Herpes Simplex Virus: Molecular Pathogenesis, Type-Specific Disease Burden, and Advances in Prevention and Treatment.
- 1Division of HIV/AIDS and Sex-Transmitted Virus Vaccines, Institute for Biological Product Control, National Institutes for Food and Drug Control, Beijing 102629, China.
- 2National Vaccine and Serum Institute (NVSI), Beijing 101111, China.
Abstract
Herpes simplex virus (HSV) is a highly prevalent neurotropic DNA virus that causes orolabial herpes, genital herpes, keratitis, neonatal infection, meningitis and encephalitis. HSV-1 and HSV-2 share epithelial entry, lytic replication, immune evasion, lifelong sensory-ganglion latency and periodic reactivation, yet they differ in typical transmission routes, anatomical recurrence and public-health burden. Rather than mechanically separating both viruses throughout, this review emphasizes shared HSV biology and highlights type-specific differences where they affect clinical interpretation or intervention design. We connect glycoprotein-mediated entry, receptor use, axonal transport, immune evasion and latency with mucocutaneous, ocular, neurologic, neonatal and genital disease. We then synthesize lessons from failed glycoprotein-D vaccine trials, multivalent and mRNA platforms, helicase-primase inhibitors, monoclonal antibodies, RNA-based approaches, genome editing and latency-directed strategies. A mechanism-guided HSV strategy should reduce acquisition, shedding and recurrence, prevent ocular, neurologic and neonatal complications, manage antiviral resistance and ultimately address latent infection.
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BibTeX
@article{jiang2026herpes,
title = {{Herpes Simplex Virus: Molecular Pathogenesis, Type-Specific Disease Burden, and Advances in Prevention and Treatment.}},
author = {Chenhao Jiang and Jianhui Nie and Li Zhang},
journal = {Viruses},
year = {2026},
month = oct,
doi = {10.3390/v18101116},
url = {https://europepmc.org/article/MED/42944036},
note = {CC BY},
}
RIS
TY - JOUR
TI - Herpes Simplex Virus: Molecular Pathogenesis, Type-Specific Disease Burden, and Advances in Prevention and Treatment.
AU - Chenhao Jiang
AU - Jianhui Nie
AU - Li Zhang
PY - 2026
DA - 2026/10/09
JO - Viruses
DO - 10.3390/v18101116
UR - https://europepmc.org/article/MED/42944036
AB - Herpes simplex virus (HSV) is a highly prevalent neurotropic DNA virus that causes orolabial herpes, genital herpes, keratitis, neonatal infection, meningitis and encephalitis. HSV-1 and HSV-2 share epithelial entry, lytic replication, immune evasion, lifelong sensory-ganglion latency and periodic reactivation, yet they differ in typical transmission routes, anatomical recurrence and public-health burden. Rather than mechanically separating both viruses throughout, this review emphasizes shared HSV biology and highlights type-specific differences where they affect clinical interpretation or intervention design. We connect glycoprotein-mediated entry, receptor use, axonal transport, immune evasion and latency with mucocutaneous, ocular, neurologic, neonatal and genital disease. We then synthesize lessons from failed glycoprotein-D vaccine trials, multivalent and mRNA platforms, helicase-primase inhibitors, monoclonal antibodies, RNA-based approaches, genome editing and latency-directed strategies. A mechanism-guided HSV strategy should reduce acquisition, shedding and recurrence, prevent ocular, neurologic and neonatal complications, manage antiviral resistance and ultimately address latent infection.
SN - 1999-4915
ER -