Search bioRxiv⌕ Search

bioRxiv · 10.1101/2022.07.22.501208

A Prime/Pull RR2/CXCL11 Therapeutic Vaccine that Bolsters the Number and Function of Dorsal Root Ganglia Tissue-Resident HSV-Specific CD8+ TRM Cells Protects Latently Infected Guinea Pigs from Recurrent Genital Herpes

Abstract

Reactivation of herpes simplex virus type 2 (HSV-2) from latently infected dorsal root ganglia (DRG) and subsequent virus shedding in the genital tract trigger recurrent genital herpes. Memory CD8+ T cells play a critical role in preventing HSV-2 reactivation from latently infected DRG, thus reducing recurrent genital lesions. The role of T-cell attracting chemokines in promoting CD8+ T cell protective immunity in recurrent genital herpes remains to be fully elucidated. In this study, we investigated whether and how the CXCL11/CXCR3 pathway affects the frequency and function of DRG-resident CD8+ T cells and the severity of recurrent genital herpes. Latently infected guinea pigs were primed with the HSV-1 RR2 protein, delivered intramuscularly with CpG/Alum adjuvants, and the induced T cells were "pulled" from the periphery into the latently infected DRG using T-cell attracting CXCL11 chemokine, delivered to DRG. In the guinea pigs that received the prime/pull vaccine, we detected a significant increase in both the number and function of tissue-resident IFN-{gamma}+CD103+CD44+CXCR3+CD8+ TRM cells that infiltrated healed sites of the vaginal mucosa (VM) and DRG tissues. This was associated with a significant decrease in virus shedding and a reduction in both the severity and frequency of recurrent genital herpes lesions. In contrast, in the guinea pigs that received the RR2 vaccine alone, we detected fewer functional CD8+ TRM cells and no reduction in the severity of recurrent genital herpes. These findings highlight the role of the CXCL11/CXCR3 chemokine pathway in shaping tissue-resident CD8+ TRM cell protective immunity against recurrent genital herpes. IMPORTANCERecurrent genital herpes is a common sexually transmitted disease worldwide. Currently, no FDA-approved therapeutic vaccines are available. In the present study, we used HSV-2 latently infected guinea pig to investigate a novel therapeutic prime/pull vaccine strategy based on priming T cells systemically, with a recombinantly expressed herpes envelope and tegument protein RR2 and "pulling" primed T cells into the tissues of latently infected ganglia with the T-cell-attracting chemokine, CXCL11. We discovered that this RR2/CXCL11 prime/pull vaccine elicited a significant reduction in virus shedding and a decrease in both the severity and frequency of recurrent genital herpes sores. This protection correlated with increased numbers of functional tissue-resident IFN-{gamma}+CD103+CD44+CXCR3+CD8+ TRM cells that infiltrate healed sites of the VM tissues and DRG. Our findings shed light on the role of TRM cells in protection against recurrent genital herpes and propose the prime/pull therapeutic vaccine as a new strategy against genital herpes. TWEETThe present study presents a novel RR2/CXCL11 prime/pull therapeutic vaccine that elicited a significant reduction in virus shedding and a decrease in both the severity and frequency of recurrent genital herpes sores.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dhanushkodi, N., Prakash, S., Srivastava, R., Coulon, P.-G., Vahed, H., Zayou, L., Quadiri, A., Schaefer, H., BenMohamed, L.. 2022-07-23. A Prime/Pull RR2/CXCL11 Therapeutic Vaccine that Bolsters the Number and Function of Dorsal Root Ganglia Tissue-Resident HSV-Specific CD8+ TRM Cells Protects Latently Infected Guinea Pigs from Recurrent Genital Herpes. https://doi.org/10.1101/2022.07.22.501208

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

ACE-engineered human iPSC-derived neutrophils enhance host defense against multidrug-resistant bacterial infections

