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At least 235 records · Page 13Linked to original sources
PubMed1986

Antibodies against herpes simplex virus in a group of healthy humans without reactions to herpes simplex virus antigens in blasttransformation assays.

22 healthy individuals with different reactions in humoral and cell-mediated immunity to herpes simplex virus (HSV), as found in complement-fixation, neutralization, and blasttransformation assays have been further investigated using antibody-dependent cell-mediated immunity (ADCC) as a serological test. Sera from all individuals were absorbed on HSV-infected, varicella zoster virus (VZV)-infected or uninfected cell monolayers, before they were used in ADCC with HSV-infected cells, as target. The results with absorbed sera were compared with the results from unabsorbed sera. Fresh uninactivated sera have also been used in some of the investigations. By these experiments a group of individuals was found, who were HSV-positive in ADCC, but negative in all other, above-mentioned tests. Because of these reactions they are proposed to be HSV-positives without a latent infection.

Adult↗
PubMed1999

Nucleotide sequence of thymidine kinase gene of sequential acyclovir-resistant herpes simplex virus type 1 isolates recovered from a child with Wiskott-Aldrich syndrome: evidence for reactivation of acyclovir-resistant herpes simplex virus.

Recurrent acyclovir (ACV)-resistant (ACV-r) herpes simplex virus type 1 (HSV-1) infections occurred in a patient with Wiskott-Aldrich syndrome, an X-linked recessive immunodeficiency syndrome composed of three clinical characteristics of immunodeficiency, thrombocytopenia, and an eczematous dermatitis. The patient had severe and recurrent ACV-r herpes simplex and was treated with vidarabine in a satisfactory manner from 1993 to 1997. During the 4-year observation period, two ACV-sensitive (ACV-s) HSV-1 isolates and five ACV-r HSV-1 isolates were recovered. The nucleotide sequence of the thymidine kinase (TK) gene from these sequential ACV-r isolates was compared with the ACV-s isolates. A single nucleotide deletion of cytosine (C) from homopolymer stretch of four C residues between nucleotide 1061 and 1064 of the open reading frame was found in all ACV-r isolates. No other differences were observed in the TK nucleotide sequence between ACV-s and ACV-r isolates. The TK nucleotide sequences of the two ACV-s isolates were identical to each other and those of the five ACV-r isolates were identical to one another. These results suggest that the ACV-r HSV-1 might have derived from the ACV-s strain in the patient body and that TK-associated ACV-r HSV-1 can reactivate from latency.

Acyclovir↗
PubMed2000

[Herpes simplex virus type 1-induced rising dbl quote, left (low)tumor" in the nasal vestibule. The problem of resistance development of herpes simplex in a patient with chronic lymphatic B-cell leukemia].

Herpes simplex viruses are known to be among the most common disease-causing microorganisms. Their prevalence can exceed 90% depending on the socioeconomic status of the population. Since the number of immunocompromised patients has increased because of the increased incidence in the acquired immunodeficiency syndrome and an increase in organ transplantation, herpes virus infection may have a greater clinical significance. While treatment of otherwise healthy individuals will not usually cause any clinical problems herpes infection in an immunocompromised patient can have severe consequences. Additionally, development of viral resistance can be observed that may require alternative drugs in treatment. We present a case history of a man with a B-cell chronic lymphocytic leukemia that was associated with a very unusual herpes simplex virus infection in the nasal vestibule. Possible causes for the development of resistance in herpes infections and the use of famciclovir and forscarnet as two therapeutic alternatives to aciclovir are discussed.

Antiviral Agents↗
PubMed1994

A herpes simplex virus 1 US11-expressing cell line is resistant to herpes simplex virus infection at a step in viral entry mediated by glycoprotein D.

