Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HERPES SIMPLEX”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed2001

Interventions for herpes simplex virus epithelial keratitis.

BACKGROUND: Many clinical trials have been performed on the acute treatment of dendritic epithelial keratitis. Surveys of antiviral pharmacology and of herpes simplex virus eye disease have evaluated different commercially available agents, but a systematic review of all comparative clinical studies has not previously been undertaken. OBJECTIVES: The objective of this review is to compare the effects of various treatments for dendritic or geographic herpes simplex virus epithelial keratitis. SEARCH STRATEGY: Sources searched for relevant studies were the Cochrane Eyes and Vision Group specialized register, The Cochrane Controlled Trials Register - CENTRAL, MEDLINE, EMBASE, Index Medicus, Excerpta Medica Ophthalmology, reference lists of primary reports, review articles, and corneal textbooks and conference proceedings pertaining to ocular virology. SELECTION CRITERIA: This review includes comparative clinical trials that assessed oral or topical ophthalmic antiviral agents, or physical or chemical debridement in people with active epithelial keratitis. DATA COLLECTION AND ANALYSIS: The reviewer extracted data and assessed trial quality. Interventions were compared by the proportions of participants healed at seven days and at fourteen days after trial enrollment. MAIN RESULTS: This review includes data from 96 trials which randomised a total of 4991 participants. Compared to idoxuridine, the topical application of vidarabine, trifluridine, or acyclovir generally resulted in a significantly greater proportion of participants healing within one week of treatment. Among these three antiviral agents, no treatment emerged as significantly better for the therapy of dendritic epithelial keratitis. Insufficient placebo-controlled studies were available to assess debridement and other physical and physicochemical methods of treatment. Interferon monotherapy had a slight beneficial effect on dendritic epithelial keratitis, but not better than other antiviral agents, and was useful with debridement. REVIEWER'S CONCLUSIONS: Currently available and investigational antiviral agents are effective and nearly equivalent, but the combination of an antiviral nucleoside and interferon seems to speed healing. Future trials of the acute treatment of herpes simplex virus epithelial keratitis must aim to achieve adequate statistical power for assessing the primary outcome and should consider the effect of lesion size and other characteristics on treatment response.

Administration, Oral↗
PubMed1997

Reactivation of oral herpes simplex virus: implications for clinical management of herpes simplex virus recurrence during radiotherapy.

Herpes viruses are characterized by their ability to establish and maintain latent infections that can be reactivated. Several stimuli can trigger the reactivation of herpes viruses, which are perhaps best recognized in the recurrent blisters and ulcers associated with herpes simplex virus. We present two clinical cases of reactivation of herpes simplex virus during radiation therapy for management of cancers of the head and neck. Although the role of ionizing radiation in the reactivation of herpes simplex virus has not been established, we review the viral and host events associated with the establishment of orofacial herpes simplex virus infection, latency, and reactivation of the virus. We discuss current models of viral reactivation and suggest directions for further clinical research into the reactivation of orolabial herpes simplex virus during radiotherapy.

Acyclovir↗
PubMed2004

Seroprevalence and seroincidence of herpes simplex virus type 1 and herpes simplex virus type 2 infections in a cohort of adolescents in Italy.

OBJECTIVE: The objective of this study was to improve the knowledge on the epidemiology of herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) in Italy. GOAL: The goal of this study was to study the seroincidence and seroprevalence of HSV-1 and HSV-2 infections among Italian adolescents. STUDY: We conducted a retrospective longitudinal study among 345 Italian adolescents tested for anti-HSV-1 and anti-HSV-2 on samples collected at 11 and 17 years of age. RESULTS: At 11 years of age, the HSV-1 prevalence was 51.6% and the HSV-2 prevalence was 2.6%; when 17 years old, these rates increased to 61.4% and 4.9%, respectively. The HSV-1 incidence was 1.6 per 100 person-years and was higher among females. The HSV-2 incidence was 0.4 per 100 person-years with no gender differences. CONCLUSION: HSV-1 is apparently widespread among Italian adolescents, whereas HSV-2 is limited. These data are of paramount importance when considering that HSV-1 can cause genital herpes and that HSV-2 plays a role in HIV transmission.

Adolescent↗
PubMed1980

Pathogenesis of herpes simplex labialis. I. Replication of herpes simplex virus in cultures of epidermal cells from subjects with frequent recurrences.

