Sialidase |
Removes sialic acid receptors on the cell surface, blocking interaction with the viral HA |
– |
Protease inhibitors |
Inhibit cleavage of the precursor HA0 into functional HA1/HA2 |
– |
MEK inhibitors |
Block the MAPK/ERK protein kinase cascade, suppress the function of nuclear export protein, resulting in nuclear retention of viral RNPs |
– |
NF-κB and IKK2 inhibitors |
Suppress the action of caspase and inhibit the release of viral RNP from the nucleus. |
Decrease proinflammatory cytokine and chemokine production upon H5N1 infection |
Inhibit SOCS-3 induction, removing the inhibitory effect on ISG production mediated via the JAK/STAT pathway. |
COX-2 inhibitors |
Suppress viral gene transcription, viral protein expression and progeny virus production in H5N1-infected cells |
Attenuate H5N1-hyperinduced cytokines in the proinflammatory cascade |
S1P agonists |
– |
Suppress cytokine release by T-cells and affect the antigen presentation ability of dendritic cells |
IPP and PAM expanded gamma-delta T-cells |
– |
Expanded Vγ9Vδ2 T cell population to enhance the host immune response |
PPAR agonists |
– |
Suppress inflammatory cytokine expression through trans-repression of NF-κB and AP-1 |
Statins |
– |
Suppress inducible MHC-II expression and activity of LFA-1 |