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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Agents that perturb endocytosis or that alter the pH of endosomes were shown to have little or no effect on plaque formation by herpes simplex virus (HSV), whereas plaque formation by vesicular stomatitis virus was inhibited as expected. A number of agents were tested for their ability to inhibit early events in HSV infection. Amantadine, chloroquine and trifluoperazine, whose actions are known to alter the endocytic pathway, showed no selective inhibitory effects on early events in HSV infection. Wheat germ agglutinin and heparin, known inhibitors of HSV infection, blocked the adsorption of virus to cells, as expected. Succinylated concanavalin A blocked plaque formation without inhibiting virus adsorption but could enhance the elution of bound virus. To a greater or lesser extent, succinylated concanavalin A, dithiothreitol, colchicine, monensin and cytochalasin B all inhibited or reduced the rate of events subsequent to adsorption and prior to early viral protein synthesis. Evidence is presented to suggest that each of these agents has a different mode of action. On the basis of these results and others, we conclude that endocytosis is probably not required for infection by HSV (at least not the low pH-dependent endocytic pathway) and that events occurring at the cell surface trigger virion-cell fusion leading to infection.
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PMID:Penetration of cells by herpes simplex virus does not require a low pH-dependent endocytic pathway. 164 8

We have been studying delayed hypersensitivity (DH) to herpes simplex virus (HSV) in order to examine the role of this response in host defense against acute and recurrent HSV infections. In previous reports the basic parameters of DH to HSV have been characterized by using a murine ear swelling model, and also the regulation of DH to HSV induced by i.v. injection of the virus. In this paper, we describe a murine protection system and our use of the ability to specifically regulate DH to HSV to examine the correlation between T cells that transfer DH (TDH) and cells that transfer protection from acute HSV infection. Both DH and protection can be transferred with lymph node cells from mice immunized subcutaneously 4 days previously. The effector cell appears to be a T cell, because serum from these donors confers no protection and treatment of immune cells with anti-Thy-1.2 plus complement reduced their ability to protect. Tolerance of DH to HSV was induced by i.v. injection 7 days before subcutaneous immunization. Tolerized mice were unable to generate protective cells. Furthermore, tolerized mice contained suppressor T cells that suppressed not only DH but also the development of protective cells. Regulation of protective cells was shown to be virus specific, because mice tolerized with vesicular stomatitis virus (VSV) were not impaired in their ability to generate T cells that protected from HSV infection. The correlation between the TDH cell and cells that transfer protection from acute HSV infection is discussed.
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PMID:Delayed hypersensitivity and immune protection against herpes simplex virus: suppressor T cells that regulate the induction of delayed hypersensitivity effector T cells also regulate the induction of protective T cells. 258 6

Thymidine kinase negative (dTK-) mutants of herpes simplex virus type 1 (HSV-1) multiplied well in rat brain glioma cells. A proportion (less than 1%) of glioma cells survived the infection with HSV and were designated "survivor" glioma cells. Survivor cells of dTK- mutant virus infection ceased to produce infectious virus after two passages and were highly resistant to both HSV-1 and HSV-2 but not to vesicular stomatitis virus (VSV). Flow cytometric studies indicated morphological differences between parental and survivor glioma cells, and HSV-1 specific antigens as well as DNA were detected in the survivor glioma cells, but only in early passages. Sensitivity to superinfection with HSV appears to correlate to loss of HSV-specific viral DNA in the survivor glioma cells. Survivor glioma cells after several subcultures lost their ability to resist superinfecting HSV, reverted morphologically to the appearance of parental glioma cells and also lost significant amount of HSV-1 specific DNA. These transient survivor glioma cells became persistently infected-virus producer cells upon HSV infection.
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PMID:Studies on interactions of dTK-HSV mutants with neurons in vitro. 287 27

Rat brain glioma cells were semipermissive for herpes simplex virus (HSV) replication, because the growth of HSV was multiplicity-dependent in these cells. By using this property, we successfully isolated 'survivor' glioma cells following HSV infection at low multiplicity and without using any special treatment (such as UV irradiation) either of the cells or of the virus. Under the same conditions there were no survivor BHK or 3T3 cells, which suggests the uniqueness of the glioma cell-HSV interaction. The survivor cells ceased to produce infectious virus after two subcultures, but were highly resistant to superinfection for at least 20 subcultures. Parental cells were significantly more permissive for homologous virus growth than survivor cells. Interferon was apparently not induced in the survivor cells, because they were as susceptible as the parental cells to infection with vesicular stomatitis virus. The survivor cells produced HSV-specific antigens and contained HSV-specific DNA.
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PMID:Herpes simplex virus type 1 and neuronal cells--a special cell-virus interaction. 298 13

Herpes simplex virus (HSV) infection of the hand occurs predominantly in three different population groups. Young adults with a recurrent HSV II infection of the hand account for the majority of cases. A prodromal phase of up to 72 hours and a recurrence of seven to 10 days' duration occasionally associated with lymphangitis, lymphadenopathy, and lymphedema are characteristic. HSV I infection of the hand classically occurs in children with herpetic stomatitis and in health care workers infected during patient care delivery. In health care workers, the infection may last 21 to 28 days and be associated with severe pain and lymphangitis. Recurrences appear uncommon in HSV I infections. Primary infection is usually managed conservatively. Vesicle drainage for pain relief and antiviral therapy with acyclovir may be of value. For recurrent infections, acyclovir, 800 mg orally, twice daily, initiated during the prodrome in an open study of eight patients appeared effective in aborting the attack. Evaluation of long-term suppression in recurrent HSV infection of the hand is in progress.
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PMID:Herpes simplex virus infection of the hand. Clinical features and management. 340 76

