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Evaluation of immune response profiles of individuals with chronic Hepatitis C treated with interferon alpha and ribavirin, in the foundation of tropical medicine of Amazonas
Retrovirology volume 7, Article number: P31 (2010)
The HCV is considered the main etiological agent involved in the hepatitis parenteral transmission. The most frequent genotypes in Brazil are 1, 2 and 3, and genotype 1b is the most frequent in blood donors. Data from the serological screening of the Foundation of Hematology and Hemotherapy of Amazonas (FHEMOAM) show that 0.32% of donors are seropositivity for anti-HCV. Some studies showed that 15 to 25% has good prognostic but 80% develops chronic hepatitis. The purpose study was to describe the clinical course and immunological profile of chronic infection by HCV in patients treated with interferon-alpha and ribavirin.
Clinical and laboratory evaluation, including viral genotype, viral load, and cellular and humoral immune response, during the first 24 weeks of therapy.
Partial results showed that genotype 1 (51.72%) is more prevalent in the Amazon, followed by 3 (31.03%) and 2 (17.24%). Significant changes of AST and ALT concentrations showed an increase in the 4 weeks of treatment. We observed a trend to increase cell populations in time 0 (pretreatment) to lymphocyte (63.3 ± 88.7), monocytes (10.6 ± 21.5), neutrophils (86.7 ± 126, 1), had not statistically significant difference. The analysis by flow cytometry showed an increase in total T cells and CD4 + in 4 weeks, returning to baseline at 12 and 24 weeks after treatment. Furthermore, there was a decrease of LTCD8 + in 12 and 24 weeks after treatment.
Partial results showed that HCV infection changes the profile of immune response in treated of patients with Interferon-alpha and ribavirin.
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Araújo, A.R., Fraporti, L.S., Torres, K.L. et al. Evaluation of immune response profiles of individuals with chronic Hepatitis C treated with interferon alpha and ribavirin, in the foundation of tropical medicine of Amazonas. Retrovirology 7, P31 (2010) doi:10.1186/1742-4690-7-S1-P31
- Viral Load
- Chronic Hepatitis
- Humoral Immune Response
- Etiological Agent