A baby hamster kidney [BHK(tk-)] cell line (US11cl19) which stably expresses the US11 and alpha 4 genes of herpes simplex virus 1 strain F [HSV-1(F)] was found to be resistant to infection with HSV-1. Although wild-type HSV-1(F) attached with normal kinetics to the surface of US11cl19 cells, most cells showed no evidence of infection and failed to accumulate detectable amounts of alpha mRNAs. The relationship between the expression of UL11 and resistance to HSV infection in US11cl19 cells has not been defined, but the block to infection with wild-type HSV-1 was overcome by exposing cells with attached virus on their surface to the fusogen polyethylene glycol, suggesting that the block to infection preceded the fusion of viral and cellular membranes. An escape mutant of HSV-1(F), designated R5000, that forms plaques on US11cl19 cells was selected. This mutant was found to contain a mutation in the glycoprotein D (gD) coding sequence that results in the substitution of the serine at position 140 in the mature protein to asparagine. A recombinant virus, designated R5001, was constructed in which the wild-type gD gene was replaced with the R5000 gD gene. The recombinant formed plaques on US11cl19 cells with an efficiency comparable to that of the escape mutant R5000, suggesting that the mutation in gD determines the ability of the mutant R5000 to grow on US11cl19 cells. The observation that the US11cl19 cells were slightly more resistant to fusion by polyethylene glycol than parental BHK(tk-) cells led to the selection and testing of clonal lines from unselected and polyethylene glycol-selected BHK(tk-) cells. The results were that 16% of unselected to as much as 36% of the clones selected for relative resistance to polyethylene glycol fusion exhibited various degrees of resistance to infection. The exact step at which the infection was blocked is not known, but the results illustrate the ease of selection of cell clones with one or more sites at which infection could be blocked.

Animals↗
PubMed1979

Characterization of pyrimidine deoxyribonucleoside kinase (thymidine kinase) and thymidylate kinase as a multifunctional enzyme in cells transformed by herpes simplex virus type 1 and in cells infected with mutant strains of herpes simplex virus.

Pyrimidine deoxyribonucleoside kinase (thymidine kinase [TK]) was purified from two herpes simplex virus type 1 (HVS-1)-transformed TK-deficient mouse (LMTK-) cell lines and from LMTK- cells infected with HSV-1 mutant viruses coding for variant TK enzymes. These preparations exhibited normal or variant virus-induced thymidylate kinase activities correlating with their relative TK activities. Neither virus-induced activity was detected in LMTK- cells infected with an HSV-1 TK-deficient mutant. These results suggest that HSV-1 thymidylate kinase activity and TK activity are mediated by the same protein.

Animals↗
PubMed1985

Virion component of herpes simplex virus type 1 KOS interferes with early shutoff of host protein synthesis induced by herpes simplex virus type 2 186.

Herpes simplex virus (HSV) strains HSV type 1 (HSV-1) KOS and HSV-2 186 are representative of delayed and early shutoff strains, respectively, with regard to their ability to inhibit protein synthesis in Friend erythroleukemia cells. When these cells were simultaneously infected with HSV-1 KOS and HSV-2 186, HSV-1 KOS interfered with the rapid suppression of globin synthesis induced by HSV-2 186. The observed interference was competitive and not due to exclusion of HSV-2 by HSV-1 at the level of adsorption. Furthermore, UV-irradiated HSV-1 KOS was also effective at interfering with the early shutoff function of HSV-2 186, indicating that a virion component is responsible for the observed interference.

Animals↗
PubMed1975

Herpes simplex virus type 2 and acute aseptic meningitis. Clinical features of cases with isolation of herpes simplex virus from cerebrospinal fluids.

Herpes simplex virus (HSV) was recovered from the cerebrospinal fluids (CSF) of 10 patients with acute aseptic meningitis. HSV type 1 was isolated from the CSF of a 6-month-old boy. The other 9 HSV isolates from CSF were from adults in the age-group 15 to 29 years; 7 of these isolates were available for typing and were identified as HSV type 2. In a further 9 patients with acute aseptic meningitis and belonging to the same age-group a HSV infection was suggested by a significant titre rise in complement-fixing antibodies against HSV. The clinical features of the 10 patients with HSV isolation from CSF are presented. The 6-month-old boy with HSV type 1 had an acute benign aseptic meningitis. Seven of the 9 adults with HSV isolation from CSF (type 2 in all isolates available for typing) had an acute uncomplicated aseptic meningitis, one patient (with type 2 isolated) had an acute meningoencephalitis and one (isolate untyped) an acute meningomyelitis.

