TABLE 1.
Summary of previous investigations examining the antiviral effects of CEP and its mechanism of action.
| Virus | EC50/IC50 (µg/mL) | TC50/CC50 (µg/mL) | Pharmacologic action | Mechanism of action | References |
|---|---|---|---|---|---|
| HIV-1 | 0.016 | 2.2 | Dampening the virus’s pathogenicity;Crossing the blood–brain barrier and inducing neural cell death | Suppresses HIV-1 long-terminal repeat-driven gene expression by inhibiting the activation of NF-κB | Baba (1997), Okamoto et al. (1998), Baba et al. (2001), Okamoto et al. (2001) |
| — | — | Suppresses the production of inflammatory cytokines and a chemokine, i.e., TNF-alpha, interleukin (IL)-1 beta, IL-6, and IL-8 | Okamoto et al. (2001) | ||
| — | — | Inhibition of the HIV-1 entry process by reducing plasma membrane fluidity | Matsuda et al. (2014) | ||
| HBV | — | — | Inhibits viral replication and suppresses viral HBeAg antigen production | Suppresses HBV via downregulation of host Hsc70 expression, thereby inhibiting viral replication and HBeAg production | Rogosnitzky et al. (2020) |
| HSV-1 | 1.56 | 7.52 | — | — | Liu et al. (2004) |
| 0.835 | 5.4 for Vero cell; 9.0 for HeLa cell | Reducing HSV-1 infection and subsequent reproduction | Arrests the cell cycle in the G2/M phase and induces apoptosis in infected cells by inhibiting the PI3K/Akt and p38 MAPK signaling pathways | Liu et al. (2021b) | |
| To promote interferon-independent autophagy through the STING/TBK1/P62-mediated signaling pathways | Liu et al. (2021a) | ||||
| HTLV-1 | — | — | Triggers apoptosis of HTLV-1-infected cells through the caspase-dependent pathway | Inhibits NF-kB signaling pathway and suppresses viral replication and then reduces viral titer | Toyama et al. (2012) |
| PRRSV | — | — | Alleviation of PRRSV infection | Inhibits the expression of integrins β1 and β3, integrin-linked kinase (ILK), RACK1, and PKCα, leading to NF-κB suppression | Yang et al. (2021) |
| Inhibition of integrins/ILK/RACK1/PKCα/NF-κB, and therefore downregulation of inflammatory responses | |||||
| PCV2 | — | 8.048 ± 0.614 | CEP has a significant antiviral effect | Inhibits mitochondrial apoptosis induced by PCV2 | Xu et al. (2020) |
| SARS -CoV | 6.0–9.5 | — | Inhibits viral replication | Inhibits viral RNA replication, blocks the expression of viral proteins, and suppresses production of pro-inflammatory molecules toward preventing an exacerbated cytokine response to the viral infection | Zhang et al. (2005), Rogosnitzky et al. (2020), Wang and Yang (2020) |
| HCoV -OC43 | 0.443 | 6.395 | Inhibits viral replication and infectivity | Blocks the expression of the viral spike protein and nucleoprotein | Kim et al. (2019) |
| Dampens virus-induced host response | Inhibits the binding of the spike protein to membrane receptors (9-O-acetylated sialic acid glycan-based receptors) | ||||
| Expression of the new spike protein and nucleoproteins |
HIV-1: human immunodeficiency virus type 1; HBV: hepatitis B virus; HSV-1: herpes simplex virus type 1; HLTV-1: human T-lymphocytic virus type 1; PRRSV: porcine reproductive and respiratory syndrome virus; PCV2: porcine circovirus type 2; SARS-CoV: severe acute respiratory syndrome coronavirus; HCoV-OC43: human coronavirus type OC43.