Sergio Isaac De La Cruz Hernández1, Henry Puerta-Guardo2, Hilario Flores-Aguilar3, Silvia González-Mateos4, Irma López-Martinez4, Vianney Ortiz-Navarrete5, Juan E Ludert6, Rosa María Del Angel7. 1. Department of Virology, Institute for Diagnosis and Epidemiological Reference (InDRE), Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico; Department of Infectomics and Molecular Pathogenesis, Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico. 2. Department of Infectomics and Molecular Pathogenesis, Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico. 3. Department of Inmunology and Inmunogenetics-InDRE, Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico. 4. Department of Virology, Institute for Diagnosis and Epidemiological Reference (InDRE), Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico. 5. Department of Biomedicine, Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico. 6. Department of Infectomics and Molecular Pathogenesis, Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico. Electronic address: jludert@cinvestav.mx. 7. Department of Infectomics and Molecular Pathogenesis, Center for Research and Advanced Studies (CINVESTAV-IPN), Mexico D.F., Mexico. Electronic address: rmangel@cinvestav.mx.
Abstract
BACKGROUND: Type 1 interferon (IFNα/β) has a significant role in establishing protection against virus infections. It has been well documented by in vitro studies that dengue virus (DENV) activates a robust IFNα/β response. However, DENV also induces a down-regulation of the JAK/STAT pathway, inhibiting the induction of interferon regulated genes. As a consequence, the role played by the IFN type 1 response in the protection of dengue patients is not fully understood. OBJECTIVE: To compare IFN-α levels in dengue patients with dengue fever (DF) or dengue hemorrhagic fever (DHF) undergoing primary or secondary infections. STUDY DESIGN: Two hundred and four serum samples were analyzed for IFN-α level by cytometric bead array. Patients' clinical condition was assigned following the WHO 1997 criteria and specific IgG and IgM antibodies were measured using commercial assays to determine primary and secondary infections. The infecting serotype was determined by qRT-PCR. RESULTS AND CONCLUSION: The IFN-α levels were found significantly higher in DF than DHF patients irrespective of the infecting serotype (DENV1 or 2), and were found to decline rapidly at day 3 after fever onset. For DENV2 infections, higher IFN-α level was found during primary than secondary infections. These results suggest that an early strong interferon response correlates with a better clinical condition.
BACKGROUND: Type 1 interferon (IFNα/β) has a significant role in establishing protection against virus infections. It has been well documented by in vitro studies that dengue virus (DENV) activates a robust IFNα/β response. However, DENV also induces a down-regulation of the JAK/STAT pathway, inhibiting the induction of interferon regulated genes. As a consequence, the role played by the IFN type 1 response in the protection of dengue patients is not fully understood. OBJECTIVE: To compare IFN-α levels in dengue patients with dengue fever (DF) or dengue hemorrhagic fever (DHF) undergoing primary or secondary infections. STUDY DESIGN: Two hundred and four serum samples were analyzed for IFN-α level by cytometric bead array. Patients' clinical condition was assigned following the WHO 1997 criteria and specific IgG and IgM antibodies were measured using commercial assays to determine primary and secondary infections. The infecting serotype was determined by qRT-PCR. RESULTS AND CONCLUSION: The IFN-α levels were found significantly higher in DF than DHF patients irrespective of the infecting serotype (DENV1 or 2), and were found to decline rapidly at day 3 after fever onset. For DENV2 infections, higher IFN-α level was found during primary than secondary infections. These results suggest that an early strong interferon response correlates with a better clinical condition.
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