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PubMed1993

[Herpes simplex encephalitis].

Herpes simplex encephalitis (HSE) is a severe disease with high mortality and morbidity. As effective antiviral therapy improves the outcome of younger patients, the early diagnosis of the disease has become important, especially in children. The annual incidence of HSE in Japan among children is estimated to be about 100-200 cases, and the mortality is 10-20%. Instead of brain biopsy, we applied the polymerase chain reaction (PCR) assay to the early diagnosis. The DNA of herpes simplex virus was detectable in CSF of all HSE patients in the acute phase. Serial quantitation of viral genome by PCR also revealed that the amount of DNA decreased gradually corresponding to antiviral therapy, and it turned to be negative 3 to 18 days after the onset of neurological signs and symptoms (mean 10.1 days). These results show the PCR assay is a useful diagnostic tool for the early and non-invasive diagnosis of HSE.

Child, Preschool↗
PubMed1980

Identification of the herpes simplex virus DNA sequences present in six herpes simplex virus thymidine kinase-transformed mouse cell lines.

We have used a novel filter hybridization approach to detect and map the herpes simplex virus (HSV) DNA sequences which are present in four HSV thymidine kinase (HSVtk+)-transformed cell lines which were derived by exposure of thymidine kinase negative (tk-) mouse cells to UV light-irradiated HSV type 2 (HSV-2). In addition, we have mapped the HSV-1 DNA sequences which are present in two HSV-1tk+-transformed cell lines produced by transfection of tk- mouse cells with sheared HSV-1 DNA. The results of these studies can be summarized as follows. (i) The only HSV DNA sequences which were common to all HSVtk+-transformed cells were those located between map coordinates 0.28 and 0.32. Thus, this region contains all of the viral DNA sequences which are necessary for the expression of HSV-mediated tk transformation. (ii) Many of the cell lines also contained variable amounts of non-tk gene viral DNA sequences located between map coordinates 0.11 to 0.57 and 0.82 to 1.00, suggesting that incorporation of the viral DNA sequences located between these map coordinates is a relatively random event. (iii) The viral DNA sequences located between map coordinates 0 to 0.11 and 0.57 to 0.82 were uniformly absent from all of the HSVtk+ cell lines tested, suggesting that there is a strong negative selective pressure against incorporation of these viral DNA sequences.

Animals↗
PubMed2005

Anti-viral activity of the extracts of a Kenyan medicinal plant Carissa edulis against herpes simplex virus.

Herpes simplex virus (HSV) infection is a major opportunistic infection in immunosuppressed persons. It is therefore a serious disease in high HIV/AIDS prevalence areas as in sub-Saharan Africa where infections due to HSV have risen significantly. The development of resistant strains of HSV to the available drugs for infection management, as is evident in the first drug of choice acyclovir, has further compounded this situation. There is therefore an urgent need to identify and develop new alternative agents for management of HSV infections, more so, for those due to resistant strains. We report here on an aqueous total extract preparation from the roots of Carissa edulis (Forssk.) Vahl (Apocynaceae), a medicinal plant locally growing in Kenya that has exhibited remarkable anti-HSV activity in vitro and in vivo for both wild type and resistant strains of HSV. The extract significantly inhibited formation of plaques in Vero E6 cells infected with 100PFU of wild type strains of HSV (7401H HSV-1 and Ito-1262 HSV-2) or resistant strains of HSV (TK(-) 7401H HSV-1 and AP(r) 7401H HSV-1) by 100% at 50 microg/ml in vitro with minimal cell cytotoxicity (CC(50)=480 microg/ml). When the extract was examined for in vivo efficacy in a murine model using Balb/C mice cutaneously infected with wild type or resistant strains of HSV, the extract at an oral dose of 250 mg/kg significantly delayed the onset of HSV infections by over 50%. It also increased the mean survival time of treated infected mice by between 28 and 35% relative to the infected untreated mice (p<0.05 versus control by Student's t-test). The mortality rate for mice treated with extract was also significantly reduced by between 70 and 90% as compared with the infected untreated mice that exhibited 100% mortality. No acute toxicity was observed in mice at the oral therapeutic dose of 250 mg/kg. These results suggest that this herbal extract has potent anti-viral agents against herpes simplex viruses that can be exploited for development of an alternative remedy for HSV infections.

