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We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. Genital herpes is an intractable disease caused mainly by herpes simplex virus (HSV) type 2 (HSV-2), and is a major concern in public health.
Herpes simplex virus (HSV) type 1 (HSV-1) and type 2 (HSV-2) belong to the alphaherpesvirus family.
In the past, efforts to develop an HSV vaccine have included development of inactivated whole-virus vaccines, subunit glycoprotein preparations, DNA plasmids, and attenuated replication-competent viruses.
Vero cells (African green monkey kidney epithelial cells) were grown in Eagle’s minimal essential medium (MEM) supplemented with 10% calf serum.
All experiments were approved by the University Committee and conducted in accordance with the Guidelines for Animal Experimentation of Nagoya University. Four weeks after immunization, blood samples were collected via laparotomy from the abdominal aortic arch.
The statistical significance of differences in disease scores and viral titers on individual days was determined using a Student’s t-test. To determine neutralizing antibody titers against HSV-2 strain 186 in HF10-immunized mice, we collected serum 1 month after HF10 immunization and investigated its ability to neutralize HSV-1 strains HF10 and KOS and HSV-2 strain 186 based as determined by reductions in plaque formation (Figure 4A). Furthermore, to investigate cellular responses to HSV-2 genital infection, we performed immunohistochemical studies in mouse vaginas on days 1 and 3 after challenge (Figure 6).
In this study, we evaluated the ability of the spontaneously occurring HSV type 1 mutant HF10 to serve as a vaccine against HSV-2-mediated genital disease. Extracts from Cleome rosea were investigated for their activity against acyclovir-resistant strains of Herpes simplex type 1 (ACVr-HSV-1) and type 2 (ACVr-HSV-2). ReferencesAlmagboul AZ, Farouk A, Bashir AK, Karim A, Salih M (1985) Antimicrobial activity of certain Sudanese plants used in folkloric medicine. Laboratorio Experimental de Drogas Antivirais e Citotoxicas (LEDAC), Departamento de Virologia, Instituto de Microbiologia Prof. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser. The adrenal glands are the primary site for herpes simplex virus type 1 (HSV-1) replication in the intraperitoneal (IP) route of inoculation. The mdr-1 (multidrug resistance) gene is normally expressed in the adrenal glands and is apparently involved in hormone secretion. ReferencesBecker Y, Tavor E, Asher Y, Berkowitz C, Moyal M (1993) Effect of herpes simplex virus type 1 UL41 gene on the stability of mRNA from the cellular genes: (3-actin, fibronectin, glucose transporter 1 and docking protein and on virus intraperitoneal pathogenicity to newborn mice. Inspired by reports that viral infection might be capable of promoting tumor regression published in the early 20th century, investigators have struggled to identify a suitable virus, which though unable to cause disease, retained the capability to replicate in cancer cells. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. A previous infection with HSV type 1 (HSV-1) enhances protection against primary HSV-2 infection to some extent. We have demonstrated that HF10 can be attenuated, and that it does not cause any neurotropic effects in mice. The HSV-1 mutant HF10, the wild-type HSV-1 strains KH7 and KOS, and wild-type HSV-2 strain 186 were titrated in Vero cells. On days 1 and 5 after infection, mice were sacrificed, and skin samples were harvested for histological and immunohistochemical studies to detect HSV-1 antigens.
After incubation at 37°C for 30 min, blood samples were centrifuged at 3000 rpm for 10 min and serum was collected. To examine the distribution of CD4+ and CD8+ cells, frozen sections were stained with a variety of antibodies.
Tissues were crushed through a 100-μm nylon cell strainer (BD Biosciences, Franklin Lake, NJ, USA). Survival rates were estimated by the Kaplan–Meier method, and statistical significances were determined by the log-rank test. After 1 month, each group was challenged by intravaginal inoculation of wild-type HSV-2 stain 186. In unimmunized mice, HSV-2 antigens were present in mucosal epithelial cells and subepithelial lamina propria of vaginal tissue at days 1 and 4 after challenge, and mucosa in the infective focus dropped out from the epithelium 6 days after challenge.
