Article

Immunogenicity and protective effect of a DNA construct encoding certain neutralizing epitopes of herpes simplex virus type-1 glycoprotein B.

Department of Virology, School of Medical Sciences, Tarbiat Modarres University, Tehran, Iran.
Folia biologica (Impact Factor: 0.78). 02/2005; 51(4):109-13.
Source: PubMed

ABSTRACT Much attention is presently focused on the vaccination with certain epitopes of an antigen. To further study the ability of neutralizing epitopes mapped in the first 1515 nucleotides of glycoprotein B of herpes simplex virus type-1 (gB-1) to induce neutralizing antibodies, a DNA immunization approach was employed. Vaccination of mice with a plasmid expressing the neutralizing epitopes induced humoral immune responses, although the antibody titre was significantly lower than that of antibodies induced by the full-length gB-1 gene. Furthermore, the plasmid DNA could not protect the mice against HSV-1 lethal challenge, but could significantly prolong the survival time compared to mock-vaccinated group.

Download full-text

Full-text

Available from: Hoorieh Soleimanjahi, Aug 17, 2015
0 Followers
 · 
89 Views
  • Source
    • "Wild HSV-1 was isolated from a cold sore lesion of a patient. The virus was confirmed as HSV-1 with an HSV-1 by IFA using HSV-1 specific monoclonal antibody [33]. The neurovirulence of the virus was proven by injection of the virus into mice and isolation of the virus from brains of dead mice. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The immunomodulatory effects of exogenous opioids on induction of acquired immunity during microbial infection are now well known; however, our knowledge about the relationship between endogenous opioid response and microbial infections is rudimentary. Here, we report the effect of administration of Naloxone (NLX), an opioid receptor antagonist, on induction of acquired immunity during primary herpes simplex virus type 1 (HSV-1) infection. BALB/c mice received NLX, twice daily, 2 h before infection with HSV-1 until 7 days after infection. Cell-mediated immunity was assessed by evaluating lymphocyte proliferation, interferon-gamma (IFN-gamma) production, delayed type hypersensitivity (DTH) and mortality rate after acute HSV-1 challenge. The findings showed that a higher level of cell-mediated immunity was induced in the NLX-treated animals compared to the control group after induction of HSV-1 infection. However, the data indicate similar neutralizing antibody production in NLX-treated animals and control animals. This observation and further studies in this field may lead to the use of NLX as an adjuvant for designing microbial vaccines and adjunctive therapy of viral infections.
    Microbial Pathogenesis 11/2007; 43(5-6):217-23. DOI:10.1016/j.micpath.2007.06.001 · 2.00 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The vast majority of the world’s population is infected with Herpes simplex virus (HSV). Although antiviral therapy can reduce the incidence of reactivation and asymptomatic viral shedding and limits morbidity and mortality from active disease, it cannot cure infection. Therefore, the development of an effective vaccine is an important global health priority. In this study, the induction of IFN-γ production was compared in different herpes simplex virus 1 (HSV-1) vaccines. Glycoprotein D (gD1) as a major immunogenic HSV-1 glycoprotein was chosen to our study. Balb/c mice were administered with DNA vaccine encoding gD1, subunit glycoprotein vaccine including insect cells infected by a gD1 recombinant Baculovirus, prime DNA vaccine boosted by subunit glycoprotein vaccine, inactivated KOS strain as a positive control, pcDNA3 plasmid and Sf9 cells as negative controls. Evaluation tests showed that the amount of IFN-γ mRNA at 8, 16 and 32 hours after restimulation sharply decreased whereas, the IFN-γ protein level is significantly increased. Our results revealed that at 14 days after immunization IFN-γ secretion of stimulated cells in all of the vaccinated groups dramatically raised rather than secreted IFN-γ levels in mice that were analyzed at 7 days after vaccination. In comparison to other groups; Prime-Boost immunization dramatically caused vigorous and prompt IFN-γ production at 7 days after immunization and 8 hours after restimulation.
    Molecular Biology 06/2009; 43(3):388-393. DOI:10.1134/S0026893309030066 · 0.74 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: It has been reported that acute morphine administration modulates innate immune response to herpes simplex virus 1 (HSV-1) infection. In this study, the effect of acute morphine on innate resistance and its probable mechanisms in increasing the mortality rate during HSV-1 infection were investigated. Mice were infected with HSV-1 24 h prior to different doses of morphine or saline administration and the mortality rate was recorded. Spleen cells were obtained from morphine- or saline-treated mice, then natural killer (NK) cell activity and interferon-gamma (IFN-gamma) production were evaluated. The effect of morphine on white blood cells' capacity to induce protection against HSV-1 infection was evaluated by adoptive transfer of spleen cells to cyclophosphamide-treated mice that were previously infected with HSV-1. Furthermore, in a separate experiment, a different group of mice received corticosterone 24 h after HSV-1 infection. Mortality rate in high-dose acute morphine-treated mice increased significantly compared to saline-treated mice (p = 0.035). NK cell cytotoxicity and IFN-gamma mRNA levels also showed a significant reduction compared to those of control groups (p < 0.001 and p = 0.014, respectively). Corticosterone administration reduces innate resistance against HSV-1 infection compared to saline-treated mice (p = 0.044). Furthermore, adoptive transfer of normal but not morphine-treated spleen cells induces resistance against HSV infection in cyclophosphamide-injected mice (p = 0.009). The current study shows that acute morphine administration reduces white blood cells' capability to induce protection against HSV-1 infection via suppression of IFN-gamma production and NK cells activity. This may be due to the increase in corticosteroids. Further studies are needed to test the effect of acute morphine on other immune cells.
    NeuroImmunoModulation 01/2007; 14(1):16-23. DOI:10.1159/000107284 · 1.78 Impact Factor
Show more