Animals↗
PubMed1992

Analysis of intrastrain recombination in herpes simplex virus type 1 strain 17 and herpes simplex virus type 2 strain HG52 using restriction endonuclease sites as unselected markers and temperature-sensitive lesions as selected markers.

The viral and host factors involved in herpes simplex virus (HSV) recombination are little understood. To identify features of the process, recombination in HSV-1 and HSV-2 has been studied by analysing the segregation of unselected markers in the form of restriction endonuclease (RE) sites. By confining parental interactions to only one strain of virus of each serotype, restrictions imposed by non-homology are overcome and differential growth phenotypes can be discounted. The analysis of unselected and selected recombinants using RE sites in conjunction with temperature-sensitive mutations is consistent with (i) HSV being highly recombinogenic, (ii) parental and progeny molecules taking part in the process, (iii) the four genomic isomers participating in recombination, (iv) genome alignment being part of the recombination process and (v) cellular factors in conjunction with genome homology influencing the efficiency of recombination.

Animals↗
PubMed1978

Identification of a common antigen of herpes simplex virus bovine herpes mammillitis virus, and B virus.

In immunoelectrophoretic analyses one common antigen was demonstrated in antigen preparations from herpes simplex virus types 1- and 2- (HSV-1 and HSV-2), bovine herpes mammillitis (BHM) virus-, and B virus-infected cells solubilized by Triton X-100. The antigen was also demonstrated in solubilized purified HSV-1 and BHM virus. The common antigen was identified as antigen 11 of HSV-1 or HSV-2. Differences were found in the polypeptide composition of the related antigens when isolated from the four different herpesviruses, but a glycopolypeptide with a molecular weight of 125,000 was present in each of the four different antigen preparations, indicating that this polypeptide carried the common antigenic determinants.

Antigens, Viral↗
PubMed1986

The herpes simplex virus type 2 equivalent of the herpes simplex virus type 1 US7 gene and its flanking sequences.

Nucleotide sequencing studies (D. J. McGeoch, A. Dolan, S. Donald, and F. Rixon, 1985, J. Mol. Biol. 181, 1-14) have indicated that herpes simplex virus type 1 (HSV-1) has a coding sequence, referred to as US7, between the genes for the glycoproteins D and E (gD and gE). Northern blot analysis and nucleotide sequencing have been carried out to show that the type 2 virus (HSV-2) has an equivalent to the US7 gene. A comparison with the HSV-1 sequence has revealed some surprising similarities and differences. At the nucleotide level, HSV-2 has inserted a large sequence into the gE promoter, retained a large palindrome present in the coding sequence but not some tandem repeats, and deleted a region beside those repeats. At the amino acid level, the putative transmembrane sequence has been remarkably well conserved, and hydrophobic moment analysis indicates that it could be interacting with polar species within the plane of the membrane. Immediately after the deletion in the HSV-2 sequence, there is an N-glycosylation signal, and HSV-2 has one more such signal than HSV-1. The longest conserved sequence at the nucleotide level codes for a region of polypeptide that is strongly predicted to fold into alpha-helix. Implications of these analyses to the structure and possible function of these molecules are discussed.

Amino Acid Sequence↗
PubMed2006

Herpes simplex keratitis.

Herpes simplex keratitis (HSK) results from an infection with the herpes simplex virus type 1 (HSV-1) also known as human herpesvirus type 1 (HHV-1). Primary infection may involve an ocular or non-ocular site, following which latency might be established principally in the trigeminal ganglion but also in the cornea. During latency, the virus appears as a circular episome associated with histones with active transcription only from the region encoding the latency-associated transcript (LAT). The LAT region is implicated in neuronal survival, anti-apoptosis, virulence, suppression of transcription, establishment of and reactivation from latency. The initial keratitis may develop after infection through the "front door route" (entry into the ocular surface from droplet spread) or "back door route" (spread to the eye from a non-ocular site, principally the mouth). The initial ocular infection may be mild. Visual morbidity results from recurrent keratitis, which leads to corneal scarring, thinning and neovascularisation. Although, recurrent disease may potentially occur through anterograde axonal spread from the trigeminal ganglion to the cornea, recent evidence suggests that HSV-1 in the cornea may be another source of recurrent disease. The pathogenesis and severity of HSK is largely determined by an interaction between viral genes encoded by the strain of HSV-1 and the make up of the host's immune system. Herpetic stromal disease is due to the immune response to virus within the cornea and the ability of the strain to cause corneal stromal disease is correlated with its ability to induce corneal vascularisation. The pathogenesis of corneal scarring and vascularisation is uncertain but appears to be a complex interaction of various cytokines, chemokines and growth factors either brought in by inflammatory cells or produced locally in response to HSV-1 infection. Evidence now suggests that HSV-1 infection disrupts the normal equilibrium between angiogenic and anti-angiogenic stimuli leading to vascularisation. Thrombospondin 1 and 2, matricellular proteins, involved in wound healing are potent anti-angiogenic factors and appear to be one of the key players. Elucidating their roles in corneal scarring and vascularisation may lead to improved therapies for HSK.

