PURPOSE: This study determined the seroprevalence of herpes virus 2 in gravidas and the differences between herpes virus 2-infected and healthy gravidas. The need to screen gravidas for herpes virus 2 was also evaluated. MATERIALS AND METHODS: A retrospective analysis involving 500 gravidas who underwent herpes virus 2 serologic testing and delivery in our hospital between January 2009 and August 2010 was performed. All patients in the study group were classified as herpes simplex virus 2 (HSV2) positive, and all cases were analyzed with respect to the clinical course of the pregnancy, pregnancy outcome, obstetric complications, and neonatal outcomes. SPSS software (version 14.0) was used for statistical analysis. A chi-square test and Student's t-test were used for statistical analysis. RESULTS: In the current study, the herpes virus 2 seroprevalence rate in gravidas was 17%. There was no significant difference in the rates of preterm delivery, premature rupture of membranes, preterm labor, and intrauterine growth restriction between the herpes virus 2-infected gravidas and the healthy control group. The rates of spontaneous abortion and sexually transmitted disease were higher in the herpes virus 2 infection group than the healthy control group. CONCLUSION: After educating gravidas on genital herpes and, if gravidas thereafter consent to herpes virus 2 screening, the risk of neonatal herpes virus 2 infections can be reduced. In addition, examination of gravidas for sexually transmitted diseases would increase as would appropriate treatment.
Adult ; Female ; Herpes Genitalis/*diagnosis/epidemiology/virology ; Herpes Simplex ; Herpesvirus 2, Human/*pathogenicity ; Humans ; Pregnancy ; Pregnancy Complications, Infectious/diagnosis/epidemiology/virology ; Retrospective Studies

OBJECTIVETo investigate the immune responses and protection from virus challenge, induced by the coinjection of IL-2cDNA with herpes simplex virus type 1 (HSV-1) glycoprotein-D (gD) DNA vaccine.

METHODSTwo DNA vaccines (pgD and pIL-2) were constructed by inserting the gD gene and IL-2 cDNA into the eukaryotic expression vector pcDNA3.1, respectively. The BALB/c mice were inoculated intramuscularly three times at 2-week intervals. Two weeks after the final immunization, mice were bled for antibody assay and spleen cells were separated for Th cell proliferation and cytokine assays. Delayed type hypersensitivity (DTH) response was detected by the pinna-swelling test. Corneal protection under HSV-1 virus challenge was continuously observed with slit-lamp microscope.

RESULTSIL-2 cDNA coinjection remarkably enhanced the specific IgG2a level when compared with gD plasmid vaccination alone. Th cell proliferation and secretion of cytokines (IL-2 and IFN-gamma) were significantly increased by IL-2 cDNA coinjection. However, the production of IL-10 was inhibited. The DTH response was also enhanced by IL-2 coinjection. When the mice were challenged with HSV-1, the cornea epithelial lesions were significantly alleviated by IL-2 coinjection as compared with gD vaccination alone.

CONCLUSIONIL-2 cDNA can enhance both the humoral and cellular immune responses, and thus increase the vaccine potency.

Animals ; Antibodies, Viral ; blood ; COS Cells ; Cell Proliferation ; Cercopithecus aethiops ; DNA ; genetics ; Female ; Herpesvirus 1, Human ; pathogenicity ; Hypersensitivity, Delayed ; immunology ; Immunization ; Immunoglobulin G ; blood ; Interferon-gamma ; blood ; Interleukin-2 ; biosynthesis ; genetics ; Mice ; Mice, Inbred BALB C ; Random Allocation ; Th1 Cells ; cytology ; Transfection ; Vaccines, DNA ; immunology ; Viral Envelope Proteins ; biosynthesis ; genetics ; Viral Vaccines ; immunology

GITR (glucocorticoid-induced TNF receptor) is a recently identified member of the TNF receptor superfamily. The receptor is preferentially expressed on CD4+CD25+ regulatory T cells and GITR signals break the suppressive activity of the subset. In this study, we wanted to reveal the in vivo function of GITR in herpes simplex virus type 1 (HSV-1) infection. A single injection of anti-GITR mAb (DTA-1) immediately after viral infection significantly increased the number of CD4+ and CD8+ T cells expressing CD25, an activation surface marker, and secreting IFN-gamma. We confirmed these in vivo observations by showing ex vivo that re-stimulation of CD4+ or CD8+ T cells with a CD4+ or CD8+ T-cell-specific HSV-1 peptide, respectively, induced a significant elevation in cell proliferation and in IFN-gamma secretion. Our results indicate that GITR signals play a critical role in the T-cell immunity to HSV-1.
Animals ; Antibodies, Monoclonal/pharmacology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Proliferation ; Female ; Glucocorticoids/*pharmacology ; Herpes Simplex/*immunology ; Herpesvirus 1, Human/pathogenicity ; *Immunity, Cellular ; Interferon Type II/secretion ; *Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Peptide Fragments/metabolism ; Receptors, Interleukin-2/metabolism ; Receptors, Nerve Growth Factor/genetics/immunology/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/immunology/*metabolism ; Research Support, Non-U.S. Gov't ; T-Lymphocytes/*immunology/metabolism/virology