Abstract
DENGUE viruses, types 1–4, are arthropod-borne flaviviruses which cause dengue shock syndrome (DSS) in humans possessing pre-infection antibody, passively acquired or derived from heterotypic infection1. Although the immuno-pathological mechanism of DSS is not fully understood, experimental studies suggest that dengue virus production is immunologically regulated. Monkeys with monotypic immunity to dengue types 1, 3 or 4 viruses, when challenged with dengue 2, had significantly higher levels of circulating virus than did similarly infected susceptible animals2. This may be attributable to the replication of virus in leukocytes. In infected monkeys, virus was frequently recovered from buffy coat cells and from lymphatic tissues3. The role of leukocytes in enhanced infection is further supported by the observation that dengue replicates readily in cultures of peripheral blood leukocytes (PBL) prepared from immune simian or human donors, but poorly or not at all in leukocytes from non-immune hosts4–6. Studies on the immunological specificity of this phenomenon have been hindered by the requirement either for expensive experimental hosts (monkeys) or for human donors with chronologically defined dengue infections. Here we describe the in vitro enhancement of dengue infection in PBL by antibody. This system provides a provisional model for DSS in young infants during primary dengue infections7,8.
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