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At least 343 records · Page 19Linked to original sources
PubMed1992

Asymptomatic reactivation of herpes simplex virus in women after the first episode of genital herpes.

OBJECTIVE: To determine frequency, anatomic site, and host factors associated with asymptomatic shedding of herpes simplex virus after initial episodes of genital herpes. DESIGN: Cohort study with follow-up for a median of 63 weeks. SETTING: Referral clinic. PATIENTS: Women (306) with first episode of herpes; 43 had primary herpes simplex virus type 1, and 227 and 36 had primary and nonprimary herpes simplex virus type 2, respectively. MEASUREMENTS: Cultures were obtained for herpes simplex virus every 4 to 6 weeks at times in which genital lesions and symptoms were not present. MAIN RESULTS: Asymptomatic shedding was detected among 11.9%, 18.3%, and 22.9% of women with primary herpes simplex virus type 1, primary HSV type 2, and nonprimary HSV type 2, respectively. Among patients with type 2 infection, previous type 1 antibody was associated with a lower rate of asymptomatic vulvar shedding. Asymptomatic cervical shedding was 3 times more frequent during the first three months after resolution of primary type 2 disease than during later time periods. In contrast, the rate of symptomatic recurrent herpes did not change over time. CONCLUSIONS: Asymptomatic genital herpes simplex type 2 is more common than type 1. Asymptomatic genital shedding occurs more often during the first 3 months after acquisition of primary type 2 disease than during later periods. Patients with HSV type 2 should be advised of this high early rate of asymptomatic shedding and of potential transmission to sexual partners.

Adult↗
PubMed1984

Immunity in the female genital tract after intravaginal vaccination of mice with an attenuated strain of herpes simplex virus type 2.

Herpes simplex virus type 2 is a common human venereal pathogen which causes lethal neurological illness after intravaginal inoculation into BALB/cJ mice. To investigate whether an attenuated, nonlethal strain of this virus would confer immunity after inoculation of mice, we constructed a strain containing a partial deletion of the thymidine kinase gene, which is necessary for viral replication and spread in sensory ganglia. Unlike its wild-type counterpart, this deletion-containing strain of herpes simplex virus type 2 caused mild clinical disease and was not lethal when studied in an age-dependent murine model of intravaginal infection. Furthermore, after intravaginal infection, the deletion-containing strain could not be isolated from sensory ganglia at a time when wild-type virus was abundant. Of greater significance, intravaginal inoculation with the deletion-containing strain rendered mice completely resistant to rechallenge with a 10-fold 50% lethal dose of wild-type virus. These results suggest that a strain of herpes simplex virus type 2 containing a deletion of the thymidine kinase gene will be useful in studying the cellular basis of mucosal immunity in the genital tract.

Animals↗
PubMed2006

Roles for herpes simplex virus type 1 UL34 and US3 proteins in disrupting the nuclear lamina during herpes simplex virus type 1 egress.

Cells infected with wild type HSV-1 showed significant lamin A/C and lamin B rearrangement, while UL34-null virus-infected cells exhibited few changes in lamin localization, indicating that UL34 is necessary for lamin disruption. During HSV infection, US3 limited the development of disruptions in the lamina, since cells infected with a US3-null virus developed large perforations in the lamin layer. US3 regulation of lamin disruption does not correlate with the induction of apoptosis. Expression of either UL34 or US3 proteins alone disrupted lamin A/C and lamin B localization. Expression of UL34 and US3 together had little effect on lamin A/C localization, suggesting a regulatory interaction between the two proteins. The data presented in this paper argue for crucial roles for both UL34 and US3 in regulating the state of the nuclear lamina during viral infection.

Animals↗
PubMed1999

Rapid detection of glycoprotein G gene for the diagnosis and typing of herpes simplex virus infection in genital herpes.

OBJECTIVE: To develop a new, rapid, and convenient technique for the diagnosis and typing of herpes simplex virus (HSV) in genital herpes (GH). METHODS: Using samples from skin vesicle fluid and urogenital mucosal swabs of subjects with GH, conventional polymerase chain reaction (PCR) (directed to polymerase gene: PCRpG) were compared with a newly developed PCR (directed to HSV glycoprotein gene: PCRgG). Both PCR methods were compared with virus isolation culture (VI) with indirect immunofluorescent staining (IIF). RESULTS: 80 samples from 40 GH patients (25 males) were tested. Positive results were seen in 52.5% (42/80) using PCRgG compared with 40% (32/80) by VI. Most of PCRgG positive samples (95.1%) were caused by HSV-2 infection. In samples from healing lesions, HSV was detected more often by PCRgG, than by VI. The results of typing by PCRgG and IIF were highly consistent. CONCLUSION: PCRgG is more sensitive than VI and PCRgG in detecting HSV in urogenital samples from subjects with GH. PCRgG is a convenient technique for the rapid detection and typing of GH.

Female↗
PubMed2005

Glycoprotein D adjuvant herpes simplex virus vaccine.