The sensitivities to human leukocyte interferon of 10 strains of Herpes simplex virus (HSV) type 1 and 3 strains of type 2 were compared. All the strains were sensitive to interferon, although their sensitivities were less than that of vesicular stomatitis virus (VSV). There was no significant difference in the sensitivities to interferon of HSV type 1 and type-2 or among different strains of a given type of HSV. Nor was there any difference between the sensitivities of 5-iodo-2'-deoxyuridine (IDU)-sensitive and resistant strains isolated from the same patients. These results suggest that interferon should be useful in therapy of HSV infection.
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PMID:Comparative studies on the inhibitory effects of interferon on various strains of herpes simplex viruses in vitro. 616 4

The protective effect of crude rat interferon against infection by vesicular stomatitis virus (VSV) and herpes simplex virus (HSV) was assessed in two culture systems: the PC12 cell line and dissociated rat neurons derived from the superior cervical ganglion (SCG). Interferon was induced in rat embryo cells by inactivated Newcastle disease virus, and its effect was assessed by reduction of viral yields and prevention of viral cytopathology. Interferon protected PC12 cells, both in the presence and absence of nerve growth factor (NGF), against infection by both viruses, although at differing concentrations: protection against VSV was noted at approximately a 10-fold lower interferon concentration than that required to inhibit HSV infection. Dissociated SCG neurons were also protected, but higher interferon concentrations were required. These results demonstrate that the antiviral state can be established in neurons in response to interferon.
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PMID:Interferon protects neurons in culture infected with vesicular stomatitis and herpes simplex viruses. 618 2

Typical herpetic stomatitis that developed in a premature 6-day-old infant was initially diagnosed cytologically. The cytomorphologic characteristics of herpes simplex virus (HSV) infection in smears of scrapings from the oral mucosa helped to establish the diagnosis of a neonatal HSV infection, permitting early treatment with cytosine arabinoside (ara-C) and subsequent complete recovery from the generalized infection. The diagnosis was later confirmed by rises in the serologic titer of complement-fixing antibodies for HSV type 2.
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PMID:Cytodiagnosis of herpes simplex virus infection in the newborn infant: report of a case. 627

The relationship between oral shedding of Herpes simplex virus (HSV) and cytotoxic cancer chemotherapy was studied. HSV seropositive outpatients receiving cytotoxic chemotherapy had HSV recovered from throat washings in eight of 114 patients (7.0%), significantly more often than HSV seropositive outpatients with malignancy who were not receiving cytotoxic chemotherapy (one of 91 patients; 1.1%; P = 0.04). Twenty-eight HSV seropositive chemotherapy patients and 11 HSV seropositive healthy hospital personnel were studied serially 2-3 times per week over a 3-4 week period for oral HSV shedding. Although a comparable percentage of each group shed HSV at least once (57.1% of chemotherapy patients versus 36.4% of controls), chemotherapy patients had a strikingly higher incidence of multiple positive cultures: 40/218 attempts (18.7%) versus 4/156 attempts (2.6%) for controls (P less than 10(-5)). Among chemotherapy patients who developed clinically evident stomatitis, 12 of 14 (85.7%) had HSV recovered compared to four of 14 (28.6%) without lesions (P = 0.004). We conclude that while oral mucosal HSV infection is associated with symptomatic stomatitis following chemotherapy, HSV does not account for all mucosal lesions in chemotherapy patients.
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PMID:Cancer chemotherapy associated symptomatic stomatitis: role of Herpes simplex virus (HSV). 628 88

Dependence of the primary antiviral immune response on costimulatory interactions between CD28/CD80-86 and between CD40/CD154 (CD40 ligand) has been correlated with the extent of viral replication in two models of systemic infection, lymphocytic choriomeningitis virus and vesicular stomatitis virus. To determine the role of these costimulatory interactions in the context of an acute cytolytic, but locally replicating viral infection, herpes simplex virus (HSV) infection was assessed in mice that had the CD28/CD80-86 or CD40/CD154 interactions disrupted either genetically or with blocking reagents (CTLA4Ig and MR1, respectively). CTLA4Ig treatment greatly reduced paralysis-free survival during primary acute HSV infection. This reflected an almost total ablation of the anti-HSV CD4(+) and CD8(+) T-cell responses due to anergy and reduced cell numbers, respectively. Disruption of CD40/CD154 interactions impaired survival, but the effect was less severe than that observed in CTLA4Ig-treated mice, with reductions observed in the CD4(+) T-cell but not CD8(+) T-cell responses. These two costimulatory pathways functioned in part independently, since disruption of both further impaired survival. The dependence on these costimulatory interactions for the control of primary HSV infection may represent a more widespread paradigm for nonsystemic viruses, which have restricted sites of replication and which employ immunoevasive measures.
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PMID:Role of CD28/CD80-86 and CD40/CD154 costimulatory interactions in host defense to primary herpes simplex virus infection. 1113 74


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