Animals↗
PubMed1986

Prospective study on the relationship between cervical neoplasia and herpes simplex type 2 virus. III. Presence of herpes simplex type-2 antibody in sera of subjects who developed cervical neoplasia later in the study.

Paired sera taken from 63 subjects who developed cervical neoplasia in the course of a prospective study on this disease were examined for the presence of herpes simplex virus type 2 (HSV-2) antibody. The first serum was taken at enrollment into the study, while the second was obtained after development of the disease, i.e. 2-4 years later. Simultaneously, paired sera from a group of control subjects, who remained free of any cytological and colposcopical abnormalities throughout the study, were also investigated. Controls were matched with patients by age, age at first intercourse, number of sexual partners, smoking habits and history of diathermoelectrocoagulation of ectopic epithelium and transformation zone of the cervix. The first sera from these subjects were obtained at enrollment while the second ones were taken at the end of the study, i.e. 5 to 7 years later. Antibody titres were remarkably stable in both patients and control subjects. Seroconversions from HSV-2 negativity to HSV-2 positivity as measured by the increase in the II/I ratio or development of antibody reactive with HSV-2-specific glycoprotein G were rare and no significant differences between the patients and control subjects were detected. This indicates that the development of the disease was apparently not followed by immediate or early activation of latent HSV-2 infection.

Antibodies, Viral↗
PubMed1989

Recombinant vaccinia virus expressing the herpes simplex virus type 1 glycoprotein C protects mice against herpes simplex virus challenge.

The gene encoding the herpes simplex virus type 1 (HSV-1) glycoprotein C (gC) was isolated and cloned into a vaccinia virus insertion vector, and the resulting vaccinia-gC vector was used to construct a recombinant vaccinia virus that expressed gC (VVgC5). Infection of cells with VVgC5 resulted in cell surface expression of authentic HSV-1 gC. HSV-1 gC-specific neutralizing antibodies were produced in VVgC5-immunized mice, and lymphocytes exhibited an HSV-1-specific proliferation response in vitro following infection. More importantly, VVgC5-immunized mice were resistant to subsequent lethal HSV-1 challenge.

Animals↗
PubMed1999

Two-centre study comparing DNA preparation and PCR amplification protocols for herpes simplex virus detection in cerebrospinal fluids of patients with suspected herpes simplex encephalitis.

In a two-centre study, the routine DNA preparation and PCR amplification protocols were compared for herpes simplex virus (HSV) detection in cerebrospinal fluids (CSFs) of 43 patients with suspected herpes simplex encephalitis (HSE). The combined clinical, radiological and laboratory results indicated HSE in 6/43 (14%) patients. Discrepant PCR results between the two centres were obtained in 8 (18%) cases consisting of 5 false-positive and 3 false-negative results. Seven out of 8 (88%) discrepant results were associated with the method of CSF preparation using protease K digestion followed by heat inactivation. In contrast, CSF digestion with proteinase K followed by DNA purification on silica spin columns was better yielding discrepant PCR results in only 1 of 78 analyses (1.3%). The results point to the need for standardization and inter-laboratory quality control for routine clinical work.

DNA, Viral↗
PubMed1995

Brain irradiation and antioedematous dexamethasone treatment--risk factors for herpes simplex encephalitis?