Herpes simplex virus (HSV) Type-1 and -2 are common infections that can cause primary and recurrent herpes labialis and genitalis, as well as gingivostomatitis, keratoconjunctivitis, encephalitis, disseminated infections in immunocompromised persons and neonatal infections. Despite several decades of HSV vaccine development, no effective vaccine has been developed until recently. The following review of the genital HSV-2 glycoprotein D (gD2t, t is for truncated) subunit vaccine formulated with a new adjuvant (AS04) containing alum and 3-O deacylated monophosphoryl lipid A (MPL) provides a background in which to evaluate the vaccine as well as a brief review of other approaches to herpes vaccines. The gD2t-AS04 vaccine has been demonstrated to be safe in several large clinical trials. In two trials, the vaccine reduced genital herpes disease by 73 and 74%, but only in females with no previous HSV infection. A large ongoing trial in HSV seronegative females will provide additional data on protection from HSV disease and infection.

Adjuvants, Immunologic↗
PubMed1991

Cutaneous herpes simplex infection.

Cutaneous Herpes simplex infections occur either as a result of direct inoculation or in conjunction with primary genital or orolabial herpes. Lesions can occur anywhere on the body. However, when they occur in conjunction with genital herpes the commonest sites are the buttock, thigh and fingers. Cutaneous lesions may recur. In immunosuppressed patients recurrences may lead to 2 serious mucocutaneous complications; chronic progressive mucocutaneous herpes where lesions spread locally to leave large non-healing ulcers; or acute mucocutaneous dissemination where the infection disseminates widely over the skin. In dermatological conditions, especially atopic eczema, widespread cutaneous dissemination (Kaposi's varicelliform eruption) may occur. This usually occurs in association with primary herpes although recurrences do sometimes occur.

Herpes Simplex↗
PubMed2006

Chronic herpes simplex virus encephalitis in childhood.

Although herpes simplex virus is a major cause of acute encephalitis in childhood, chronic herpes simplex virus encephalitis has only rarely been reported. This report presents a case of chronic herpes simplex virus encephalitis in a 6-year-old female. Diagnosis was based on the detection of herpes simplex virus deoxyribonucleic acid by polymerase chain reaction in combination with the cerebrospinal fluid/serum ratio of herpes simplex virus-specific immunoglobulin G, the presence of herpes simplex virus-specific oligoclonal immunoglobulin G bands in cerebrospinal fluid, and calcifications in the temporal regions found on cerebral computed tomographic scan. Prolonged antiviral therapy was beneficial to later mental development.

Antiviral Agents↗
PubMed1980

Serum antibodies to herpes simplex virus type 1 during active oral herpes infection.

Subjects with oral herpes lesions at the time of serum sampling had higher-efficiency antibody (higher proportion of neutralizing antibody as determined by plaque reduction, compared with total antibody as detected by radioimmunoassay) to herpes simplex virus type 1 (HSV-1) than did subjects with no lesions at the time of serum sampling. These higher-efficiency sera also had higher antibody titers to structural components of herpes simplex virus type 1 than did the low-efficiency sera. Absorption of high- and low-efficiency sera with purified herpes simplex virus type 1 particles removed all neutralizing antibody but not all antibody detected by radioimmunoassay. High-efficiency serum was depleted of more antibody to particulate antigen that was the low-efficiency serum, indicating that the high-efficiency serum contained a higher proportion of antibody to the virus particle.

Adult↗
PubMed2000

Treatment of common cutaneous herpes simplex virus infections.

Herpes simplex virus infection is increasingly common in the United States. New antiviral medications have expanded treatment options for the two most common cutaneous manifestations, orolabial and genital herpes. Acyclovir therapy remains an effective and often less expensive option. Famciclovir and valacyclovir offer improved oral bioavailability and convenient oral dosing schedules but are more expensive than acyclovir. Patients who have six or more recurrences of genital herpes per year can be treated with one of the following regimens: acyclovir, 400 mg twice daily; valacyclovir, 1 g daily; or famciclovir, 250 mg twice daily. These regimens are effective in suppressing 70 to 80 percent of symptomatic recurrences. Episodic treatment of recurrent genital herpes is of questionable benefit, but it may be helpful in appropriately selected patients. There is little evidence indicating benefit from treatment of recurrent orolabial herpes, which tends to be mild and infrequent.

2-Aminopurine↗
PubMed2007

Apoptosis during herpes simplex virus infection.

Herpes simplex virus (HSV) infection triggers apoptosis in infected cells. However, proteins synthesized later in infected cells prevent apoptotic cell death from ensuing. In vivo data showing that apoptosis accompanies herpes stromal keratitis and encephalitis suggest that apoptotic modulation plays a role in the development of herpetic disease. Tremendous progress has been made toward identifying the viral factors that are responsible for inducing and inhibiting apoptosis during infection. However, the mechanisms whereby they act are still largely unknown. Recent studies have illustrated a wide diversity in the cellular response to HSV-triggered apoptosis, emphasizing the importance of host factors in this process. Together, these findings indicate that apoptosis during HSV infection represents an important virus-host interaction process, which likely influences viral pathogenesis.

