HSV2 Specific Neutra™ Antibody Products

Are prolonged therapeutic development timelines or challenges in generating high-specificity antiviral antibodies hindering your HSV2 research? Creative Biolabs' HSV2 specific Neutra™ antibody products accelerate breakthroughs with advanced phage display screening and structural epitope mapping, enabling rapid development of neutralizing antibodies that precisely block viral entry and fusion.

Introduction to HSV2

Herpes simplex virus-2 (HSV2), a neurotropic alphaherpesvirus, is the primary causative agent of genital herpes, a lifelong infection marked by recurrent lesions and asymptomatic viral shedding. Its double-stranded DNA genome encodes 11 envelope glycoproteins, with glycoprotein D (gD) serving as a critical mediator of viral entry through interactions with host receptors such as nectin-1 and HVEM. HSV2 establishes latency in sensory ganglia, evading immune surveillance and complicating therapeutic interventions.

• Structure

The HSV2 virion comprises an icosahedral capsid surrounded by a tegument layer and a lipid envelope embedded with glycoproteins. Glycoprotein D (gD) forms a trimeric structure essential for receptor binding, while gB and the gH/gL complex drive membrane fusion. High-resolution structural studies reveal that neutralizing antibodies targeting conformational epitopes on gD disrupt receptor binding or inhibit fusion by blocking gD-gH/gL interactions.

• Related Signaling Pathways

HSV2 exploits host cell signaling to evade immune detection. Key pathways include:

- Interferon (IFN) suppression: HSV2 downregulates IFN production via viral proteins like ICP0, impairing innate antiviral responses.

- NF-κB activation: Viral glycoproteins trigger pro-inflammatory cytokine release, contributing to tissue damage.

- Apoptosis inhibition: HSV2 enhances survival of infected cells to sustain replication.

Fig.1 HSV-2's survival strategies and impact on host defense mechanisms.¹

• Associated Pathologies

HSV2 infections cause genital ulcers, neonatal herpes, and increased susceptibility to HIV. Persistent inflammation and neuronal damage underscore the need for therapies targeting viral entry and immune evasion mechanisms.

Applications of HSV2 Neutralizing Antibodies

• Antiviral Therapeutic Development

Neutralizing antibodies reduce viral load in preclinical models by targeting entry and fusion. Early administration correlates with diminished lesion severity and transmission rates, supporting their use in acute and recurrent infection management.

• Diagnostic Tool Development

High-affinity anti-gD antibodies enable rapid HSV2 detection in clinical samples. Applications include ELISA-based serology and point-of-care lateral flow assays, critical for early diagnosis and epidemiological studies.

• Vaccine Efficacy Evaluation

Quantifying neutralizing antibody titers post-vaccination using standardized assays (e.g., CPE-based neutralization) provides critical data for optimizing immunogen design. Creative Biolabs' antibodies serve as reference standards for validating vaccine-induced immune responses.

Our Anti-HSV2 Neutralizing Antibody Products

Neutralizing antibodies against HSV2 gD are pivotal for antiviral strategies. Monoclonal antibodies (mAbs) can bind distinct gD epitopes:

- Stabilize the N-terminal α-helix of gD, preventing conformational changes required for fusion.

- Blocks gD-nectin-1 binding, inhibiting viral attachment.

Creative Biolabs' antibodies exhibit nanomolar affinity validated via SPR and ELISA, ensuring specificity for research applications. We deliver rigorously validated HSV2 specific Neutra™ antibody products, engineered to meet the demands of antiviral research and therapeutic development. Our portfolio includes high-specificity mAbs for gD, optimized for applications ranging from structural studies to clinical assay development.

Contact our team today to explore custom solutions for your HSV2 projects.

REFERENCE

1. Borase, Hemant, and Deepak Shukla. "The interplay of genital herpes with cellular processes: a pathogenesis and therapeutic perspective." Viruses 15.11 (2023): 2195. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.3390/v15112195