Many viruses are capable of inducing cell death, leading to lysis of infected cells [1–3]. In late stages of PEDV infections, morphological changes commonly known as CPE, microscopically observed. The morphology of Vero cells after infection with PEDV was greatly decreased from that of PEDV by addition of Q7R. However, the addition of ribavirin to PEDV-infected Vero cell proved to be impossible in preventing CPE.
Viral infections such as rhinovirus, influenza virus, human immunodeficiency virus and bovine viral diarreha virus frequently result in the generation of oxidative stress in the infected cells [4–7]. The events leading to the generation of ROS during viral infections are still unclear. Also, antioxidants have been shown to have antiviral activities against a variety of unrelated viruses by alleviating the oxidative stress generated by viruses [16–20]. Mechanistically, it is believed that these viruses induce apoptosis by oxidative stress mediated via ROS. Interference with this pathway by antioxidants is believed to inhibit virus-induced apoptosis and thus inhibit efficient virus multiplication. In contrast, there are also reports indicating that under certain conditions compounds act as a pro-apoptotic drug [21–23]. Depending on the viral system analyzed, antioxidative compounds differ in their ability to reduce virus growth [7, 24, 25].
Flavonoids are a large class of polyphenolic compounds and Jung et al. (2003) reported that the relationship between flavonoid structure and antioxidant activity. They found that the inhibitory activities of flavonoids on total ROS are more strongly increases with the rising number of hydroxyl groups than the foavonoid glycosides on their structures .
Our previous study showed that quercetin 7-rhamnoside (Q7R) didn't directly interact with PEDV particles and affect the initial stage of PEDV infection by interfering with its viral mRNA production . In this report, we present evidence that Q7R, but not other commonly used antioxidants, are able to protect cells from PEDV induced death. Q7R are potent agents that have been shown to be involved in a number of processes, suggesting that their antiviral effects might not be due to its antioxidant functions alone. Nevertheless, further studies are needed to verify the underlying mechanism of Q7R action in inhibiting PEDV infection.
In conclusion, Q7R is an extremely potent anti-PEDV substance which reduces PEDV growth, inhibits the CPE and DNA fragment of infected cells regardless of its antioxidant activity and then didn't directly interact with PEDV particles and affect the initial stage of PEDV infection by obstructing with its viral mRNA production. It will be interesting to further investigate the antiviral activity of the Q7R in preventing various PEDV-mediated injuries in in vivo pathological situations.