Severe neutropenia predisposes patients to life-threatening infections, while donor-dependent granulocyte transfusions are limited by availability and variable cell quality. Here, we engineered human induced pluripotent stem cells (iPSCs) to constitutively or inducibly express angiotensin-converting enzyme (ACE) and differentiated them into functional ACE-engineered neutrophils (ACE-iNeu). ACE expression enhanced granulocytic maturation, reactive oxygen species generation, inflammatory cytokine production, and antimicrobial signaling. ACE-iNeu exhibited enhanced bactericidal activity against methicillin-resistant Staphylococcus aureus and multidrug-resistant Pseudomonas aeruginosa. Following adoptive transfer into neutropenic mice, ACE-iNeu significantly reduced circulating and tissue bacterial burdens. Integrated metabolomic and transcriptomic analyses revealed ACE-associated alterations in adenine nucleotide abundance and developmental and inflammatory pathways. Together, these findings establish ACE engineering as a strategy to enhance the production and antimicrobial function of human iPSC-derived neutrophils and support further preclinical development of engineered granulocyte therapies for severe drug-resistant infections.

immunology↗

Tetravalent dengue mRNA vaccination orchestrates balanced four-serotype immunity with durable memory and protection in mice.

An effective dengue vaccine must establish durable immunity across four dengue virus (DENV) serotypes, evade antibody-dependent enhancement (ADE), and overcome immune imprinting from prior exposure. Here, we developed TetprM-E mRNA-LNP, a tetravalent vaccine comprising LNP-formulated nucleoside-modified mRNAs encoding DENV1-4 precursor membrane-envelope (prM-E) antigens, and evaluated its immunogenicity, durability, protection and breath across serotype-specific immune backgrounds. Three immunization strategies elicited neutralizing titers greater than 1:1500 against each serotype. Passive transfer of immune sera conferred 100% survival and reduced viremia after lethal DENV2 challenge in immunocompromised mice. Vaccination induced DENV envelope (env)-specific CD8+T cells and CD4-dependent germinal-center responses. DENV env-binding antibodies persisted for 34 weeks alongside DENV env-specific memory B cells. Vaccine-elicited sera showed no measurable in vitro ADE. Although monovalent priming initially biased antibody responses, TetprM-E mRNA-LNP vaccination broadened neutralization across DENV1-4 regardless of priming serotype. Together, TetprM-E mRNA-LNP elicits broad, durable, and protective immunity despite serologic constraints from pre-existing immunity.

immunology↗

The antagonism of sex chromosomes and sex hormones dictates outcomes in Th17 cell-mediated central nervous system autoimmunity.

Biological sex traits are shaped by the combined effects of both sex hormones and chromosomes. How these factors interact in sex-related autoimmune diseases, such as multiple sclerosis (MS), has been a subject of intense recent interest. Here, using the Four Core Genotype (FCG) mouse model, in which these two variables can be disentangled, we describe an antagonism between sex hormones and chromosomes that potently influences outcomes in T helper 17 (Th17)-driven progressive central nervous system (CNS) autoimmunity. Male gonadal hormones dampen disease severity, irrespective of sex chromosome complement, by promoting a Wnt/{beta}-catenin signaling program associated with a homeostatic, non-pathogenic Th17 phenotype. By contrast, XY chromosomal complement exacerbates Th17 pathogenicity in a recipient sex-dependent manner; we identify the X-linked molecule SUV39H1 as an inhibitor of inflammatory Th17 cell function. Unexpectedly, we found that hormonally and chromosomally female FCG Th17 cells induced far more severe disease than WT female counterparts despite being genetically identical, pointing to a parental imprinting effect in dictating Th17 cell pathogenicity. These latter investigations uncovered Runx2, a transcription factor previously linked to developmental programs, as a novel negative regulator of the pathogenicity of Th17 cells. Together, our findings establish biological sex as a multilayered regulator of Th17 pathogenicity, revealing distinct and sometimes opposing contributions of hormones, chromosomes, and parental inheritance.

immunology↗