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Review
. 2013 Apr;9(4):729-35.
doi: 10.4161/hv.23289. Epub 2013 Feb 26.

Recent advances in vaccine development for herpes simplex virus types I and II

Affiliations
Review

Recent advances in vaccine development for herpes simplex virus types I and II

Jeffrey L Coleman et al. Hum Vaccin Immunother. 2013 Apr.

Abstract

Despite recent advances in vaccine design and strategies, latent infection with herpes simplex virus (HSV) remains a formidable challenge. Approaches involving live-attenuated viruses and inactivated viral preparations were popular throughout the twentieth century. In the past ten years, many vaccine types, both prophylactic or therapeutic, have contained a replication-defective HSV, viral DNA or glycoproteins. New research focused on the mechanism of immune evasion by the virus has involved developing vaccines with various gene deletions and manipulations combined with the use of new and more specific adjuvants. In addition, new "prime-boost" methods of strengthening the vaccine efficacy have proven effective, but there have also been flaws with some recent strategies that appear to have compromised vaccine efficacy in humans. Given the complicated lifecycle of HSV and its unique way of spreading from cell-to-cell, it can be concluded that the development of an ideal vaccine needs new focus on cell-mediated immunity, better understanding of the latent viral genome and serious consideration of gender-based differences in immunity development among humans. This review summarizes recent developments made in the field and sheds light on some potentially new ways to conquer the problem including development of dual-action prophylactic microbicides that prohibit viral entry and, in addition, induce a strong antigen response.

Keywords: T cells; adjuvant; asymptomatic; humoral; immunity; seronegative; seropositive; symptomatic.

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Figures

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Figure 1. Subunit vaccine. This illustration shows a glycoprotein subunit vaccine administered through a syringe into the oro-facial pathway inducing an accessory cell to elicit a T cell response. The antigen presentation will cause these cells to become either CD4+ cells or CD8+ cells. These will then act against HSV, which has established latency in the trigeminal or cervical ganglia.
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Figure 2. Microbivac model. This model shows a microbicide preventing viral entry into an epithelial cell while eliciting antigen presentation from an accessory cell, inducing long-term immunity. The microbivac concept is based on a hypothetical microbicide that traps virions and serves as an antigen-presenting vaccine platform.

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