HSV Specific Neutra™ Antibody Products

Herpes Simplex Virus (HSV) is a viral infection that causes the skin and mucous membranes sores. There are two types: HSV-1, primarily causing oral herpes, and HSV-2, mainly causing genital herpes. The virus has a double-stranded DNA structure. It is transmitted via direct contact with infected bodily fluids or sores. Symptoms include blisters, itching, pain, and fever. HSV can lead to complications like neonatal herpes, encephalitis, and recurrent outbreaks. The antiviral medications can help manage symptoms and reduce transmission.

HSV Cell Cycle

HSV infects host cells by binding to various receptors, causing the viral envelope to fuse with the plasma membrane and release the capsid into the cytoplasm. After reaching the nuclear pore, the capsid transports the viral DNA into the nucleus, where transcription, replication, and capsid assembly occur. Viral gene expression follows a temporal order: immediate early (alpha), early (beta), and late (gamma) proteins. Alpha gene products regulate viral replication and promote beta protein transcription. Beta proteins play a role in DNA replication and packaging. After viral DNA replication, Gamma proteins encode structural components for the capsid, tegument, and envelope. Finally, newly formed virions are packaged and released with the lipid envelope.

Fig. 1 Schematic of HSV cell cycle.¹

Immunology and Viral Defense

HSV uses multiple tactics to escape the host's immune defense. The viral protein ICP47 interferes with antigen presentation by blocking the transporter proteins TAP1 and TAP2, preventing viral and cellular peptides from reaching the endoplasmic reticulum. Proteins like Us3, gJ, and gD inhibit apoptosis that would normally occur in response to cellular stress. The viral protein VHS, encoded by the UL41 gene, degrades both host and viral mRNA, halting cellular protein synthesis. Additionally, ICP27 collaborates with VHS to further block host mRNA production. HSV also uses the viral protein γ₁34.5 to dephosphorylate eIF-2alpha, allowing viral protein synthesis while inhibiting cellular translation.

Latency, Reactivation, and Neurovirulence

Once infection begins on mucosal surfaces, HSV-1 and HSV-2 establish latency in sensory ganglia by traveling retrogradely along sensory nerves to the trigeminal and sacral ganglia. During latency, the viral genome adopts a circular form, with latency-associated transcripts (LAT) as the primary gene products. LATs protect against neuronal cell death by preventing apoptosis, aiding axon regeneration, and suppressing viral gene expression. Reactivation occurs when the virus travels back along sensory nerves to cause localized vesicular eruptions. Triggers for reactivation include stress, trauma, fever, immunosuppression, and UV light exposure. Reactivation leads to decreased LAT levels and activation of lytic gene transcripts. HSV's neurovirulence, enabled by viral proteins like γ134.5, allows the virus to invade and replicate in neural tissue by interfering with host defenses, including PKR and eIF-2alpha. Mutants lacking γ134.5 cannot replicate in the CNS, and latency is reduced.

Fig. 2 Establishment of HSV latency in neurons.¹

Anti-HSV Neutralizing Antibodies

Antibodies targeting HSV are crucial for both diagnosis and potential therapeutic strategies. These antibodies are designed to bind to specific viral antigens, such as the glycoproteins on the viral envelope. By neutralizing the virus, they prevent HSV from entering host cells and triggering infection. Additionally, antibodies targeting HSV can be used to detect viral presence in clinical samples, aiding in diagnosing HSV infections. Research into therapeutic antibodies continues to explore their potential in treating HSV-related diseases, including genital and ocular infections. Research has demonstrated one potent neutralizing and protective antibody against HSV could compete with cell receptors, disrupting viral attachment by blocking receptor binding. Another HSV-specific monoclonal antibody has shown promise in preventing reactivation and reducing viral load.

Fig. 3 Schematic representation of lateral flow assay test based on antibody for HSV-2 infections detection.²

Creative Biolabs offers high-quality anti-HSV neutralizing antibodies to support your research on HSV infections. These antibodies are suitable for various applications, including WB, ELISA, IF, Neutralization, etc.

REFERENCES

1. Zhu, Shuyong, and Abel Viejo-Borbolla. "Pathogenesis and virulence of herpes simplex virus." Virulence 12.1 (2021): 2670-2702. Distributed under Open Access license CC BY 4.0, without modification.
2. Goux, Heather J., et al. "Evaluation of a nanophosphor lateral-flow assay for self-testing for herpes simplex virus type 2 seropositivity." PLoS One 14.12 (2019): e0225365. Distributed under Open Access license CC0 1.0, without modification.