Abstract
The Bowman‒Birk inhibitor (BBI), a protease inhibitor derived from soybeans, has been extensively studied in anti-tumor and anti-inflammation research. We recently reported that BBI has an anti-HIV-1 property in primary human macrophages. Because HSV-2 infection plays a role in facilitating HIV-1 sexual transmission, we thus examined whether BBI has the ability to inhibit HSV-2 infection. We demonstrated that BBI could potently inhibit HSV-2 replication in human cervical epithelial cells (End1/E6E7). This BBI-mediated HSV-2 inhibition was partially through blocking HSV-2-mediated activation of NF-κB and p38 MAPK pathways. In addition, BBI could activate the JAK/STAT pathway and enhance the expression of several antiviral interferon-stimulated genes (ISGs). Furthermore, BBI treatment of End1/E6E7 cells upregulated the expression of tight junction proteins and reduced HSV-2-mediated cellular ubiquitinated proteins’ degradation through suppressing the ubiquitin‒proteasome system. These observations indicate that BBI may have therapeutic potential for the prevention and treatment of HSV-2 infections.
Highlights
Herpes simplex virus type 2 (HSV-2) is an enveloped double-stranded DNA virus that belongs to the herpesviridae family
Because HSV-2 infection is a cofactor promoting HIV-1 sexual transmission, we examined whether Birk inhibitor (BBI) has an inhibitory effect on HSV-2 infection of human cervical epithelial cells
End1/E6E7 cells were pretreated with BBI for 24 h and infected with HSV-2 (MOI of 0.001)
Summary
Herpes simplex virus type 2 (HSV-2) is an enveloped double-stranded DNA virus that belongs to the herpesviridae family. Due to its highly prevalent and contagious trait, HSV-2 has been considered as one of the most severe pathogens for human beings. HSV-2 infection can cause genital herpes, which plays a significant role in the spread of sexually transmitted infections (STIs). Through mother-to-child transmission, HSV-2 is the cause of neonatal herpes, responsible for high morbidity and mortality [1]. There is increasing evidence that HSV-2 is a risk factor for HIV infection and sexual transmission [3,4,5]. The coinfection with HSV-2 is associated with a severity of genital ulceration, a reduced HIV-specific T cell response, and an increased systemic inflammation [6]
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