Abstract
Herpes simplex virus type-2 (HSV-2) is a common cause of genital infections throughout the world. Currently no prophylactic vaccine or therapeutic cure exists against the virus that establishes a latent infection for the life of the host. Intravaginal microbivac is a developing out-of-the-box strategy that combines instant microbicidal effects with future vaccine-like benefits. We have recently shown that our uniquely designed zinc oxide tetrapod nanoparticles (ZOTEN) show strong microbivac efficacy against HSV-2 infection in a murine model of genital infection. In our attempts to further understand the antiviral and immune bolstering effects of ZOTEN microbivac and to develop ZOTEN as a platform for future live virus vaccines, we tested a ZOTEN/HSV-2 cocktail and found that prior incubation of HSV-2 with ZOTEN inhibits the ability of the virus to infect vaginal tissue in female Balb/c mice and blocks virus shedding as judged by plaque assays. Quite interestingly, the ZOTEN-neutralized virions elicit a local immune response that is highly comparable with the HSV-2 infection alone with reduced inflammation and clinical manifestations of disease. Information provided by our study will pave the way for the further development of ZOTEN as a microbivac and a future platform for live virus vaccines.
Highlights
Herpes simplex virus-2 (HSV-2) is a neurotropic double stranded DNA virus capable of lytic infection in multiple host cell types as well as latent infection in neuronal cells [1]
zinc oxide tetrapod nanoparticles (ZOTEN)/HSV-2 was used for the intravaginal infection of BALB/c mice
The viral titers recovered from these vaginal swabs were significantly lower in ZOTEN/HSV-2 group at 2 days post infection, with 4 out of 5 mice displaying no detectable virus. These findings confirm the potent antiviral activity displayed by ZOTEN and its ability to neutralize virus and decrease viral shedding as early as 2 days post infection (Figures 2A,B)
Summary
Herpes simplex virus-2 (HSV-2) is a neurotropic double stranded DNA virus capable of lytic infection in multiple host cell types as well as latent infection in neuronal cells [1]. The viral DNA genome is encased in an icosadeltahedral protein capsid which is surrounded by tegument proteins [2]. The capsid and tegument are enveloped in a lipid bilayer composed of multiple viral proteins and glycoproteins on the surface of the virus particle [3]. HSV-2 entry into the host cell primarily involves the interaction of the viral entry glycoproteins with various cell surface receptors that facilitate virion envelope fusion with the plasma membrane of the host cell causing capsid penetration into the cytoplasm [4]. Once the genome reaches the nucleus, viral protein production occurs in a sequential manner beginning with immediate early gene products that promote immune evasion and neurovirulence [5]. Proteins are synthesized which are required for viral
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