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Bee venom (BV) from honey bee (Apis Melifera L.) contains at least 18 pharmacologically active components including melittin (MLT), phospholipase A2 (PLA2), and apamin etc. BV is safe for human treatments dose dependently and proven to possess different healing properties including antibacterial and antiparasitidal properties. Nevertheless, antiviral properties of BV have not well investigated. Hence, we identified the potential antiviral properties of BV and its component against a broad panel of viruses. Co-incubation of non-cytotoxic amounts of BV and MLT, the main component of BV, significantly inhibited the replication of enveloped viruses such as Influenza A virus (PR8), Vesicular Stomatitis Virus (VSV), Respiratory Syncytial Virus (RSV), and Herpes Simplex Virus (HSV). Additionally, BV and MLT also inhibited the replication of non-enveloped viruses such as Enterovirus-71 (EV-71) and Coxsackie Virus (H3). Such antiviral properties were mainly explained by virucidal mechanism. Moreover, MLT protected mice which were challenged with lethal doses of pathogenic influenza A H1N1 viruses. Therefore, these results provides the evidence that BV and MLT could be a potential source as a promising antiviral agent, especially to develop as a broad spectrum antiviral agent.

The belief that honey bee venom (BV) can be used to treat certain immune-related diseases, such as arthritis and rheumatic conditions, goes back to antiquity. A growing number of reports have demonstrated that BV contains at least 18 pharmacologically active components, including phospholipase A2 (PLA2). Recent research has shown that bee venom PLA2 (bvPLA2) induces protective immune responses against several diseases including asthma, Parkinson’s disease, and drug-induced organ inflammation. However, the antiviral properties of bvPLA2 have not been well investigated. Hence, we examined the potential inhibitory effects of bvPLA2 and its possible mechanism of action against a broad panel of pathogenic viruses in vitro. Pre-treatment with bvPLA2 significantly inhibited the replication of vesicular stomatitis virus (VSV), coxsackie virus (H3), enterovirus-71 (EV-71), herpes simplex virus (HSV) and Adenovirus (AdV) dramatically. However, bvPLA2 did not show antiviral activity against Influenza A virus (PR8) and Newcastle disease virus (NDV). Such inhibitory effects were explained by blocking of the attachment of the virus to cells upon bvPLA2 treatment. Additionally, we observed that Heparan sulfate (HS) has an inhibitory effect on the attachment of HSV to the cell surface dose dependently, which was inconsistent with bvPLA2 treatment. These findings suggest that bvPLA2 has an inhibitory effect on the replication of diverse viruses by blocking their attachment to the cell surface and could be a promising source of natural antiviral agents.