| ORIGINAL ARTICLE |
|
| Year : 2018 | Volume
: 11
| Issue : 3 | Page : 214-221 |
|
|
Andrographolide inhibits chikungunya virus infection by up-regulating host innate immune pathways
Swati Gupta1, Kamla Prasad Mishra1, Paban Kumar Dash2, Manmohan Parida2, Lilly Ganju1, Shashi Bala Singh1
1 Defence Institute of Physiology & Allied Sciences, Lucknow Road, Timarpur, Delhi-110054, India
2 Defence Research and Development Establishment, Jhansi Road, Gwalior-474002, India
Correspondence Address:
Kamla Prasad Mishra
Sc. ‘E’, Immunomodulation Laboratory, Defence Institute of Physiology & Allied Sciences, Lucknow Road, Timarpur, Delhi
India
 Source of Support: Defence Research & Development Organization (DRDO) is gratefully
acknowledged for the financial support in the form NBC subproject, Conflict of Interest: None  | 4 |
DOI: 10.4103/1995-7645.228436
|
|
|
Objective: To investigate the therapeutic efficacy of andrographolide, a plant derived compound, against chikungunya virus (CHIKV) infection. Methods: Using flow cytometry and immunoblotting assay, in vitro viral protein expression was studied in THP-1 cells line. In Balb/c mouse neonates, viral RNA copy number was determined by real time PCR. Results: The results showed reduced CHIKV protein expression on andrographolide treatment in CHIKV-infected human peripheral blood mononuclear cells, Vero cells and THP-1 cell line. In vivo, andrographolide treatment to CHIKV-infected neonates reduced viral RNA copy number. Further, andrographolide also increased cytotoxic T lymphocytes both in vitro and in vivo. Andrographolide also activated host innate immune pathways, viz., protein kinase R, phosphorylated eukaryotic initiation factor 2α , retinoic acid inducible gene-I and interferon regulatory factor 3/7, thereby increasing IFN- α secretion. CHIKV-induced nuclear factor κ light chain enhancer of activated B cells and tumor necrosis factor- α was also reduced on andrographolide treatment. Conclusion: Andrographolide inhibits CHIKV by suppressing viral protein expression and up-regulating host innate immunity and hence could be an effective therapeutic agent against CHIKV infection.
|
|
|
|
| [FULL TEXT] [PDF]* |
|
 |
|
