SUMMARYThe recently established virus family Flaviviridae contains at least 68 recognized members. Sixty-six of these viruses were tested by cross-neutralization in cell cultures. Flaviviruses were separated into eight complexes [tick-borne encephalitis (12 viruses), Rio Bravo (six), Japanese encephalitis (10), Tyuleniy (three), Ntaya (five), Uganda S (four), dengue (four) and Modoc (five)] containing 49 viruses; 17 other viruses were not sufficiently related to warrant inclusion in any of these complexes.

The family Flaviviridae comprises the genus Flavivirus, which contains 65 related species and two possible members. They are small, enveloped RNA viruses (diameter 45 nm) with peplomers comprising a single glycoprotein E. Other structural proteins are designated C (core) and M (membrane-like). The single strand of RNA is infectious and has a molecular weight of about 4 × 10⁶ and an m⁷G ‘cap’ at the 5’ end but no poly(A) tract at the 3’ end; it functions as the sole messenger. The gene sequence commences 5’-C-M-E... The replication strategy and the mode of morphogenesis are distinct from those of the Togaviridae which are slightly larger and morphologically similar in some respects. Flaviviruses infect a wide range of vertebrates, and many are transmitted by arthropods.

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SUMMARYCross-neutralization studies on 42 flaviviruses and their respective antisera were performed by a plaque assay in a line of pig kidney cells. Six tick-borne viruses fell into one subgroup; seven viruses associated with bats and small rodents and a further tick-borne virus fell into a second subgroup. Twenty-two mosquito-borne viruses fell into one major and four minor subgroups. Four mosquito-borne, one tick-borne and one bat virus showed no relationship to any other ftavivirus.

Interactions between animal viruses and antiviral antisera may exceptionally result in an apparent increase in viral infectivity. Halstead and coworkers demonstrated enhanced replication of dengue virus (a Flavivirus, family Togaviridae) in human or simian peripheral blood leucocytes carrying Fc receptors at subneutralising concentrations of antidengue antibody. We have used three continuous cell lines which express macrophage markers to explore the mechanism of this phenomenon. Dengue virus failed to replicate in these cells, but West Nile virus, another Flavivirus, replicated in all three, and we were able to demonstrate reproducibly 50--100-fold enhancement of virus yields in the presence of Flavivirus antisera, the effect also being directly demonstrable in P388D1 cells by increased numbers of virus-induced plaques. The phenomenon of antibody-dependent enhancement of viral replication is not unique to dengue virus, and may have far wider relevance in other viral infections.