In HF10-immunized mice, CD4+ cells localized to the infective focus and invaded the mucosal subepithelial lamina propria on both 1 and 3 days after challenge (Figure 6A). Accumulation of CD4+ and CD8+ T cells in the infection focus of vagina after HSV-2 challenge.
The safety of the vaccine must be considered because HF10 is a replication-competent virus. After replication in the adrenal glands, the virus penetrates the neurons that innervate the glands and reaches the spinal cord.
The effect of HSV-1 infection of the adrenal glands on the expression of the mdr-1 gene was studied. In principal, the productive growth of the virus would kill or lyse malignant cells and the newly minted viral progeny would spread the infection, resulting ultimately in the destruction of the tumor by a process termed viral oncolysis. In this study, we evaluated the ability of HF10, a naturally occurring replication-competent HSV-1 mutant, to protect against genital infection in mice caused by HSV-2.
The most successful vaccine in human trials was a subunit glycoprotein vaccine that included HSV-2 gD, a major viral envelope antigen, as an immunogen with alum and 2-o-deacylated monophosphoryl lipid A as adjuvants (Bernstein et al., 2005).
Intranasal vaccination of mice with HF10 conferred significant protection against lethal challenge with HSV-1 and HSV-2 (Mori et al., 2005). Mice were challenged 4 weeks or 4 months after immunization, and 7 days prior to challenge they were subcutaneously injected in the neck ruff with 3 mg Depo-Provera (Sigma-Aldrich). To estimate neutralization titers, diluted sera were added to 100 PFUs of HSV-1 strains HF10 and KOS or HSV-2 strain 186, incubated for 30 min at 37°C, and the remaining infectious virus was detected on duplicate Vero cell monolayers. Erythrocytes were depleted using lysis buffer (BD Biosciences), and spleen cells were suspended in RPMI-1640 medium containing 10% FCS. Mice immunized with HF10 had significantly lower titers of virus shedding in the vaginal mucosa 1 day after challenge (Figure 2A). One month after immunization with HF10, 5 × 105 PFUs of wild-type HSV-2 strain 186 were inoculated into mice vagina. In contrast, in HF10-immunized mice, HSV-2 antigen staining was restricted to the mucosal surface at days 1 and 4 and was undetectable 6 days after challenge. After inoculation of wild-type HSV-2 strain 186 into HF10-immunized mice or unimmunized mice vagina; vaginal mucosal lesions were excised at days 1, 4, and 6 after challenge, and HSV-2 antigens were stained.
The titers producing a 50% reduction in plaque formation by HF10 and KOS were between 16 and 32. To confirm that protein synthesis was necessary, we stimulated splenocytes with 186-infected NIH3T3 cells treated with ganciclovir or cycloheximide. Unimmunized and HF10-immunized mice were challenged with HSV-2 by intravaginal infection, and vagina was excised 1 or 3 days later. The extracts presented low cytotoxicity and caused virus titer reduction above 70%, with different mechanisms of action. HSV-1 infection leads to shutoff of both cellular and viral genes, due to the activity of the UL41 gene product.
N Engl J Med 35: 1608–1614Chirgwin JM, Przybyla AE, MacDonald RS, Rutter WS (1979) Isolation of biologically active ribonucleic acids from sources enriched in ribonucleases. Fueled by revolutionary advances in molecular biology that enabled a new understanding of viral virulence at the genetic level, nonpathogenic strains of human viruses have been engineered in the laboratory and their oncolytic ability evaluated in animal models of human cancer. Subcutaneous inoculation of HF10-immunized mice against lethal infection by HSV-2, and attenuated the development of genital ulcer diseases. Both exert neurotropic effects and spread to the nervous system (Corey and Spear, 1986; Whitley and Roizman, 2001).
