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] |