Herpes simplex encephalitis (HSE) could result from the reactivation of an endogenous latent herpes simplex virus (HSV) in sensory ganglia or in brain parenchyma. Virus replication and a new lytic virus cycle may be triggered by a wide variety of factors. One of these might be irradiation as suggested by experimental evidence obtained in mouse trigeminal ganglia. Here we report the occurrence of HSE in a 52 years old woman two months after brain irradiation (40 Gray in 20 fractions) and dexamethasone administration for a metastatic brain tumor. HSE has already been observed in a clinical context very similar to that reported here, suggesting that brain irradiation together with corticoid therapy may, in some rare patients, favour the occurrence of HSV reactivation and HSE.

Antineoplastic Agents, Hormonal↗
PubMed1977

Expression of an early, nonstructural antigen of herpes simplex virus in cell transformed in vitro by herpes simplex virus.

Hyperimmune rabbit antiserum to an early, nonstructural herpes simplex virus type 2 (HSV-2)-induced polypeptide (VP143) reacted in immunofluorescence tests with a variety of cell lines transformed by HSV-2. Cytoplasmic fluorescence was observed in 10 to 50% of HSV-2-transformed cells, whereas no fluorescence was observed in cells transformed by other oncogenic DNA viruses or by a chemical carcinogen. VP143-specific reactivity could be absorbed from anti-VP143 serum with HSV-2-transformed cells but not with cells transformed by other agents. When HSV-2-transformed cells were synchronized in mitosis and examined at various times postmitosis for VP143-specific fluorescence, the expression of VP143 was shown to be cell cycle dependent.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1993

Diagnostic impression cytology for herpes simplex keratitis.

Herpes simplex virus (HSV) antigens in corneal or conjunctival epithelial lesions were detected by impression cytology. Specimens were obtained using a nitrocellulose membrane and were stained by the peroxidase-antiperoxidase method. HSV antigens were demonstrated in 30 of 32 patients with herpes simplex keratitis or conjunctivitis. Impression specimens of dendritic or stellate keratitis lesions exhibited precise replicas of corneal lesions with numerous antigen-positive cells. HSV antigens were also detectable in some of the minute stellate and/or punctate epithelial keratitis lesions even during the course of antiviral treatment. Impression cytology is noninvasive and useful for a rapid etiological diagnosis of herpetic epithelial lesions.

Antigens, Viral↗
PubMed2004

Sexually transmitted herpes simplex viruses.

Herpes simplex virus type 2 (HSV-2) is the dominant primary causative agent in genital ulcerative infections. Since infections with HSV-2 usually are acquired through sexual contacts, antibodies are rarely found before the age of onset of sexual activity. Although most genital infections are caused by HSV-2, a rising proportion has become attributable to primary type 1 herpes simplex virus (HSV-1) infection. Genital HSV-1 infections are usually both less severe clinically and less prone to recur. HSV-1 infection might render a certain protection against an HSV-2 infection and seems to mitigate the HSV-2 illness. It is not yet clear whether the advent of HSV-1 genitally will reduce the general occurrence of HSV-2. Increased efforts to protect against sexual transmission of the herpes viruses should have an effect on the transmission of other chronic diseases, such as the human immunodeficiency virus (HIV). In conclusion, it seems that increased sexual promiscuity and more advanced sexual techniques contribute to an unnecessary rise in prevalence of genital HSV infections, thus also affecting transmission of other genitally manifested diseases in targeted populations.

Disease Transmission, Infectious↗
PubMed1981

Repair of psoralen-treated DNA by genetic recombination in human cells infected with herpes simplex virus.

Herpes simplex virus type 1 was treated with 4,5'-8-trimethylpsoralen (psoralen) plus near-ultraviolet light in order to produce lesions (monoadducts and DNA cross-links) in the viral DNA. Human fibroblasts were infected by damaged virus under conditions in which either a single virus particle or several particles entered a given cell, and the fraction of virus-producing cells was determined. This fraction was significantly greater for multiply infected cells than for singly infected cells, indicating that the psoralen lesions are repaired more efficiently in the present of homologous, damaged DNA (multiplicity reactivation). Evidence is presented that herpes simplex virus may code for functions which participate in its own repair, both during multiplicity reactivation and during repair which occurs in singly infected cells: (a) host cells deficient in repair of lesions induced by psoralen (xeroderma pigmentosum) or the DNA cross-linking agent mitomycin C (Fanconi's anemia) exhibited normal levels of multiplicity reactivation of psoralen-treated herpes virus; (b) while xeroderma pigmentosum cells have been previously shown to be deficient in repair of psoralen-treated adenovirus under conditions of single infection, herpes virus is repaired at near normal levels in these same cells. Recombination levels between genetically marked pairs of herpes viruses were found to increase after treatment of the parental viruses with psoralen, suggesting that psoralen damage stimulates genetic recombination. This stimulation provides convincing evidence for a repair pathway in which genetic recombination between damaged viral genomes can lead to the production of viable virus.

