17, respectively) but not in 1a1b (1.28 ¡À 0.40). Socs1 transcript was absent in three patients infected with HCV genotype 1b. A weak correlation between ifnar1 and socs1 transcription was found, when Spearman's correlation coefficient was calculated.Our results suggest that HCV infection may up-regulate ifnar1 transcription. HCV genotypes differ in their capacity to affect ifnar1 and socs1 transcription, as well as in the ability to evade the antiviral response.Hepatitis C virus (HCV) is a public health concern worldwide and a major cause of chronic liver inflammation, cirrhosis and hepatocellular carcinoma (HCC) [1]. In Mexico, the prevalence of HCV is ~1.4% in the open population and 35% in patients with active hepatitis [2].HCV is a single-stranded positive RNA virus that codes for a precursor polyprotein, which is processed into 10 active proteins: C, P7, E1, E2, NS2, NS3, NS4A, NS4B, NS5A and NS5B. Due to high genetic diversity, HCV is classified according to several genotypes and subtypes, which differ in geographic distribution, virulence and sensitivity
%U http://www.virologyj.com/content/7/1/243