A recent study conducted by the Shanghai University of Traditional Chinese Medicine has shed light on the remarkable antiviral properties of Prunella vulgaris, a herbaceous plant from the Labiatae family. The study focused on the effects of Prunella vulgaris polysaccharide extract (PVE30) on herpes simplex virus (HSV) infections, revealing its potential as a powerful antiviral agent.
Herpes simplex virus (HSV) infections, caused by HSV-1 and HSV-2, are common and can lead to oropharyngeal and genital infections. The study sought to understand how PVE30 functions against these viruses by targeting their attachment and entry into host cells.
The findings of the study demonstrated that PVE30 effectively inhibits viral attachment and penetration. By interacting with HSV surface glycoproteins, PVE30 hinders the virus’s ability to attach to host cells. Additionally, PVE30 restricts viral replication by downregulating the expression of specific genes, thereby limiting the production of viral gene products.
Another significant mechanism through which PVE30 exerts its antiviral effects is by suppressing Toll-like receptor (TLR) signaling. TLRs play a crucial role in recognizing viral proteins and nucleic acids, initiating host defense mechanisms. PVE30 inhibits TLR2 and TLR3 signaling, leading to the suppression of nuclear factor-kappa B (NF-κB) activation. NF-κB is a transcriptional regulator that influences cell survival, differentiation, inflammation, and antiviral responses.
Furthermore, PVE30 has been found to block HSV-1-induced necroptosis, a form of programmed cell death triggered by viral intermediates. By reducing the phosphorylation of a key protein involved in necroptosis, PVE30 maintains a delicate balance between cell death, proliferation, and differentiation during HSV-1 replication.
The study also investigated the direct interactions between PVE30 and HSV glycoproteins. It was confirmed that PVE30 competes with heparan sulfate for interaction with viral glycoproteins, resulting in a strong inhibition of HSV attachment to cells. Additionally, the study revealed that PVE30 downregulates the expression of immediate early genes and subsequently affects the expression of early and late viral gene products, effectively restricting the production of progeny virus.
Moreover, PVE30 was found to regulate the activity of specific molecules involved in the NF-κB pathway, reducing the secretion of inflammatory cytokines. It also decreased the percentage of necroptotic cells and reduced the expression of a key protein involved in necroptosis. Interestingly, PVE30 may inhibit HSV-induced necroptosis through a TLR signaling pathway independent of MyD88.
The comprehensive findings of this study provide a deeper understanding of the multifaceted antiviral mechanisms of Prunella vulgaris polysaccharide extract PVE30 against HSV infections. Its ability to inhibit viral attachment and penetration, restrict viral replication, suppress TLR-mediated NF-κB activation, and block HSV-induced necroptosis positions PVE30 as a promising candidate for antiviral therapies. These findings not only validate the traditional uses of Prunella vulgaris in Chinese medicine but also open up new avenues for further research and pharmaceutical development in the field of antiviral treatments.