TY - JOUR
T1 - Highly permissive infection of microglial cells by Japanese encephalitis virus
T2 - a possible role as a viral reservoir
AU - Thongtan, Thananya
AU - Cheepsunthorn, Poonlarp
AU - Chaiworakul, Voravasa
AU - Rattanarungsan, Chutima
AU - Wikan, Nitwara
AU - Smith, Duncan R.
PY - 2010/1/1
Y1 - 2010/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=73149084851&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=73149084851&partnerID=8YFLogxK
U2 - 10.1016/j.micinf.2009.09.013
DO - 10.1016/j.micinf.2009.09.013
M3 - Article
C2 - 19786116
AN - SCOPUS:73149084851
VL - 12
SP - 37
EP - 45
JO - Microbes and Infection
JF - Microbes and Infection
SN - 1286-4579
IS - 1
ER -