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PubMed2000

An appraisal of screening for maternal type-specific herpes simplex virus antibodies to prevent neonatal herpes.

Almost all neonatal herpes simplex virus infections occur as a result of first-episode maternal infection during late pregnancy when delivery occurs before the development of protective maternal antibodies. Screening of pregnant women for the presence of type-specific herpes simplex virus antibodies has therefore been suggested as a means of identifying women vulnerable to herpes simplex virus acquisition and subsequent transmission of herpes simplex virus to their neonates. Couples in whom herpes simplex virus serotype discordance is identified could be counseled regarding sexual behavior modification to avoid maternal herpes simplex virus infection. However, the ramifications of routine screening for herpes simplex virus susceptibility during pregnancy could be profound in terms of costs, prenatal care delivery, and even social duress. The recent US Food and Drug Administration approval of type-specific herpes simplex virus antibody assays for clinical use lends temporal urgency to the need for a critical examination of the relevant data. After we performed such an evaluation and created a decision analysis model to assess the potential cost-effectiveness of herpes simplex virus antibody screening, we concluded that screening for maternal type-specific herpes simplex virus antibodies cannot be recommended to prevent neonatal herpes.

Antibodies, Viral↗
PubMed1981

Expression of herpes simplex virus common surface antigens and malignancy by clonal cells of a herpes simplex virus type 2-transformed line.

Herpes simplex virus (HSV) type common surface antigens (CSA) were examined by indirect immunofluorescence with rabbit antiserum to HSV type 1 in a clonal hamster cell line 155-4 transformed by HSV type 2. The tumor formation was examined in hamsters transplanted with various transformed and tumor cells. The examination of subclones derived from 1554-cell line gave the following results. (1) Thirty subclones were isolated and classified into three phenotypes as to CSA expression: (i) in CSA-positive type (20% of the clones isolated), the number of CSA-positive cells increased soon (5 hr) after seeding at 37 degree; (ii) in CSA-inducible type (33% of the clones), the number of CSA-positive cells increased after treatment with actinomycin D (ACT-D, 2 micrograms/ml), but not without ACT-D; (iii) CSA-negative type (47% of the clones), the number of CSA-positive cells did not increase after seeding or after ACT-D treatment. (2) In tumor cell lines derived from the parent line and from three representative clones, CSA expressions were similar to that by CSA-negative type. (3) Transformed cells expressing CSA after seeding or after ACT-D treatment formed tumors and metastases less efficiently than cells expressing little CSA in transplanted hamsters. (4) Tumor cell lines formed tumors and metastases more efficiently than transformed cells expressing little CSA in transplanted hamsters.

Animals↗
PubMed1984

Expression of a herpes simplex virus glycoprotein in two clonal lines of hamster cells transformed by herpes simplex virus type 2.

Expression of herpes simplex virus type 2 (HSV-2) glycoproteins on the cell surface of two clones of a hamster cell line transformed by HSV-2 was examined by immunofluorescence tests with hamster antisera prepared against three size-class glycoprotein fractions obtained from hamster embryo fibroblast cells infected with HSV-2. Enhanced expression of one of the three size-class glycoprotein fractions (molecular weight, 82,000-94,000) was found in one clone (155-4-213) after replating of the cells, and in the other (155-4-03) after actinomycin D treatment. Enhanced expression of the antigen in clone 155-4-213 was inhibited by 2-deoxy-D-glucose, but not by puromycin or protease inhibitors, antipain and p-nitrophenyl-p'-guanidinobenzoate. On the other hand, the antigen expression induced by actinomycin D in clone 155-4-03 was inhibited by these four drugs. These results indicate that the expressions of the antigen in the two clones are enhanced by different mechanisms.

Animals↗
PubMed1983

Herpes simplex virus and human cancer. III. Search for relationship of herpes simplex antibodies and cervical dysplasia and labial neoplasia.

We employed the enzyme-linked immunosorbent assay (ELISA), indirect hemagglutination (IHA), and complement fixation (CF) methods to measure antibody titer to herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) in patients affected by labial tumors or cervical dysplasias. No relationship of antibody titer to HSV-1 and labial tumors was detected by any of the three methods. Association between antibody titer to HSV-2 and cervical dysplasias was revealed by IHA (p less than 0.05) and ELISA (p less than 0.001); CF tests were negative. Moreover, we assayed for HSV-specific antigens in cell cultures derived from labial tumors and cervical dysplasias. In cultures from labial tumors, it was not possible to detect HSV-specific antigens. Of the 25 cultures derived from cervical dysplasias, HSV antigens were found in only 3 cultures.

Adult↗
PubMed2006

Herpes simplex and varicella-zoster virus infections during pregnancy: current concepts of prevention, diagnosis and therapy. Part 1: herpes simplex virus infections.

