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At least 19 recordsLinked to original sources
PubMed1978

Cytologic examination and viral and bacterial culture in herpes simplex, herpes zoster, and varicella.

Cytologic examination of epithelial cells from the base of vesicles, virus isolation, and bacterial culture were carried out in thirty-one patients with herpes simplex, in eleven patients with herpes zoster, and in three patients with varicella. Determination of herpes simplex complement fixation reaction was made in the patients with herpes simplex. Cytologic manifestations consistent with herpes were found 65 percent of patients with herpes simplex, while herpesvirus hominis was isolated in 77 percent of these patients. Diagnostic cytologic manifestations were found in 82 percent of the patients with herpes zoster or varicella. Varicella-zoster virus was isolated in 27 percent of these patients. The presence of pathogenic bacteria did not seem to influence the frequency of virus isolation or finding of characteristic cytologic features.

Bacteria↗
PubMed1976

Gastroesophageal involvement in herpes simplex.

Herpes simplex in the gastric mucosa has not been previously described. The case presented here describes gastritis and esophagitis resulting from herpes simplex in a patient being treated with immunosuppressive agents. These changes were confirmed endoscopically and radiographically. Biopsy specimens of the gastric and esophageal mucosa showed eosinophilic intranuclear inclusion bodies typical of herpes simplex. The pathogenesis and pathological appearance of herpetic gastritis and esophagitis are presented.

Adult↗
PubMed1975

Viral warts, herpes simplex and herpes zoster in patients with secondary immune deficiencies and neoplasms.

The incidence of viral warts, recurrent herpes simplex and herpes zoster has been assessed in a group of patients with possible secondary immune deficiency states and compared to a control group. Patients with cell-mediated immune deficiency appear to be more prone to warts and zoster infection as compared to patients with humoral immune deficiency. Recurrent herpes simplex infection was not increased in either group.

Adolescent↗
PubMed1978

Double blind trial in the treatment of herpes simplex and herpes zoster with adenine arabinoside and idoxuridine.

In a double blind trial adenine arabinoside (Vidarabine) and Idoxuridine (IDU) were tested in herpes simplex and herpes zoster infections. Adenine arabinoside covered 19 patients with HSV and 6 with HZ while IDU 19 with HSV and 6 with HZ. From the statistical analysis it was found that Vidarabine acts shorter than IDU in HSV P less than 0.01, while in HZ no significant difference P less than 0.5 was found, possibly due to the small number of patients tested.

Adolescent↗
PubMed1977

The use of betadine antiseptic paint in the treatment of Herpes simplex and Herpes Zoster.

Twenty-two patients with Herpes Simplex were treated with Betadine (povidone iodine) Antiseptic paint and seven with 5% idoxuridine in dimethyl sulphoxide, also one patient with bilateral lesions was treated with the two solutions, one on each side. The povidone iodine alcohol solution appeared to be at least as effective as the idoxuridine with minimal side-effects (some stinging in two patients). Good results were also obtained with this solution in twelve patients with Herpes Zoster.

Adolescent↗
PubMed1988

Differences in the mechanism of induction of interferon-alpha by herpes simplex virus and herpes simplex virus-infected cells.

The cellular source of IFN alpha after induction with Herpes simplex virus type-1 (HSV) and HSV-infected fibroblasts was investigated by using human peripheral blood mononuclear cell (PBMC) populations, purified according to conventional procedures, and which included T- and B-lymphocytes as well as monocytes. It appears that the cells responding to HSV virions are monocytes, whereas the PBMC population induced by HSV-infected cells is represented by B-lymphocytes. Furthermore, by using monoclonal antibody (MoAb) to HLA class I and class II products, it appears that different membrane structures are involved in the induction of IFN by HSV virions, as opposed to HSV-infected cells. In fact, most anti-HLA class II MoAbs inhibit IFN induction by HSV-infected cells, and not IFN induction by HSV virions.

Antibodies, Monoclonal↗
PubMed1991

Mechanism and mode of action of 5-iodo-2-pyrimidinone 2'-deoxyribonucleoside, a potent anti-herpes simplex virus compound, in herpes simplex virus-infected cells.

The anti-herpes simplex virus type 2 (-HSV-2) action of 5-iodo-2-pyrimidinone deoxyribonucleoside (IPdR) was found to be exerted through inhibition of HSV DNA synthesis. The inhibition of viral DNA synthesis was not caused by inhibition of the synthesis of HSV-2-specified proteins or HSV-2 mRNA species involved with viral DNA synthesis or by depletion of deoxynucleotides. The inhibition of viral DNA synthesis may be due to damage to the DNA template in the nuclei or to an action at the DNA replication complex, because nuclei isolated from HSV-2-infected cells treated with IPdR could not support DNA synthesis in vitro. Moreover, the addition of exogenous template to the reaction enabled nuclear DNA synthesis to occur at the level of control. The major cellular metabolite of IPdR in HeLa S3 cells infected with HSV-2 was IPdR monophosphate, which was formed through virally specified kinase. Attempts to either identify or synthesize IPdR diphosphate and triphosphate were unsuccessful. The accumulation of IPdR monophosphate was dependent on the extracellular concentration of IPdR. IPdR monophosphate did not have any inhibitory effect on nuclear DNA synthesis, even at 200 microM. Thus, the action of IPdR could be due to an unidentified metabolite of IPdR or the depletion of a cellular metabolite that is essential for viral DNA synthesis.

Antiviral Agents↗
PubMed1976

Immunology of herpes simplex virus infection: relevance to herpes simplex virus vaccines and cervical cancer.

The immunology of herpes simplex infections has been reviewed, particularly in relation to potential herpes simplex virus (HSV) vaccines, and to the association between HSV and cervical cancer. Relevant data from humans, experimental animals, and in vitro systems implicate both specific immune mechanisms and nonspecific factors in the course of HSV infections. There appear to be complex interactions between the various populations of mononuclear cells, marcrophages, and lymphokines or other humoral factors. It is not yet possible, however, to pinpoint the crucial factors determining the different manifestations of the viral infection (primary infection, endogenous recurrence, or exogenous reinfection) in the various human hosts, although genetic factors may be important. While numerous animal models of HSV infection are available for the evaluation of HSV vaccines, models of HSV-induced cervical cancer require further exploration.

Age Factors↗
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↗