Antiviral Perspectives for Chikungunya Virus

Table 2

Some of the major cellular inhibitors against chikungunya virus.

Cellular factors	Assays	Target/effectors	Pros	Cons	References
Furin inhibitors	In vitro (myoblast cells).	Intracellular furin-mediated cleavage of viral envelope glycoproteins: the E2E3 or p62 precursor.	Able to induce a stronger inhibition of viral infection.	Not tested in invivo system.	Ozden et al., 2008 [54]
2′,5′-Oligoadenylate synthetase (OAS3)	Human epithelial HeLa cell lines.	Affects CHIKV replication through a RNase L-dependent pathway.	Ability of OAS3 to inhibit alphavirus growth may be important for the development of antiviral molecules against CHIKV.	Cannot rule out the possibility that OAS3-mediated inhibition of CHIKV was also due to a block early in virus life cycle, for example, viral entry and uncoating of virus particles.	Bréhin et al., 2009 [56]
Cellular IMPDH enzyme	In vitro (vero cells).	Depletion of intracellular guanosine pool.	CHIKV utilizes IMPDH activity for its growth and multiplication which is a potential and effective target to prevent its infection.	It would be useful to explore similar findings by targeting IMPDH in case of other alphaviruses which are more lethal than chikungunya like Sindbis virus, Semliki forest virus, and so forth.	Khan et al., 2011 [62]
Viperin	In vivo (monocytes).	Endoplasmic reticulum.	Critical antiviral host protein that controls CHIKV infection and provides a preclinical basis for the design of effective control strategies against CHIKV.	Large gaps in our understanding of the precise mechanisms at play for viperin to exert such a wide variety of roles within the cell.	Teng et al., 2012 [63]