Antiviral Activity of Crude Polysaccharide Derived from Seaweed against IHNV and IPNV In Vitro

Abstract

Both infectious hematopoietic necrosis virus (IHNV) and infectious pancreatic necrosis virus (IPNV) are the causative agents of acute and highly contagious diseases of juvenile salmonids, resulting in severe economic losses to these cold-water fish globally. There is an urgent need to explore antiviral agents against IHNV and IPNV due to the lack of commercially available vaccines and antiviral drugs. More importantly, the co-infection of IHNV and IPNV is prevalent in nature, which not only aggravates extensive damage to the salmonids but also poses challenges to its prevention and control. The antiviral effects of a crude polysaccharide derived from seaweed (CSP) on IHNV and IPNV were evaluated in this study separately. Furthermore, the underlying antiviral mechanisms of CSP to IHNV and IPNV were analyzed, respectively. The results showed that CSP possessed excellent safety and good ability to inhibit IHNV, IPNV, and their co-infection. CSP preferred to act at the early stage of viral infection. The antiviral mechanism of CSP on IHNV is possibly involved in preventing viral attachment and release, while in IPNV, it is involved in suppressing viral attachment, entry, and release. Taken together, the results of this study shed new light on developing novel agents against viral infection in salmonid fish.

Keywords: IHNV; IPNV; antivirus; co-infection; polysaccharide.

Figure 1

The antiviral activity of CSP to IHNV with a MOI of 0.1 and 1.0, respectively (different letters indicate statistical significance, p < 0.05).

Figure 2

The antiviral activity and actions of CSP on IHNV. (a) The antiviral activity of CSP with different concentrations on IHNV under the pre-addition, post-addition, and inactivated treatments. (b) The changes of relative expression levels of IHNV-L gene in the viral attachment, entry, and replication processes, respectively. (c) The determination of the viral titers during the viral release process. Different letters indicate statistical significance, p < 0.05.

Figure 3

The antiviral activity of CSP on IPNV with a MOI of 0.1 and 1.0, respectively (different letters indicate statistical significance, p < 0.05).

Figure 4

The antiviral activity and actions of CSP on IPNV. (a) The antiviral activity of CSP with different concentrations on IPNV under the pre-addition, post-addition, and inactivated treatments. (b) The changes in relative expression levels of the IPNV-VP2 gene in the viral attachment, entry, and replication processes, respectively. (c) The determination of the viral titers during the viral release process. Different letters indicate statistical significance, p < 0.05.

Figure 5

The antiviral ability of CSP on the co-infection of IHNV and IPNV. (a) The antiviral activity of CSP on the co-infection of IHNV and IPNV with a MOI of 0.1 and 1.0, respectively. (b) The antiviral activity of CSP on IPNV under the pre-addition, post-addition, and inactivated treatments. (c) IFAT result of the co-infection without the presence of CSP. (d) IFAT result of the co-infection with the presence of CSP. Different letters indicate statistical significance, p < 0.05).