Primary cultures were established with epidermal cells from the skin of 11 patients with frequent episodes of herpes simplex labialis and 13 control subjects with titers of neutralizing antibody to herpes simplex virus (HSV) type 1 but no history of herpetic disease. Confluent monolayers were exposed to HSV type 1 strain E115, and the infection was monitored by assay of the rate of virus appearance in the culture medium. The mean slope of the virus growth curves ([log10 pfu/ml]/log10 hr) was 9.0 in cultures from patients vs. 9.5 in cultures from controls, and the respective mean titers of virus 53 hr after infection were 10(6.8) and 10(6.5) (differences not statistically significant). Genetically controlled host factors may play some role in the clinical response to HSV infection, but variation in the susceptibility of epidermal cells, the natural target for HSV, is not one of the critical determinations.

Adult↗
PubMed1987

Non-herpes simplex encephalitis is early exclusion of herpes simplex etiology possible?

Since effective antiviral treatment is available for herpes simplex encephalitis (HSE), early diagnosis or exclusion of herpes simplex etiology is essential for prognosis. In a retrospective study of 25 cases of acute viral encephalitis not caused by herpes simplex virus (non-HSE), we investigated whether HSE can be excluded in the early phase before serological evidence is present. Using clinical means, history, investigations of CSF (protein, cells), EEG, and CCT, HSE could not be excluded with reliability. This is because clinical signs and laboratory results are not pathognomonic for any form of viral encephalitis, even if periodic activity in EEG and temporal attenuation in CCT are more frequent in HSE than in other forms of encephalitis. Therefore, in all cases of severe encephalitis, acyclovir therapy should be initiated early.

Adolescent↗
PubMed1979

Herpes simplex virus glycoproteins: participation of individual herpes simplex virus type 1 glycoprotein antigens in immunocytolysis and their correlation with previously identified glycopolypeptides.

Tissue culture cells infected with herpes simplex type 1 virus express virus-specified glycoprotein antigens on the plasma membrane. Three of these have been previously identified and have been designated as Ag-11, Ag-8, and Ag-6. In the present study, immunoglobulins to each of the antigens were shown to be capable of mediating immunocytolysis in the presence of either complement (antibody-dependent complement-mediated cytotoxicity) or peripheral blood mononuclear cells (antibody-dependent cell-mediated cytotoxicity [ADCC]). Two herpes simplex virus type 1 strains, VR-3 and F, reacted similarly in the ADCC test in the presence of immunoglobulins to Ag-11, Ag-8, and Ag-6 in both infected Chang liver cells and HEp-2 cells. Anti-Ag-6, however, produced a lower ADCC reaction in HEp-2 cells than in Chang liver cells, suggesting differences in the Ag-6 surface expression in, or release from, these cells. Chang liver and HEp-2 cells infected with the MP mutant strain of herpes simplex virus type 1 showed reduced ADCC in the presence of anti-Ag-11 and anti-Ag-8, but no reactivity at all with anti-Ag-6. Crossed immunoelectrophoretic analysis showed that MP-infected cell extracts contain Ag-11 and Ag-8, but lack Ag-6. Polypeptide analysis of herpes simplex virus type 1 strains F, VR-3, and MP showed that Ag-11 consists of the glycoproteins gA and gB, that Ag-8 consists of gD, and that Ag-6 consists of gC. In conclusion, the present study demonstrates that either one of the glycoproteins (gC, gD, and a mixture of gA and gB) can function as a target for immunocytolysis and that the antibody preparation to gC (Ag-6) does not cross-react with any of the other glycoproteins.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1999

A novel anti-herpes simplex virus type 1-specific herpes simplex virus type 1 recombinant.

A recombinant herpes simplex virus (HSV) capable of inhibiting its own replication as well as the replication of wild-type virus would have greatly increased safety as a general purpose vector for in vivo gene transfer, antitumor therapy, and viral vaccine against HSV infection. By using a tetracycline repressor (tetR)-mediated HSV-1 viral replication switch [Yao and Eriksson (1999). Hum. Gene Ther. 10, 419-427], we have generated a novel anti-HSV-1-specific HSV-1 recombinant (CJ83193) that expresses a trans-dominant negative HSV-1 UL9 origin-binding protein, UL9-C535C. The de novo synthesis of CJ83193 can be suppressed by UL9-C535C by at least 1 x 10(6)-fold in non-tetR-expressing cells, and is subject to tetracycline regulation over a range of four to five orders of magnitude in a tetR-expressing osteosarcoma line. In particular, the UL9-C535C peptides expressed from the CJ83193 genome can inhibit the replication of wild-type HSV-1 by 100- to 200-fold in single-step growth assays. The construction of CJ83193 creates a new general strategy for developing recombinant viral vectors able to function as an intracellular therapy against wild-type viral infections.

Animals↗
PubMed1993

Quantitative analysis of herpes simplex virus DNA in cerebrospinal fluid of children with herpes simplex encephalitis.