Animals↗
PubMed1986

Thiosemicarbazones of 2-acetylpyridine, 2-acetylquinoline, 1-acetylisoquinoline, and related compounds as inhibitors of herpes simplex virus in vitro and in a cutaneous herpes guinea pig model.

A series of 111 thiosemicarbazones of 2-acetylpyridine, 2-acetylquinoline, 1-acetylisoquinoline, and related compounds were evaluated as inhibitors of herpes simplex virus in vitro and in a cutaneous herpes guinea pig model. All derivatives tested were potent inhibitors of virus replication with mean 50% inhibitory concentrations of 1.1 micrograms/ml for both type 1 and 2 herpes simplex virus. Inhibitory concentrations for cellular protein and DNA synthesis were considerably higher for many compounds resulting in in vitro therapeutic indices ranging from greater than 100 (highly selective) to less than 1 (negatively selective). All compounds were tested for dermal toxicity following topical administration of saturated solutions in 1,3-butanediol to the shaved, depilated skin of guinea pigs. Approximately 50% of the compounds produced slight to no dermal toxicity whereas the remaining compounds produced moderate to severe dermal toxicity. 28 compounds were evaluated in the cutaneous herpes guinea pig model against herpes simplex virus type 1. A number of N4-monosubstituted 2-acetylpyridine thiosemicarbazones produced highly significant reductions in days to healing and lesion score without producing untoward dermal toxicity. Structure-activity relationships revealed that a reduction of the azomethine bond in the molecule (i.e., conversion of a thiosemicarbazone to a thiosemicarbazide) greatly diminished dermal toxicity apparently without producing a proportional decrease in antiviral activity.

Animals↗
PubMed2002

Herpes Simplex Virus in Children.

Herpes simplex virus (HSV) infections are ubiquitous. Children are infected with HSV resulting in totally asymptomatic acquisition to life-threatening disease. Therapy of HSV diseases of children can be considered according to severity and time of acquisition. Neonatal herpes simplex virus infections take one of three forms--disease localized to skin, eye, or mouth (SEM), encephalitis, or multiorgan disseminated disease. Treatment consists of intravenous (IV) administration of acyclovir. Supportive care for patients with life-threatening disease is an integral component of patient management. Mucocutaneous HSV infections in the immunocompromised host can be treated with either intravenous acyclovir or one of the orally bioavailable antiviral therapies. For hospitalized patients, therapy consists of IV acyclovir at 5 mg/kg every 8 hours for 7 to 14 days. For ambulatory patients, therapy is tailored according to age. For children less than 12 years of age, oral acyclovir is administered at a dosage of 20 mg/kg every eight hours. Although no controlled studies have been performed with valaciclovir or famciclovir, the pharmacokinetics of these medications would suggest superiority over acyclovir. Dosage recommendations have not been established for young children. For postpubertal children, dosage should mirror that of adults. Valaciclovir is administered at 500 mg twice daily. Famciclovir is administered at 125 mg three times daily. Herpes simplex keratoconjunctivitis is treated with topical triflurothymidine. Two drops are applied to the infected eye five times daily until resolved. Recurrences are managed in a similar manner. Some physicians administer oral acyclovir at the doses noted above in order to prevent frequent recurrences. Genital HSV infections can be treated with acyclovir, valaciclovir, or famciclovir. Episodic treatment of recurrent episodes is usually not necessary in childhood. Importantly, all data on the use of these compounds for these conditions have been generated in adults. Physician judgment is required for the management of recurrent herpes labialis, erythema multiforme, and herpes gladitorum. No controlled studies have been performed in children, although experience with acyclovir, valaciclovir, and famciclovir have resulted in their use.

Journal Article↗
PubMedDate not supplied

Effective treatment of disseminated peritoneal colon cancer with new replication-competent herpes simplex viruses.

BACKGROUND/AIMS: Oncolytic herpes simplex virus type 1 mutants are promising therapeutic agents for malignant tumors. Their efficacy depends on the extent of both viral replication in the tumor and induction of a host anti-tumor immune response. In this study, new replication-competent, attenuated herpes simplex virus mutants, named HF10 and Hh101, have been evaluated for their oncolytic activities. METHODOLOGY: We determined the genome structures of the mutants and examined the survival rates of mice that were injected intraperitoneally with carcinoma and sarcoma cells and treated with the mutants. Tumors were examined by both histology and immunochemistry. RESULTS: HF10 and Hh101 administration effectively treated disseminated peritoneal colon carcinoma in a BALB/c mouse model and all surviving mice were resistant to rechallenge of the tumor cells. The survival rate in a C3H mouse model was improved by HF10, but not Hh101. CONCLUSIONS: HF10 and Hh101, novel agents as oncolytic viral therapy, are both safe and effective herpes simplex virus mutants for malignant tumor treatment. The Hh101, is more attenuated in its virulence than the HF10 because it is a double gene knocking-out construct. The choice of viral mutant for treatment should be made according to the type of malignancy.

Animals↗