The interactions of SEM, SEVI, and SP with HSVs are direct. Moreover, viral growth curve assays showed that SEM and SEVI amyloids, as well as SP, sped up the kinetics of HSV replication such that the virus reached its replicative peak more quickly. Viral replication was increased by about 50- to 100-fold.

Along with SP, SEM and SEVI amyloids enhanced viral entry and increased infection rates by more than 10-fold, as assessed by flow cytometry assay and fluorescence microscopy. In this study, we found that the two amyloids as well as SP strongly enhance both HSV-1 and -2 infections in cell culture. Whether SEM or SEVI amyloids or SP could also enhance other herpesvirus infections has not been examined. Previously, we demonstrated that the amyloid fibrils semenogelin (SEM) and semen-derived enhancer of viral infection (SEVI), and seminal plasma (SP) augment cytomegalovirus infection (Tang et al., J. Semen plays an important role in carrying the viral particle that invades the vaginal or rectal mucosa and, thereby, initiates viral replication. Sexual transmission is a major route for the spread of both herpes simplex virus-1 (HSV-1) and -2. Human herpesviruses cause different infectious diseases, resulting in world-wide health problems.

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