Cell Transformation, Viral↗
PubMed1995

Quantification of transcripts from the ICP4 and thymidine kinase genes in mouse ganglia latently infected with herpes simplex virus.

Herpes simplex virus establishes latency in nervous tissue in which it is maintained for the life of the mammalian host, with occasional reactivation leading to subsequent spread. Latency-associated transcripts are abundant during latency, but viral proteins and productive cycle RNAs have not been detected. Using sensitive, quantitative PCR assays, we have quantified certain viral RNAs specific to productive-cycle genes in mouse ganglia latently infected with herpes simplex virus type 1. Sense-strand RNA specific to the essential immediate-early gene, ICP4, was present in most ganglia in variable amounts relative to the amount of viral DNA, with one to seven molecules of RNA per viral genome in about 20% of ganglia. In contrast, the amount of latency-associated transcripts was much less variable, at an average of 4 x 10(4) molecules per viral genome. The amounts of ICP4-specific RNA were similar at 30 and 60 days postinfection, and at least some of these transcripts initiated within a region consistent with utilization of the ICP4 promoter. RNA specific to the thymidine kinase gene, whose transcription in productive infection is dependent on ICP4, was present in latently infected ganglia at a maximum level of 3.2 x 10(6) molecules per ganglion (500 molecules per viral genome). ICP4-specific and tk-specific RNAs measured from the same samples showed a positive correlation extending over 2 orders of magnitude. We conclude that ICP4-specific RNA is expressed in the absence of detectable reactivation and discuss possible implications of our findings for latent gene expression.

Animals↗
PubMed1992

Incorporation of the carbocyclic analog of 2'-deoxyguanosine into the DNA of herpes simplex virus and of HEp-2 cells infected with herpes simplex virus.

The carbocyclic analog of 2'-deoxyguanosine (CdG) is active against herpes simplex virus (HSV), human cytomegalovirus, and human hepatitis-B virus. In order to understand the mechanism of action of this compound against HSV, we have evaluated (a) the incorporation of [3H]CdG into viral and host DNA in HEp-2 cells infected with HSV and (b) the interaction of the 5'-triphosphate of CdG (CdG-TP) with the HSV DNA polymerase and human DNA polymerases alpha, beta, and gamma (EC 2.7.7.7). Incubation of HSV-1-infected HEp-2 cells with [3H]CdG resulted in the incorporation of CdG into both the HSV and the host cell DNA. These results indicated that CdG-TP was used as a substrate for HSV DNA polymerase and for at least one of the cellular DNA polymerases. Degradation of both viral and host DNA with micrococcal nuclease and spleen phosphodiesterase indicated that CdG was incorporated primarily into internal positions in both DNAs. The viral DNA containing CdG sedimented in neutral and alkaline sucrose gradients in the same way as did viral DNA labeled with [3H]thymidine, indicating that the HSV DNA containing CdG was similar in size to untreated HSV DNA. CdG-TP was a competitive inhibitor of the incorporation of dGTP into DNA by the HSV DNA polymerase (Ki of 0.35 microM) and the human DNA polymerase alpha (Ki of 1 microM). CdG-TP was not a potent inhibitor of either DNA polymerase beta or gamma. Using DNA-sequencing technology, CdG-TP was found to be an efficient substrate for HSV DNA polymerase. Incorporation of CdG monophosphate (CdG-MP) into the DNA by HSV DNA polymerase did not interfere with subsequent chain extension. These results suggested that the antiviral activity of CdG was due to its incorporation into the DNA and subsequent disruption of viral functions. In contrast, CdG-TP was not as good as dGTP as a substrate for DNA synthesis by DNA polymerase alpha, and incorporation of CdG-MP by DNA polymerase alpha inhibited further DNA chain elongation.

Base Sequence↗