Three possible triggers to induce thrombocytopenia in dengue virus infection.

Changes in platelet count by dengue virus-platelet interaction and the participation of anti-DV antibody to such changes were studied in vitro with the aim to investigate a mechanism of how the DV causes prominent thrombocytopenia characteristically seen in DHF. The results obtained showed that: (1) DV antigen attached to human platelets without immune-mediated reaction, (2) a decrease in platelet count was more markedly demonstrated by the binding of anti-DV antibody on the DV antigen associated with platelets than by the binding of the antigen-antibody complex on platelets, (3) a modulation of endothelial cell by the infection of DV to the cell was suggested as one of the causes of the thrombocytopenia.

Flavivirus infections in Chiang Mai area, Thailand, in 1982.

Infection by JE virus still constitutes major cause of encephalitis in Chiang Mai Area, although some cases of possible dengue encephalopathy were observed. In spite of many apparent encephalitis cases, infection of vector mosquitoes by JE virus was not demonstrated. Virus isolation from hospitalized patients showed that the principal type of dengue virus circulating in Chiang Mai in 1982 was type 1 virus. Seroepidemiological survey on healthy humans indicated that the northern part of Chiang Mai Province in the region of the Maekong Valley has not yet been invaded so much by dengue viruses, compared with the Chiang Mai Valley, where dengue infection apparently became more prevalent than 12 years ago. The survey also indicated that the spread of JE virus in the study area was not uniform. Survey on vertebrates showed that anti-JE antibodies were highly prevalent among swine, horses, mules, sheep, and dogs. On the other hand, antibody prevalence was low in monkeys, ducks, and sparrows, and was negative among chickens and lizards. IgM-ELISA appeared to help differential diagnosis on JE from dengue even when the HI test did not give positive results.