Although the vaccine appeared safe and effective against genital herpes in guinea pigs, it failed to provide sufficient protection against primary infection in a clinical trial (Stanberry et al., 2002). Skin samples were obtained at days 1 and 5 after infection and evaluated by hematoxylin and eosin (HE) staining and immunohistochemistry (IHC) to detect HSV-1 antigens.
These results indicate that mice immunized with HF10 were protected against severe genital disease caused by HSV-2.
Serum had little effect on plaque formation by HSV-2 strain 186 at lower concentrations, but at a dilution of 1:2 caused a 40% reduction. In unimmunized mice, there were no detectable CD4+ and CD8+ cells 1 day after challenge (Figures 6A, B), but there were a few CD4+ cells in the infective focus 3 days after challenge. Frozen sections were stained with anti-CD4 (green), anti-CD8 (green), and anti-HSV-2 antibodies (red). Therefore, immunization with HSV-1 may be useful for preventing infection with or disease caused by HSV-2.


In addition, HF10 exhibits a relatively high divergence in proteins compared to HSV-1 strain 17. Extracts from leaves of field-grown plants inhibited viral infection mainly by affecting the virus particle itself (virucidal effect), while extracts from calli acted mainly on cell receptors.
The mutant vhs-1 expresses an inactive form of UL41 product and does not cause shutoff of gene expression.
Shutoff of the expression of the mdr-1 gene in the adrenal glands was observed in all the infected mice except for those infected with the vhs-1 mutant.
This chapter chronicles the milestones in engineering oncolytic strains of herpes simplex virus type 1, highlighting different stages of development beginning with the pioneering use of recombinant viruses produced in the laboratory, accompanied by a discussion of key design innovations which upon incorporation into HSV-1 oncolytic strains, substantially improved both their safety and efficacy, and summarizes recent experiences in phase I clinical trials.
Immunization with HF10 inhibited HSV-2 replication in the mouse vagina, reduced local inflammation, controlled emergence of neurological dysfunctions of HSV-2 infection, and increased survival. Furthermore, immunization with HSV-2 gD subunit did not reduce the rate at which women acquired HSV-2 genital herpes (Belshe et al., 2012). Plaque formation by UV-inactivated HF10-immunized mouse serum was lower than that of HF10-immunized mice (Figure 4B). After 4 weeks, serum (n = 3) collected and neutralizing ability against HF10 was assayed by the reduction in plaque formation.
There was little or no production of IFN-γ by splenocytes from unimmunized mice subjected to identical protein stimulation (Figure 5).
On the other hand, all extracts evaluated affected the virus entry across the cell membrane and the intracellular viral replication at similar percentages, causing reduction on titers in the range of 68–90%. The level of mdr-1-specific mRNA in HSV-1 vhs-l -infected glands was comparable to that in uninfected glands. In HF10-immunized mice, we observed rapid and increased production of interferon-γ in the vagina in response to HSV-2 infection, and numerous CD4+ and a few CD8+ T cells localized to the infective focus. In this study, we used HF10 as a live attenuated vaccine, and evaluated the immune response generated and protective effect against HSV-2 genital infection in mice. Stained slides were washed, incubated with DRAQ5, and mounted with Fluoromount Plus (Diagnostic Biosystems, Pleasanton, CA, USA).
Viral titers on day 5 were significantly lower in HF10-immunized mice than in unimmunized mice and UV-inactivated HF10-immunized mice. To evaluate cellular immune responses, we stimulated spleen cells from each immunized or unimmunized mouse with 186-infected NIH3T3 cells and examined IFN-γ production kinetics.
The media were collected at 5 and 20 h after addition and assayed for IFN-γ concentrations by ELISA.
This study validated the potential use of in vitro materials as sources of antiherpetic agents from C. The relevance of the shutoff phenomenon to HSV-1 pathogenicity and to future application in gene therapy is discussed in this chapter.
After primary infection via the genital tract, the virus establishes latency within the lumbosacral ganglions, and establishes a state of lifelong infection.
