Highly permissive infection of microglial cells by Japanese encephalitis virus: a possible role as a viral reservoir

Thananya Thongtan, Poonlarp Cheepsunthorn, Voravasa Chaiworakul, Chutima Rattanarungsan, Nitwara Wikan, Duncan R. Smith

Research output: Contribution to journalArticlepeer-review

62 Scopus citations

Abstract

Japanese encephalitis virus (JEV), a mosquito-borne Flavivirus, is a major cause of acute encephalitis, and neurons have been proposed to be the principle JEV target cells in the central nervous system. However, clinically, infection with JEV leads to increased levels of cytokines and chemokines in the serum and cerebrospinal fluid (CSF) the levels of which correlate with the mortality rate of patients. This research aimed to study the role of microglial cells in JEV infection. Mouse microglial cells (BV-2) supported the replication of JEV with extracellular production of virus by 10 h post-infection, and virus titer reached a maximum (2.55 × 1010 pfu/ml) by day 3 post-infection. While apoptosis was induced in response to virus infection, no alteration in nitric oxide production was observed. Microglial cells remained productively infected with JEV for up to 16 weeks without significant morphological alterations, and the released virions were infectious to mouse neuroblastoma (NA) cells. The high virus production and long persistence of JEV in microglial cells suggests that these cells may serve as viral reservoirs for the infection of neurons in the CNS.

Original languageEnglish (US)
Pages (from-to)37-45
Number of pages9
JournalMicrobes and Infection
Volume12
Issue number1
DOIs
StatePublished - Jan 2010
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported by grants no. RA043/49 from the Ratchadapiseksompotch Fund, Faculty of Medicine, Chulalongkorn University, Thailand and GRB_042_52_30_12 from the National Research Council of Thailand. NW is supported by a TRF-Mahidol University Scholarship and DRS is supported by the Thailand Research Fund.

Copyright:
Copyright 2010 Elsevier B.V., All rights reserved.

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