Table 3.

Role of mucosal chemokine in HSV-1/2 infections.

Chemokine	Genital mucosa findings (HSV-1/2)	Ocular mucosa findings (HSV-1/2)	Key reference (2022–2025)
CCL25	Primarily a gut-associated chemokine (CCR9 ligand) expressed in small intestinal and thymic epithelium. No significant findings in genital HSV – it is not known to be induced or required in vaginal HSV infection (mucosal immunity to HSV-2 does not appear to involve CCL25).	No data in ocular HSV. (CCL25 is tissue-specific to the gastrointestinal tract; it is not typically expressed in ocular mucosa)	Meurens et al., 2006 – J. Interferon Cytokine Res. (CCL25 in mucosal immunity context); Smith et al., 2022 – Front. Immunol. (notes major mucosal chemokines and need for further study in HSV).
CCL28	Protective role: Homeostatically produced in vaginal mucosa. Elevated in asymptomatic HSV-infected individuals and mice, correlating with higher HSV-specific effector memory CCR10+ CD8+ T cells and memory B cells in vaginal tissue. CCL28-CCR10 axis mobilizes antiviral lymphocytes to infection site; CCL28knockout mice have increased susceptibility to genital HSV-2 and reduced mucosal memory T/B cell infiltration.	Not studied in ocular HSV. (Ocular surface epithelial cells can secrete CCL28 during inflammation, but its role in HSV-1 ocular infection is undetermined. Excess chemokine in eye may contribute to immunopathology rather than protection.)	Dhanushkodi et al., 2023 – J. Immunol. 211(1):118–129 (demonstrates CCL28’s role in recruiting CCR10+ T and B cells for genital HSV protection; DOI: 10.4049/jimmunol.2300093).
CXCL17	Protective role: Constitutively present in vaginal mucosa and induced by HSV. Higher CXCL17 levels observed in protected mice after intravaginal HSV exposure, accompanied by increased CXCR8+ CD8+ effector memory and CD103^+ tissue-resident T cells in the vaginal mucosa. In CXCL17 knockout mice, genital HSV-1 infection leads to fewer tissue CD8 T cells, more viral replication, and more latency in ganglia, indicating CXCL17 is crucial for mobilizing protective CD8+ T cells to the genital mucosa.	Not studied in ocular HSV. (No published evidence of CXCL17’s role in HSV-1 eye infections. Ocular herpes lesions are driven by an intense chemokine/cytokine storm causing inflammation, so any CXCL17 effect is uncharacterized. It has been suggested as a mucosal immunomodulator, but no direct data in the eye.)	Srivastava et al., 2018 – J. Immunol. 200(8):2915–2926 (CXCL17 mediates recruitment of CXCR8+ CD8 TEM and TRM, protecting against vaginal HSV; DOI: 10.4049/jimmunol.1701474). Smith et al., 2022 – Front. Immunol. (review, notes chemokine CXCL17 in HSV mucosal immunity).
CXCL14	Constitutively expressed in mucosal epithelium; specific role in genital HSV infection remains unclear (no direct studies). Proposed to participate in basal immune surveillance but not confirmed in HSV-2 models.	Upregulated on ocular surface under inflammatory stress; no HSV-specific data. Ocular infection triggers broad chemokine release that mainly contributes to tissue damage rather than protection.	Dhanushkodi et al., 2023 – J. Immunol. (211(1):118–129, discusses CXCL14 as a mucosal chemokine; DOI: 10.4049/jimmunol.2300093).