Adolescent↗
PubMed1997

Quantitation of herpes simplex virus type 1 DNA in cells of cerebrospinal fluid of patients with herpes simplex virus encephalitis.

We used a nested polymerase chain reaction assay to quantitate the number of viral copies in cells of CSF of eight patients with herpes simplex virus encephalitis (HSVE). The viral load was monitored in serial CSF samples during the course of disease and correlated to clinical symptoms, radiologic manifestations, efficacy of acyclovir treatment, and overall clinical outcome. Before treatment, HSV type 1 (HSV-1) copies were detected at a mean value of 1,786/10(5) (range, 5 to 8,333/10(5) cells; median, 81/10(5) cells). During therapy, HSV-1 DNA decreased gradually to a mean value of 6 copies/10(5) cells (range, 0 to 33 copies/10(5) cells; median, 0 copies/10(5) cells) within 6 to 21 days and disappeared or was barely detectable before treatment completion in most cases. The HSV-1 burden in the CSF did not clearly correlate with the severity of clinical signs or the degree of cranial imaging findings and overall outcome. Quantitation of HSV-1 copies allows rapid and reliable monitoring of antiviral therapy. The absence of a clear correlation between viral load in the CSF and morbidity may suggest a role for indirect mechanisms of brain injury in HSVE.

Acyclovir↗
PubMed1993

Identification of renal sympathetic preganglionic neurons in hamsters using transsynaptic transport of herpes simplex type 1 virus.

Herpes viruses have been used as retrograde transsynaptic tracers to identify pathways from the CNS to specific target tissues. We used herpes simplex virus to identify central nervous system neurons responsible for control of the kidney. Herpes simplex type 1 or herpes simplex type 2 was injected into rat kidneys and herpes simplex type 1 was microinjected into hamster and guinea pig kidneys. After three to seven days, ganglia, spinal cords and brains were examined using immunohistochemistry to visualize the virus-infected neurons. Our first experiments demonstrated that rats were not susceptible to infection with neurotropic strains of herpes simplex type 1. Injections of a wildtype strain of herpes simplex type 2 into rat kidneys led to nonspecific infection of many central nervous system neurons and glia. In contrast, herpes simplex type 1 injections in hamsters and guinea pigs caused specific infection of limited numbers of neurons in approximately one-third of the animals and the study was continued using hamsters. Sympathetic preganglionic neuron labelling was found in the ipsilateral intermediolateral cell column of the spinal cord as well as the lateral funiculus. Most infected preganglionic neurons were located in the seventh to the ninth thoracic spinal segments. Infected neurons were not found in the dorsal or ventral horn of the spinal gray matter and only one or two cells were found in the brainstem. Sympathetic preganglionic neuron morphology was usually normal, showing detailed dendritic arborizations, and lysis was infrequent. Small infected cells were sometimes observed close to sympathetic preganglionic neurons. Because herpes simplex type 1 virus was not detected immunocytochemically in ganglionic neurons in these same hamsters, the polymerase chain reaction was used in some additional hamsters to detect viral DNA in the T12 and T13 chain ganglia and splanchnic ganglia ipsilateral to the kidney injected with herpes simplex type 1. Finally, the overall distribution of renal postganglionic and splanchnic preganglionic neurons in hamsters was examined for comparison to the number and locations of virus-labelled neurons. Retrograde transport of the fluorescent dye FluoroGold demonstrated that (i) renal postganglionic neurons are distributed in the T10-L1 chain ganglia and in the prevertebral splanchnic ganglion and (ii) splanchnic preganglionic neurons are located in the T3-T12 spinal segments, predominantly in the intermediolateral and funicular spinal autonomic nuclei. In conclusion, herpes simplex type 1 virus infected an exclusive population of "renal" neurons in hamsters without lysis and with little cellular reaction to the infection after a survival period of three days, permitting these neurons to be studied in detail.

Animals↗
PubMed2006

Maternal herpes simplex virus antibody avidity and risk of neonatal herpes.