Herpes simplex virus (HSV) DNA in the cerebrospinal fluid (CSF) of children with herpes simplex encephalitis (HSE) was quantified and typed using the polymerase chain reaction (PCR) assay. During the acute phase, HSV-DNA was detected in the CSF of 13 patients with HSE, including 5 neonates. A restriction profile of the PCR products cleaved with the restriction enzymes XhoI and BglII showed that 2 neonatal samples were HSV-2, and the remainder were HSV-1. The amount of HSV-DNA in the initial CSF ranged from 10(2)-10(5) copies/ml. A significantly greater number of HSV-DNA copies was detected in neonates than in older children (mean 3.9 vs. 2.5, log 10 copies/ml p < .05). Except for one patient, the amount of HSV-DNA decreased gradually with acyclovir therapy. These results show that a quantitative PCR assay is applicable not only to the diagnosis of HSE but also for monitoring the response to antiviral drugs.

Adolescent↗
PubMed1984

Ribonucleotide reductase of herpes simplex virus type 2 resembles that of herpes simplex virus type 1.

The ribonucleotide reductase (ribonucleoside-diphosphate reductase; EC 1.17.4.1) induced by herpes simplex virus type 2 infection of serum-starved BHK-21 cells was purified to provide a preparation practically free of both eucaryotic ribonucleotide reductase and contaminating enzymes that could significantly deplete the substrates. Certain key properties of the herpes simplex virus type 2 ribonucleotide reductase were examined to define the extent to which it resembled the herpes simplex virus type 1 ribonucleotide reductase. The herpes simplex virus type 2 ribonucleotide reductase was inhibited by ATP and MgCl2 but only weakly inhibited by the ATP X Mg complex. Deoxynucleoside triphosphates were at best only weak inhibitors of this enzyme. ADP was a competitive inhibitor (K'i, 11 microM) of CDP reduction (K'm, 0.5 microM), and CDP was a competitive inhibitor (K'i, 0.4 microM) of ADP reduction (K'm, 8 microM). These key properties closely resemble those observed for similarly purified herpes simplex virus type 1 ribonucleotide reductase and serve to distinguish these virally induced enzymes from other ribonucleotide reductases.

Adenosine Triphosphate↗
PubMed2000

High prevalence of herpes simplex virus type 2 in acute retinal necrosis syndrome associated with herpes simplex virus in Japan.

PURPOSE: To determine the type of herpes simplex virus in acute retinal necrosis syndrome associated with herpes simplex virus. METHODS: Herpes simplex virus type 1, herpes simplex virus type 2, varicella-zoster virus, Epstein-Barr virus, and cytomegalovirus were examined by polymerase chain reaction in intraocular specimens from 16 patients with acute retinal necrosis syndrome. Anti-herpes simplex virus type 1 and anti-herpes simplex virus type 2 type-specific antibodies in serum from the patients were detected by enzyme immunoassay. RESULTS: Of 16 patients with acute retinal necrosis syndrome, seven were polymerase chain reaction positive for herpes simplex virus type 2 and nine were positive for varicella-zoster virus. Anti-herpes simplex virus type 2 antibody was positive and anti-herpes simplex virus type 1 antibody was negative in the sera of the seven patients with herpes simplex virus type 2 DNA-positive acute retinal necrosis syndrome. In contrast, anti-herpes simplex virus type 2 antibody was absent in all nine varicella-zoster virus DNA-positive acute retinal necrosis syndrome patients. CONCLUSION: Herpes simplex virus type 2 has been demonstrated to be the major causative agent in acute retinal necrosis syndrome associated with herpes simplex virus by molecular biological and serological methods. Negative preexisting anti-herpes simplex virus type 1 antibody may play an important role in acute retinal necrosis syndrome associated with herpes simplex virus type 2.

Adolescent↗
PubMed2002

[Cloning and expression of simplex herpes virus ? US4 fragment].

BACKGROUND: To get early laboratory study of type specific antigenicity of herpes simplex virus II. METHODS: PCR and prokaryotic expression technique. RESULTS: Herpes simplex virus II type specific gene fragment was expressed in E.coli and the products can be used as specific antigen for the detection of anti\HSV in the recovery sera. CONCLUSIONS: Cloning and express of HSVII type specific antigen found the basis for developing specific diagnosis methods and vaccine of HSV.

Antigens, Viral↗
PubMed1984

Prospective study on the relationship between cervical neoplasia and herpes simplex type-2 virus. II. Herpes simplex type-2 antibody presence in sera taken at enrollment.

