Recapitulations on changes in dengue virus properties and the etiology of dengue hemorrhagic fever.

The relation of changes in virus properties and the pathophysiology of dengue hemorrhagic fever is examined in view of previous and present evidences of host-induced modification of virus surface antigens in Aedes albopictus cells. Small (or avirulent) and large (or virulent) plaque variants were assayed in vivo and in vitro; changes in electrophoretic patterns accompanied the transition from virulence to avirulence as well as the alteration in immunological reactivity. Mosquito -adapted virus is not lethal to suckling mice and does not initiate plaque formation in mammalian cells; however, its presence is established by the virus interference test. Host-induced modification or the acquisition of host cell membrane components in the viral coat might predispose to either an abrogation of self-tolerance (an auto-immune process) or to the accummulation is subsequent infections with heterologous dengue virus of antigen-antibody complexes which activate complement and trigger the changes in the blood vascular system that lead to hemorrhagic tendencies. (Summary)