Archives of Virology

, Volume 158, Issue 7, pp 1445–1459

Secondary infection as a risk factor for dengue hemorrhagic fever/dengue shock syndrome: an historical perspective and role of antibody-dependent enhancement of infection

Authors

    • Institute of Tropical Medicine “Pedro Kouri”
    • Department of VirologyPAHO/WHO Collaborating Center for the Study of Dengue and its Vector, “Pedro Kouri” Tropical Medicine Institute
  • Mayling Alvarez
    • Institute of Tropical Medicine “Pedro Kouri”
  • Scott B. Halstead
    • Dengue Vaccine Initiative
Brief Review

DOI: 10.1007/s00705-013-1645-3

Cite this article as:
Guzman, M.G., Alvarez, M. & Halstead, S.B. Arch Virol (2013) 158: 1445. doi:10.1007/s00705-013-1645-3

Abstract

Today, dengue viruses are the most prevalent arthropod-borne viruses in the world. Since the 1960s, numerous reports have identified a second heterologous dengue virus (DENV) infection as a principal risk factor for severe dengue disease (dengue hemorrhagic fever/dengue shock syndrome, DHF/DSS). Modifiers of dengue disease response include the specific sequence of two DENV infections, the interval between infections, and contributions from the human host, such as age, ethnicity, chronic illnesses and genetic background. Antibody-dependent enhancement (ADE) of dengue virus infection has been proposed as the early mechanism underlying DHF/DSS. Dengue cross-reactive antibodies raised following a first dengue infection combine with a second infecting virus to form infectious immune complexes that enter Fc-receptor-bearing cells. This results in an increased number of infected cells and increased viral output per cell. At the late illness stage, high levels of cytokines, possibly the result of T cell elimination of infected cells, result in vascular permeability, leading to shock and death. This review is focused on the etiological role of secondary infections (SI) and mechanisms of ADE.

Copyright information

© Springer-Verlag Wien 2013