BACKGROUND/AIMS: Interaction of platelets with HCV is presumed to be one of the pathogenic mechanisms implicated in HCV-associated thrombocytopenia. Nevertheless, analysis of factors influencing the detection of HCV in platelets is not well understood. In this study, we investigated the relationship between the detection of HCV in platelets from a cohort of 39 chronically HCV-infected patients and several viral and host factors. METHODOLOGY: This study comprised of 14 males and 25 females with a median age of 53 years, followed-up in Rio de Janeiro, Brazil, between August 2003 and December 2004. HCV-RNA was detected in serum and platelet samples by reverse transcription-nested polymerase chain reaction. Genotypes were determined by using direct nucleotide sequencing of the PCR products and plasma viral loads by using HCV-Amplicor Monitor 2.0. RESULTS: When compared on the basis of the results of the detection of HCV-RNA in platelets, patients did not differ significantly in relation to viral load and genotype, platelet count, aminotransferases and degree of hepatic fibrosis. CONCLUSIONS: Our data suggest that HCV can be detected in platelets of chronically HCV-infected patients independent of these cofactors, including circulating HCV load. Studies on HCV dynamics are needed to provide new insights into HCV binding to platelets.
BACKGROUND/AIMS: Interaction of platelets with HCV is presumed to be one of the pathogenic mechanisms implicated in HCV-associated thrombocytopenia. Nevertheless, analysis of factors influencing the detection of HCV in platelets is not well understood. In this study, we investigated the relationship between the detection of HCV in platelets from a cohort of 39 chronically HCV-infectedpatients and several viral and host factors. METHODOLOGY: This study comprised of 14 males and 25 females with a median age of 53 years, followed-up in Rio de Janeiro, Brazil, between August 2003 and December 2004. HCV-RNA was detected in serum and platelet samples by reverse transcription-nested polymerase chain reaction. Genotypes were determined by using direct nucleotide sequencing of the PCR products and plasma viral loads by using HCV-Amplicor Monitor 2.0. RESULTS: When compared on the basis of the results of the detection of HCV-RNA in platelets, patients did not differ significantly in relation to viral load and genotype, platelet count, aminotransferases and degree of hepatic fibrosis. CONCLUSIONS: Our data suggest that HCV can be detected in platelets of chronically HCV-infectedpatients independent of these cofactors, including circulating HCV load. Studies on HCV dynamics are needed to provide new insights into HCV binding to platelets.
Authors: Adriana Vieira-de-Abreu; Robert A Campbell; Andrew S Weyrich; Guy A Zimmerman Journal: Semin Immunopathol Date: 2011-08-06 Impact factor: 9.623