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Updated: Aug 21, 2026
Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
Herpesvirus infection of ICAM-1-deficient mice
Hyo W Jung1, Cho-Rok Jung, Beom K Choi
1Immunomodulation Research Center, University of Ulsan, 29 Mukeo-dong, Nam-ku, Ulsan, Korea 680-749.
Purpose:
To determine the effect of ICAM-1 deficiency on viral infection of the cornea.
Materials And Methods:
Wild-type and intercellular adhesion molecule 1 (ICAM-1)-deficient mice were infected with the RE strain of herpes simplex virus type 1 (HSV-1). Corneal swabs and trigeminal ganglia were obtained and analyzed for infectious virus. Corneas and trigeminal ganglia were evaluated for signs of inflammation by immunohistochemical staining and for interferon-gamma (IFN-gamma)-producing cells by enzyme-linked immunospot assay (ELISPOT). Serum anti-HSV-1 antibody titers were determined by enzyme-linked immunosorbent assay (ELISA).
Results:
Viral titers in corneal swabs from the wild-type and ICAM-1-deficient mice were not significantly different during the 21-day study. Infectious virus was present in the trigeminal ganglia of wild-type and ICAM-1-deficient mice through day 6 after infection. Serum anti-HSV-1 antibody titers were significantly higher in wild-type mice 6 days after infection, compared with ICAM-1-deficient mice; by day 8 and thereafter, however, antibody titers were not significantly different. Production of interferon gamma was greater in trigeminal ganglion cells from wild-type mice stimulated with interleukin 12 and interleukin 18 on days 4, 6, and 8 after infection compared with cells from ICAM-1-deficient mice. Histopathologic analysis of corneal and ganglion sections from wild-type and ICAM-1-deficient mice showed no significant differences in the time-course of appearance or the intensity of the inflammatory infiltrate. Immunohistochemical staining for CD3(+) T-lymphocytes and CD11b(+) neutrophils and macrophages demonstrated equivalent numbers of these cells in the corneas and trigeminal ganglia of wild-type and ICAM-1-deficient mice.
Conclusions:
The results of these experiments indicate that ICAM-1 deficiency has only a modest effect on viral infection of the cornea and the development of an acquired immune response.
Insights
Intercellular adhesion molecule 1 (ICAM-1) deficiency minimally impacts herpes simplex virus type 1 (HSV-1) corneal infection and immune response. ICAM-1 deficient mice showed similar viral loads and inflammation compared to wild-type mice.
Area of Science:
- Immunology
- Virology
- Ophthalmology
Background:
- Intercellular adhesion molecule 1 (ICAM-1) plays a role in immune cell trafficking and inflammation.
- Herpes simplex virus type 1 (HSV-1) is a common cause of infectious eye disease.
Purpose of the Study:
- To investigate the impact of ICAM-1 deficiency on HSV-1 corneal infection and the subsequent immune response in a mouse model.
Main Methods:
- Wild-type and ICAM-1-deficient mice were infected with HSV-1.
- Viral loads in corneas and trigeminal ganglia were quantified.
- Inflammation, immune cell infiltration, and antibody titers were assessed.
- Interferon-gamma (IFN-γ) production was measured.
Main Results:
- No significant difference in viral titers was observed in corneas between wild-type and ICAM-1-deficient mice.
- Infectious virus was detected in trigeminal ganglia of both groups.
- While initial antibody titers were higher in wild-type mice, they became comparable later.
- IFN-γ production was greater in wild-type mice, but inflammation and immune cell infiltration were similar.
Conclusions:
- ICAM-1 deficiency has a modest effect on HSV-1 corneal infection.
- The development of the acquired immune response to HSV-1 is only slightly altered by the absence of ICAM-1.
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