Primary herpes simplex virus (HSV) infection may lead to severe illness in pregnancy and may be associated with transplacental virus transmission and fetal infection. The consequences may be abortion, stillbirth and congenital malformations. In neonates, the clinical findings after intrauterine HSV infection are characterized by skin lesions, diseases of the eye and neurologic damage. Herpes genitalis of pregnant women at the time of labor may result in life-threatening neonatal herpes. Currently, neither active nor passive immunization is available to prevent HSV infections during pregnancy and in the newborn infant. Therefore, antiviral treatment using aciclovir and/or valaciclovir must be considered in all primary episodes of genital herpes as well as in neonates who show signs of either infection. Clinical herpes lesions of the genitalia and/or positive test for virus detection at the time of delivery are an indication for cesarean section. However, this surgical intervention may be reduced by suppressive treatment of recurrent genital herpes with aciclovir or valaciclovir.

Acyclovir↗
PubMed1987

Expression of herpes simplex virus 1 glycoprotein B by a recombinant vaccinia virus and protection of mice against lethal herpes simplex virus 1 infection.

The herpes simplex virus 1 (HSV-1) strain F gene encoding glycoprotein gB was isolated and modified at the 5' end by in vitro oligonucleotide-directed mutagenesis. The modified gB gene was inserted into the vaccinia virus genome and expressed under the control of a vaccinia virus promoter. The mature gB glycoprotein produced by the vaccinia virus recombinant was glycosylated, was expressed at the cell surface, and was indistinguishable from authentic HSV-1 gB in terms of electrophoretic mobility. Mice immunized intradermally with the recombinant vaccinia virus produced gB-specific neutralizing antibodies and were resistant to a lethal HSV-1 challenge.

Animals↗
PubMed2000

[Specific skin infiltration of extracutaneous B-cell lymphoma in healing herpes simplex skin].

Both herpes simplex and herpes zoster are not uncommon in patients affected by malignant lymphoma or leukemia. Of particular interest, the herpetic lesions may be followed by specific cutaneous infiltrates. We report on a patient with a centrocytic-centroblastic non-Hodgkin lymphoma who showed primary skin infiltrates within the area affected by herpes simplex. After effective therapy with aciclovir, papules and plaques developed at the site of the herpetic scars. Histologic investigation confirmed dense B-lymphocytic infiltrates with immunoglobulin light chain restriction and a granulomatous reaction. Although the chemotherapeutical regiment was modified, the patient died one month later of a lethal blast crisis. The occurrence of so called isotopic skin reactions and their prognostic significance is discussed.

Blast Crisis↗
PubMedDate not supplied

High prevalence of herpes simplex virus type 1 in female anogenital herpes simplex in Newcastle upon Tyne 1983-92.

This retrospective study was undertaken to evaluate the prevalence of the viral types and temporal epidemiology in patients with ano-genital herpes between 1983-92. One thousand one hundred and thirty-five patients with anogenital herpes were available for analysis. The annual incidence of anogenital herpes nearly tripled over the period of 7 years (1986-92) from 59 to 171 cases. The percentage of HSV-1 infection in female cases (63-79%) was much higher than in other reported studies and remained relatively constant over the study period.

Anus Diseases↗
PubMed1977

Efficacy of herpes simplex virus type 1 immunization in protecting against acute and latent infection by herpes simplex virus type 2 in mice.

ICR mice were immunized with herpes simplex virus type 1 (HSV-1) and later challenged with HSV-2 by footpad inoculation. Both immunized animals and age-matched, nonimmunized controls were observed for ascending neurological disease and latent infection of spinal ganglia resulting from the HSV-2 challenge. Control animals had a 78% incidence of acute and latent infection compared with a 1.7% incidence in immunized mice. The data show immunity to HSV-1 is protective against both acute and latent infection by HSV-2.

Acute Disease↗
PubMed1989

Herpes simplex virus type 1 immediate-early protein Vmw110 reactivates latent herpes simplex virus type 2 in an in vitro latency system.

Reactivation of latent herpes simplex virus type 2 (HSV-2) by the immediate-early protein Vmw110 was studied by using an in vitro latency system. Adenovirus recombinants that express Vmw110 reactivated latent HSV-2. An HSV-1 mutant possessing a deletion in a carboxy-terminal region of Vmw110 reactivated latent HSV-2, whereas mutant FXE, which has a deletion in the second exon, did not. Therefore, Vmw110 alone is required to reactivate latent HSV-2 in vitro, and the region of Vmw110 defined by the deletion in FXE is important for this process.

Adenoviridae↗
PubMed1984

Recovery of herpes simplex virus genetic information from human trigeminal ganglion cells following superinfection with herpes simplex virus type 2 temperature-sensitive mutants.

Explant cultures of human trigeminal ganglia were derived from 36 individuals. Those cultures which failed to release herpes simplex virus (HSV) spontaneously were superinfected at various times after establishment in vitro with a range of HSV-2 temperature-sensitive (ts) mutants. Eight cultures from six individuals contained HSV-specific genetic information which could be detected or rescued following superinfection. Restriction enzyme analysis of ts+ virus recovered from the ganglia of two individuals following superinfection was identical to that of endogenous HSV-1 spontaneously released from parallel cultures. Retrieval of ts+ virus by this technique suggests products of the superinfecting virus activated expression of whole genomes or that spontaneous virus expression occurred unrelated to the act of superinfection.

