INDUCTION OF INTERFERON a FROM HUMAN LYMPHOCYTES BY AUTOLOGOUS, DENGUE

Monocytes appear to play an important role in dengue virus infection. They have been identified as cells that support dengue virus replication (1) . Dengue virus has been recovered from circulating mononuclear cells and lymphoid organs of dengue virus-infected humans and monkeys (2-4). Cell separation experiments showed that dengue virus replicates in monocyte fractions, but did not replicate in the monocyte-depleted fractions (1) . Furthermore, monocytes containing dengue virus-like structures have been detected in the skin and kidney of dengue hemorrhagic fever patients (5, 6) . Therefore, dengue virusinfected monocytes may be active in inducing responses from immune-competent lymphocytes. It has been hypothesized that immune elimination of dengue virusinfected monocytes (DV-monocytes)' may lead to the severe complications of dengue infection, hemorrhagic manifestations, and shock, which are more commonly observed in secondary dengue infections (7) . In the report we analyzed the in vitro interaction between DV-monocytes and lymphocytes as a model of primary dengue infection. We used autologous monocytes and lymphocytes from dengue nonimmune donors . Lymphocytes produce high titers ofinterferon a (IFN-a) after being exposed to DV-monocytes . The IFN-a induced was able to inhibit infection of other monocytes by dengue virus . These results suggest that IFN induction from lymphocytes by DVmonocytes is an important defense mechanism in primary dengue infections.