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Abstract
Herpes simplex virus type 1 (HSV1) is a complicated structural agent with a sophisticated transcription process and a high infection rate. A vaccine against HSV1 is urgently needed. As multiple viral-encoded proteins, including structural and nonstructural proteins, contribute to immune response stimulation, an attenuated or deficient HSV1 vaccine may be relatively reliable. Advances in genomic modification technologies provide reliable means of constructing various HSV vaccine candidates. Based on our previous work, an M6 mutant with mutations in the UL7, UL41, LAT, Us3, Us11 and Us12 genes was established. The mutant exhibited low proliferation in cells and an attenuated phenotype in an animal model. Furthermore, in mice and rhesus monkeys, the mutant can induce remarkable serum neutralizing antibody titers and T cell activation and protect against HSV1 challenge by impeding viral replication, dissemination and pathogenesis.
Highlights
Herpes simplex virus type 1 (HSV1), a double-stranded DNA virus with a complicated genomic structure and transcriptional mechanism [1, 2], is an agent that leads to various herpes infections, more commonly causing oral vesicles, corneal herpes and approximately 47% of first-time genital herpes cases [3, 4]
Previous studies have indicated that attenuated or deficient HSV1 vaccines are capable of safely eliciting a comprehensive protective immune response
A series of HSV1 mutants with deficiencies in different genes, including the UL7 gene involved in viral transcriptional regulation, the UL41 gene related to virulence and the LAT gene involved in latency establishment, were constructed and identified to present different levels of attenuation [24, 25]
Summary
Herpes simplex virus type 1 (HSV1), a double-stranded DNA virus with a complicated genomic structure and transcriptional mechanism [1, 2], is an agent that leads to various herpes infections, more commonly causing oral vesicles, corneal herpes and approximately 47% of first-time genital herpes cases [3, 4]. Recent reports on deficient HSV vaccines suggest that multiple proteins encoded during viral infection, including structural and nonstructural molecules, contribute to the comprehensive antigenic signals required for a specific immune response [13,14,15]. In this case, it is reasonable to develop an attenuated or deficient HSV1 vaccine because these vaccines are capable of eliciting a comprehensive protective immune response with the premise of ensured safety [16,17,18,19]. The biological characteristics and attenuated phenotype of this mutant, especially its potential to elicit immunoprotective effects, were analyzed and evaluated in cells and animal models in this work
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