PubMed ID: 42475334
Author(s): Kolb AW, Sauter MM, Ferguson S, Jain AS, Sheibani NK, Sorenson CM, Brandt CR. Herpes simplex virus type-1 ocular infection in thrombospondin-1 deficient C57BL/6J mice. PLoS One. 2026 Jul 20;21(7):e0352457. doi: 10.1371/journal.pone.0352457. eCollection 2026. PMID 42475334
Journal: Plo S One, Volume 21, Issue 7, 2026
Herpes simplex virus type 1 (HSV-1) corneal infection triggers an immunopathological response and corneal neovascularization leading to vision impairment. Thrombospondin-1 (TSP-1) is a matricellular protein shown to regulate inflammatory processes and vascularization in the cornea. The purpose of this study was to determine if loss of TSP-1 alters the pathology of HSV-1 keratitis. The recombinant virus INV-2C or the low passage orolabial HSV-1 isolate, Ikey, were administered to scarified corneas of 8-week-old Thbs1-/- and control C57BL/6J mice. Blepharitis, corneal neovascularization, corneal clouding, weight loss, viral titers, and mortality were determined on multiple days post infection. Corneal nerve loss was evaluated on day 2 and day 7. Neutralizing antibody, T-cell responses, and infiltrating cells in the aqueous and vitreous humors were quantified. There was no significant difference between Thbs1-/- and C57BL/6J control mice when comparing any corneal disease outcome with either virus. Severe pan-uveitis developed in both C57BL/6J and Thbs1-/- mice infected with the Ikey strain of virus. There were no significant differences in antibodies to HSV or in the number of HSV-1 specific IFN-g secreting T-cells in the spleen between C57BL/6 or TSP-1-/- mice. The lack of TSP-1 did not affect the severity of corneal disease, immune responses to HSV-1, or sensory nerve loss suggesting either TSP-1 functions are not involved in HSV-1 pathogenesis or that other members of the TSP family can substitute for the loss of TSP-1.
Copyright: © 2026 Kolb et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.