Conclusion
These results as a whole suggest that the upregulation of TNF-α could be part of the process that induces cell damage and death in cases of dengue encephalitis.
Methods
Susceptibility and permissiveness of the SH-SY5Y line to infection by DENV-2 was analyzed, showing that the proportions of viral infection and production are similar to those of primate cells used as positive control for infection.
Objective
To evaluate the possible mechanisms involved in the onset of neurological signs in a cell line of human neurons as a model of infection with dengue virus type 2 (DENV-2). Materials and
Results
Infection induced a cytopathic effect on the neuroblastoma line characterized by apoptotic cell death process, increasing the proportion of annexin V and TUNEL positive cells and an upregulation of TNF-α. Treatment with anti-TNF-α antibody increased slightly cell survival of infected cells. The addition of exogenous TNF-α to the infected cultures enhanced cell death.