OBJECTIVE: The objective of the study was to assess whether herpes simplex virus antibody avidity is associated with risk of transmission of herpes simplex virus to the neonate. STUDY DESIGN: We developed a novel herpes simplex virus type 1 avidity test based on the commercially available Focus HerpeSelect-1 enzyme-linked immunosorbent assay kit using sera from nonpregnant subjects with genital herpes simplex virus-1 infection. We used this test, and the previously developed herpes simplex virus type 2 avidity test, to compare maternal herpes simplex virus-1 and herpes simplex virus-2 antibody avidity in women who transmitted herpes simplex virus to the neonate and women who had herpes simplex virus isolated from genital secretions at delivery but who did not transmit herpes simplex virus to their infants. RESULTS: Among nonpregnant subjects with genital herpes simplex virus-1 infection whose sera were used to develop the herpes simplex virus-1 avidity test, a significant relationship between herpes simplex virus-1 antibody avidity and time since herpes simplex virus-1 acquisition was observed (P < .001, mixed-effects model), with median avidity values increasing over time after primary infection. Among pregnant, herpes simplex virus-1, or herpes simplex virus-2 seropositive women, 4 of 8 women (50%) with avidity 40 or greater transmitted herpes simplex virus to the neonate, compared with only 12 of 97 (12%) of women with avidity greater than 40 (P = .02). CONCLUSIONS: Herpes simplex virus-1 antibody avidity increased over time after genital herpes simplex virus-1 acquisition, as has been previously observed for herpes simplex virus-2. Among women with herpes simplex virus antibody at delivery, low antibody avidity was associated with herpes simplex virus transmission to the neonate and may be a useful marker for recent seroconversion.

Adult↗
PubMed1995

Protection against herpes simplex virus-induced eye disease after vaccination with seven individually expressed herpes simplex virus 1 glycoproteins.

PURPOSE: To compare the efficacy of each of seven expressed herpes simplex virus 1 (HSV-1) glycoproteins as vaccines to protect against ocular disease after primary ocular HSV-1 infection. METHODS: Mice were vaccinated three times with equal amounts of each of seven individually expressed HSV-1 glycoproteins (gB, gC, gD, gE, gG, gH, and gI) and then ocularly challenged with McKrae, a corneal disease-producing strain of HSV-1. Viral clearance from the eye, blepharitis, keratitis, and neovascularization were determined at various times after infection. RESULTS: Mice vaccinated with gD or gB had the best protection against eye disease. Vaccination with gI, gC, or gE produced moderate protection against eye disease. Vaccination with gG produced less protection, and vaccination with gH produced no apparent protection against eye disease. CONCLUSIONS: These results suggest that when used as vaccines, different HSV-1 glycoproteins provide different levels of protection against HSV-1-induced eye disease. Based on comparison with the authors' previously published results, the ability of each glycoprotein to protect against eye disease correlated with the ability of the glycoprotein to induce high serum neutralizing antibody titers and killer cell activity. Results suggest that the effectiveness of these seven glycoproteins in protecting against eye disease can be ranked as follows: gD > gB > gI > (gC = gE) > gG > gH.

Animals↗
PubMed1984

Physical mapping of the herpes simplex virus type 2 nuc- lesion affecting alkaline exonuclease activity by using herpes simplex virus type 1 deletion clones.

The nuc- lesion affecting alkaline exonuclease activity in the herpes simplex virus type 2 (HSV-2) mutant ts1348 had previously been mapped to the EcoRI-D restriction enzyme fragment of HSV-1. Eight clones with deletions representing most of HSV-1 EcoRI fragment D were selected with lambda gtWES hybrids. These clones were tested for their ability to rescue the alkaline exonuclease activity of HSV-2 nuc- ts1348 virus. The sequences colinear with the HSV-2 nuc- lesion were found to map between 0.169 and 0.174 map units on the HSV-1 Patton genome, representing an 0.8-kilobase-pair region that is 12.9 to 13.7 kilobase pairs from the left end of HSV-1 EcoRI fragment D.

Animals↗