Gene Expression Regulation↗
PubMed1952

HERPES simplex.

Explore the source record for details and available documents.

Herpes Simplex↗
PubMed1996

Seroepidemiology and control of genital herpes: the value of type specific antibodies to herpes simplex virus.

Herpes simplex virus (HSV) type 2 is the main cause of genital herpes infections. Conventional serological techniques cannot discriminate between antibodies specific to HSV types 1 and 2, so these methods cannot be used in the seroepidemiological investigation of genital herpes infections. The discovery of type specific antigens in HSV-1 and HSV-2, most notably glycoprotein G (gG), has been successfully exploited to develop assays for the detection of type specific HSV antibody. The presence of type specific antibodies provides evidence for infection with HSV-1, HSV-2, or both. Tests which detect humoral responses to HSV-2 have been used during the past decade to investigate populations in various countries. Most surveys of general adult populations in the developed world have found a relatively low seroprevalence of HSV-2, although this does differ between countries. Studies of HSV-2 antibody in developing countries have revealed higher rates of infection in adults. People attending sexually transmitted diseases (STD) clinics have higher rates of HSV-2 infection than general populations sampled in the same country. Assays of HSV type specific antibodies have been used in seroepidemiological surveys that include information about demography and sexual behaviour to identify risk factors for HSV-2 infection. The surveys show that people with a large number of sexual partners are at increased risk of acquiring HSV-2 infection and that a high proportion of HSV-2 infections are asymptomatic. Assays of HSV type specific antibody have been used to show that the presence of pre-existing HSV-1 antibody may reduce the severity of genital HSV-2 infection. Such assays have also been used in studies of the transmission of genital herpes. Proposed interventions to counter the spread of genital herpes include targeted education and vaccination programmes. Assays of HSV type specific antibodies may be used to monitor the effectiveness of such policies.

Adult↗
PubMed1975

Herpes simplex virus infection in guinea pigs: an animal model for studying latent and recurrent herpes simplex virus infection.

Footpad infection of guinea pigs with herpes simplex virus led to an acute local inflammatory reaction, followed by a persistent latent infection of lumbosacral dorsal root ganglia. Spontaneous reactivation of the latent virus occurred, leading to recurrent lesions at the site of the initial infection. Clinical observations and virological studies during the acute latent and recurrent infection are reported.

Animals↗
PubMed1983

Genetic variability of herpes simplex virus: development of a pathogenic variant during passaging of a nonpathogenic herpes simplex virus type 1 virus strain in mouse brain.

Herpes simplex virus type 1 ANG (HSV-1 ANG) is originally nonpathogenic for inbred mice upon intraperitoneal intravenous, or intravaginal inoculation. In contrast, mice died of encephalitis within 4 to 5 days after intracerebral inoculation with this strain. HSV-1 ANG was serially passaged in mouse brains. In two independent series, peripherally pathogenic virus variants had developed and accumulated in the virus progeny after 12 to 15 intracerebral passages. In mixed infections both nonpathogenic and pathogenic viruses replicated at the primary site of infection and spread to various organs. However, only the pathogenic phenotype could be recovered from the spinal cord and the brain. Comparison of the restriction enzyme cleavage patterns of pathogenic ANG and nonpathogenic ANG virus DNAs revealed distinct alterations in the S-segment (US) sequences bounded by coordinates 0.953 and 0.958 in the prototype orientation and by coordinates 0.862 to 0.867 in the IS orientation of the viral genome. However, it is not known whether these alterations are physiologically relevant to the observed changes in pathogenicity. When coinjected intraperitoneally at 50 to 100-fold excess, the nonpathogenic HSV-1 ANG protected mice against its own pathogenic variant as well as against other pathogenic HSV-1 strains. Pathogenic HSV-1 ANG proved to be genetically and phenotypically stable for at least 25 serial passages in tissue culture at either high or low multiplicity of infection.

Animals↗
PubMed1982

Herpes simplex antigen in immune complexes of patients with erythema multiforme: presence following recurrent herpes simplex infection.

Serum samples from patients with erythema multiforme (EM) were examined for the presence of herpes simplex virus (HSV) antigen in immune complexes using the Raji cell radioimmunoassay. Raji-cell-bound immune complexes from eight of 12 patients with EM after HSV infection and four of four patients with EM of uncertain cause had increased anti-HSV binding, while patients with EM after drug exposure and patients with recurrent HSV infections without EM had binding in the same range as controls. Viral cultures for HSV of immune complexes eluted from Raji cells were negative. Sucrose density gradient ultracentrifugation studies of serum samples of patients with EM after HSV infection showed HSV antigen in large molecular weight fractions. The HLA typing of lymphocytes from 16 patients with EM after HSV infection was not different from that of controls. Immune complexes composed of antibody and HSV antigen are present in serum samples of patients with EM after HSV infection and some cases of EM of uncertain cause and may mediate the pathogenesis of these disorders.

Antigen-Antibody Complex↗