Faculty Opinions recommendation of Microglia retard dengue virus-induced acute viral encephalitis.

Author(s):  
Anirban Basu ◽  
Sourish Ghosh
2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Tsung-Ting Tsai ◽  
Chia-Ling Chen ◽  
Yee-Shin Lin ◽  
Chih-Peng Chang ◽  
Cheng-Chieh Tsai ◽  
...  

Author(s):  
Ting-Jing Shen ◽  
Ming-Kai Jhan ◽  
Jo-Chi Kao ◽  
Min-Ru Ho ◽  
Tsung-Ting Tsai ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3181
Author(s):  
Ming-Kai Jhan ◽  
Chia-Ling Chen ◽  
Ting-Jing Shen ◽  
Po-Chun Tseng ◽  
Yung-Ting Wang ◽  
...  

Infection with flaviviruses causes mild to severe diseases, including viral hemorrhagic fever, vascular shock syndrome, and viral encephalitis. Several animal models explore the pathogenesis of viral encephalitis, as shown by neuron destruction due to neurotoxicity after viral infection. While neuronal cells are injuries caused by inflammatory cytokine production following microglial/macrophage activation, the blockade of inflammatory cytokines can reduce neurotoxicity to improve the survival rate. This study investigated the involvement of macrophage phenotypes in facilitating CNS inflammation and neurotoxicity during flavivirus infection, including the Japanese encephalitis virus, dengue virus (DENV), and Zika virus. Mice infected with different flaviviruses presented encephalitis-like symptoms, including limbic seizure and paralysis. Histology indicated that brain lesions were identified in the hippocampus and surrounded by mononuclear cells. In those regions, both the infiltrated macrophages and resident microglia were significantly increased. RNA-seq analysis showed the gene profile shifting toward type 1 macrophage (M1) polarization, while M1 markers validated this phenomenon. Pharmacologically blocking C-C chemokine receptor 2 and tumor necrosis factor-α partly retarded DENV-induced M1 polarization. In summary, flavivirus infection, such as JEV and DENV, promoted type 1 macrophage polarization in the brain associated with encephalitic severity.


1970 ◽  
Vol 5 (2) ◽  
pp. 63-65
Author(s):  
MY Ali ◽  
SA Fattah ◽  
MM Islam ◽  
MA Hossain ◽  
SY Ali

Nipah viral encephalitis is one of the fatal re-emerging infections especially in southeast Asia. After its outbreak in Malaysia and Singapore; repeated outbreaks occurred at western part of Bangladesh especially in Faridpur region. Besides, sporadic attacks appear to occur in the country throughout the year. Here two Nipah outbreaks in greater Faridpur district in 2003 and 2004 are described along with brief review on transmission of the virus. Where the history of illness among patients are very much in favour of man to man transmission. Moreover the death of an intern doctor from Nipah encephalitis who was involved in managing such patients in Faridpur Medical College Hospital strongly suggests man to man transmission of this virus. So, aim of this review article to make the health personnel and general people be aware about man to man transmission of virus, so that they can adapt personal protection equipment (PPE) for their protection against this deadly disease. DOI: 10.3329/fmcj.v5i2.6825Faridpur Med. Coll. J. 2010;5(2):63-65


ENTOMON ◽  
2019 ◽  
Vol 44 (3) ◽  
pp. 213-218
Author(s):  
Suresh Chand Kaushik ◽  
Sukhvir Singh ◽  
Purnima Srivastava ◽  
R. Rajendran

Detection of viruses in human sera particularly in endemic areas is cumbersome and laborious. Therefore, an alternative approach, Immuno-fluorescence assay (IFA) was performed to determine dengue virus (DENV) positivity in mosquitoes. A total of 1055 adult Aedes aegypti female mosquitoes were tested for IFA test against DENV. Minimum infection rate (MIR) for DENV was found higher during August to November 2016 ranging from 10.75 to 20.83. The average yearly MIR was about 6.64. Higher MIR for Ae. aegypti was found in Sarfabad, Noida (12.71) and Khoda Colony, Ghaziabad (11.90). Minimum MIR (4.67) was observed in Sanjay colony (Faridabad). The main contribution of this study resides in the development of a more suitable monitoring system for early detection of viral circulation and to prioritize early intervention in the non-transmission season.


Author(s):  
Gerhard Dobler

• TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from oth-er forms of viral encephalitis or other diseases. • Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. • Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detec-tion of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. • During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. • Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either Infection with other flaviviruses or with other flavivirus vaccines.


The first case of tick-borne encephalitis (TBE) in Lithuania, diagnosed by clinical and epidemiologic criteria only, was reported in 1953. A forest worker became ill with the disease in April after a tick bite, had a typical clinical presentation with shoulder girdle muscle paralysis and bulbar syndrome, and died after 12 days from the start of clinical symptoms. Autopsy data were compatible with viral encephalitis.1 Serological diagnosis of TBE in Lithuania was started in 1970.2


TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from other forms of viral encephalitis or other diseases. Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detection of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either infection with other flaviviruses or with other flavivirus vaccines.


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