Sera obtained at enrollment in the study from patients suffering from moderate to sever dysplasia (cervical intraepithelial neoplasia grade II), carcinoma in situ (cervical intraepithelial neoplasia grade III) and invasive carcinoma, or developing any of these conditions in the course of the prospective study, and from control subjects, were examined for herpes simplex type-2 (HSV-2) antibody presence. The controls were matched with the patients by age, age at first intercourse, number of sexual partners, smoking habits and history of diathermoelectrocoagulation of the ectopic epithelium and transformation zone of cervix. Only those subjects were selected as controls who remained free of pathological colposcopical and cytological findings throughout the observation period, i.e. for at least 4 years after their serum sample was obtained. The microneutralization test (MNT) and type-2-specific solid-phase radioimmunoassay (SPRIA) were used as serological tests. No difference in the prevalence of HSV-2 antibody between the patients and controls was revealed by either test. Various combinations of the results from the two tests also failed to show any difference between patients and controls. Moreover, no significant differences were observed in the prevalence of HSV-2 antibody between patients suffering from the various pathological conditions and those diagnosed at enrollment and later in the course of the study. These results do not provide any support for the hypothesis of the involvement of HSV-2 in cervical neoplasia.

Animals↗
PubMed1984

Mapping of a herpes simplex virus type 2-encoded function that affects the susceptibility of herpes simplex virus-infected target cells to lysis by herpes simplex virus-specific cytotoxic T lymphocytes.

A function(s) involved in the altered susceptibility of herpes simplex virus type 2 (HSV-2)-infected cells to specific lysis by cytotoxic T lymphocytes was mapped in the S component of HSV-2 DNA by using HSV-1 X HSV-2 intertypic recombinants (RH1G44, RS1G25, R50BG10, A7D, and C4D) and HSV-1 MP. Target cells infected with R50BG10, A7D, and C4D exhibited reduced levels of cytolysis, as did HSV-2-infected cells, whereas RH1G44 and RS1G25 recombinant-infected and HSV-1 MP-infected cells showed levels of lysis equal to that of HSV-1 KOS-infected cells. The intertypic recombinants R50BG10, RS1G25, RH1G44, and HSV-1 MP induced cross-reactive cytotoxic T lymphocytes. Coinfection of cells with HSV-1 KOS and either HSV-2 186 or R50BG10 recombinant also resulted in a decrease in the level of specific lysis by anti-HSV cytotoxic T lymphocytes.

Animals↗
PubMed1990

Rapid detection of herpes-simplex-virus DNA in cerebrospinal fluid of patients with herpes simplex encephalitis.

Herpes-simplex-virus (HSV) DNA in cerebrospinal fluid was amplified by use of the polymerase chain reaction and identified by hybridisation to a specific oligonucleotide probe. Specimens of cerebrospinal fluid (CSF) from 4 of 4 patients with herpes simplex encephalitis were positive for HSV DNA, whereas CSF specimens from 6 patients with other central-nervous-system infections were negative. This technique may expedite diagnosis of herpes simplex encephalitis.

Adult↗
PubMed1997

Nonneutralizing antibody against the glycoprotein K of herpes simplex virus type-1 exacerbates herpes simplex virus type-1-induced corneal scarring in various virus-mouse strain combinations.

PURPOSE: To determine whether the exacerbation of herpes simplex virus type-1 (HSV-1) induced corneal scarring that the authors reported previously in HSV-1 glycoprotein K (gK) vaccinated BALB/c mice challenged with HSV-1 strain McKrae was a general phenomenon independent of virus and mouse strains. To determine the gK-induced immune response leading to exacerbation of HSV-1-induced corneal scarring. METHODS: BALB/c or C57BL/6 mice were vaccinated with gK, ocularly challenged with HSV-1 strain KOS or McKrae, and the relative amount of corneal scarring determined 28 days after challenge. The T cells, total serum, or purified immunoglobulin G (IgG) isolated from gK-vaccinated mice was transferred individually to naive mice, and the affects on corneal scarring after HSV-1 challenge were determined. RESULTS: The KOS challenge of gK-vaccinated BALB/c mice resulted in significant corneal scarring (P = 0.0003), despite the fact that KOS normally produces no corneal scarring. McKrae challenge of gK-vaccinated C57BL/6 mice resulted in significant corneal scarring (P < 0.0001), despite the fact that C57BL/6 mice are normally refractory to HSV-1-induced corneal scarring. Passive transfer of total anti-gK mouse sera or purified anti-gK mouse IgG, but not adoptive transfer of total anti-gK T-cells to naive mice, resulted in exacerbation of corneal scarring after HSV-1 challenge (P < 0.0001). Mice defective for T-cell-dependent antibody production were not susceptible to exacerbation of HSV-1-induced corneal scarring by gK vaccination (P < 0.0001). CONCLUSIONS: The ability of gK vaccination to exacerbate HSV-1-induced corneal scarring was not mouse strain or HSV-1 strain specific. The gK-induced exacerbation of corneal scarring was related to anti-gK IgG. How anti-gK IgG exacerbated HSV-1 induced corneal scarring remains to be determined.

Animals↗