Subcutaneous inoculation of HF10-immunized mice from lethal infection by HSV-2, and attenuated the development of genital ulcer diseases. Finally, slides were visualized using an LSM 510 laser-scanning confocal microscope (Carl Zeiss, Jena, Germany). To produce viral antigens, UL46 and US6 genes and ICP0 cDNA from HSV-2 strain 186 were amplified by polymerase chain reaction and cloned into pcDNA 3.1(+) expression vectors (Invitrogen, Carlsbad, CA, USA). N Engl J Med 314:686–691De Bruyne T, Pieters L, Witvrouw M, De Clercq E, Berghe DV, Vlietinck AJ (1999) Biological evaluation of proanthocyanidin dimers and related polyphenols.
Thus, the protective effect of HF10 was related to induction of cellular immunity, mediated primarily by Th1 CD4+ cells. Killed viral vaccines have proven to be inferior to live vaccines, in terms of naturally acquired immunity, preventing infection or re-infection, and producing durable immunity.
In contrast, all mice in the control group developed severe genital symptoms and hind paralysis (Figure 2B).
We then investigated IFN-γ concentrations in vaginal washes after challenge (Figure 4D).
Supernatants from three mice were combined and assayed for IFN-γ concentrations using an ELISA. These data indicate that the live attenuated HSV-1 mutant strain HF10 is a promising candidate antigen for a vaccine against genital herpes caused by HSV-2.
HF10 also induced rapid accumulation of CD4+ and CD8+ cells in the infective focus, and protected mice against HSV-2 genital disease via induction of a cellular immune response. Anti-mouse CD4 antibody and fluorescein isothiocyanate (FITC)-labeled anti-mouse CD8 antibody were purchased from Chemicon International (Temecula, CA, USA) and Thermo Scientific (Rockford, IL, USA), respectively. Plasmid-transfected or HSV-2-infected cells were frozen, thawed, and added to dishes containing splenocytes acquired as described above.
Disease scores were not significantly different between UV-inactivated HF10-immunized mice and unimmunized mice (P = 0.065). Although IFN-γ production was recognized in mouse vaginas immunized with UV-inactivated HF10, the quantity was not statistically significantly different from that produced by unimmunized mice. A vaccine would provide a more effective means of preventing or limiting infection, and would greatly relieve the social and economic burden of HSV-2 infection.
Genital symptoms and paralysis in mice immunized with UV-inactivated HF10 were slightly weaker than those in unimmunized mice, albeit without statistical significance (Figure 2B). In contrast, IFN-γ concentration in HF10-immunized mice was significantly higher than that in unimmunized mice.
Genital tracts of unimmunized, UV-inactivated HF10-immunized, and HF10-immunized mice were washed 0, 1, and 3 days after challenge with strain 186, and the washes were assayed for IFN-γ concentrations by ELISA.
In developed countries, while childhood acquisition of HSV-1 has decreased, HSV-2 seroprevalence has increased, suggesting the possible protective effect of HSV-1 against HSV-2 infection (Xu et al., 2006). Anti-mouse IgG-conjugated FITC and anti-rabbit IgG-conjugated tetramethylrhodamine-5-(6)-isothiocyanate (TRITC) were obtained from Sigma-Aldrich (St.
Cann AJ Am J Cardiol 64: 1310–1316Genlach JH, Endicott A, Juranka PF, Herdrson G, Sarangi F, Deuchass KL, Ling V (1986) Homology between P-glycoprotein and a bacterial haemolysis transport protein suggests a model for multidrug resistance. Thus, immunization with UV-inactivated HF10 partially protected mice from HSV-2 genital disease. Recently, the US Food and Drug Administration approved a phase I clinical trial of HF10 against refractory head and neck cancer (Clinical Trials Gov, Identifier: NCT01017185). We then confirmed the persistent efficacy of HF10 immunization against vaginal infection by HSV-2. Chapman and Hall Ltd, New YorkHashem FA, Wahba HE (2000) Isothiocyanates in myrosinase treated herb extract of Cleome chrysantha Decne.
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