Neutrophil-mediated suppression of virus replication after herpes simplex virus type 1 infection of the murine cornea
Neutrophil-mediated suppression of virus replication after herpes simplex virus type 1 infection of the murine cornea
复制标题
DOI:
10.1128/jvi.70.2.898-904.1996
复制
发表时间:
1996-02-01
影响因子:
5.4
通讯作者:
Lausch, RN
中科院分区:
文献类型:
--
作者:
Tumpey, TM;Chen, SH;Lausch, RN
Herpes simplex virus type 1 (HSV-1) infection of the murine cornea induces the rapid infiltration of neutrophils. We investigated whether these cells could influence virus replication. BALB/c mice treated with monoclonal antibody (MAb) RB6-8C5 experienced a profound depletion of neutrophils in the bloodstream, spleen, and cornea. In these animals, virus titers in the eye were significantly higher than those in the immunoglobulin G-treated controls at 3 days postinfection. By day 9, virus was no longer detectable in the controls, whereas titers of 10(3) to 10(6) PFU were still present in the neutrophil-depleted hosts. Furthermore, virus spread more readily to the skin and brains of MAb RB6-8C5-treated animals, rendering them significantly more susceptible to HSV l-induced blepharitis and encephalitis. Only 25% of the treated animals survived, whereas all of the controls lived. Although MAb RB6-8C5 treatment did not alter the CD4(+) T-cell, B-cell, natural killer cell, or macrophage populations, the CD8(+) T-cell population was partially reduced. Therefore, the experiments were repeated in severe combined immunodeficiency mice, which lack CD8(+) T cells. Again virus growth was found to be significantly elevated in the eyes, trigeminal ganglia, and brains of the MAb RB6-8C5-treated hosts. These results strongly indicate that in both immunocompetent and immunodeficient mice, neutrophils play a significant role in helping to control the replication and spread of HSV-1 after corneal infection.