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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↗
PubMed2005

Endobronchial pseudo-tumour caused by herpes simplex.

Herpes simplex virus (HSV) causes tracheobronchitis and pneumonitis; however, to date, there has only been one report of an endobronchial mass caused by HSV type II. This case study describes a 68-yr-old female with severe kyphoscoliosis who was intubated for acute on chronic hypercapnic respiratory failure and developed blood-tinged endotracheal secretions. Fibreoptic bronchoscopy demonstrated an endobronchial mass in the right middle lobe. Cultures grew HSV type I and biopsy specimens demonstrated cytopathological changes consistent with HSV infection. This is the first reported case of HSV type I presenting as an endobronchial tumour.

Acyclovir↗
PubMed2000

Antiviral therapy of herpes simplex.

Herpes simplex virus (HSV) infections in immunocompromised patients are more severe and invasive than in non-immunocompromised patients. They are characterised by prolonged viral shedding and a tendency to heal more slowly. In addition, resistant viruses are exclusively isolated in immunocompromised patients, requiring other drugs with distinct mechanisms of action. The reference compound for the treatment of HSV infections is acyclovir (ACV) that selectively inhibits HSV DNA replication with low host-cell toxicity. Recently, two molecules, valaciclovir (VACV), the L-valyl ester of ACV and famciclovir (FCV), the diacetyl ester of 6-deoxy-penciclovir (PCV), another potent nucleoside analogue, were developed showing an increased oral bioavailability compared to the original compounds. Foscavir (PFA) and more recently cidofovir (CDV) are drugs that do not need the viral thymidine kinase (TK) to be activated and therefore are the appropriate candidates for the treatment of resistant viruses emerging under acyclovir or penciclovir.

Antiviral Agents↗
PubMed1998

In vivo production of cytokines and beta (C-C) chemokines in human recurrent herpes simplex lesions--do herpes simplex virus-infected keratinocytes contribute to their production?

Recurrent human herpes simplex lesions are infiltrated by macrophages and CD4 and CD8 lymphocytes, which secrete cytokines and chemokines. Vesicle fluid was examined by ELISA for the presence of cytokines and beta (C-C) chemokines. On the first day of the lesion, high concentrations of interleukin (IL)-1beta, and IL-6, moderate concentrations of IL-1alpha and IL-10, and low concentrations of IL-12 and beta chemokines were found; levels of macrophage inflammatory protein (MIP)-1beta were significantly higher than levels of MIP-1alpha and RANTES. At day 3, the concentrations of IL-1beta, IL-6, and MIP-1beta were lower, whereas the levels of IL-10, IL-12, and MIP-1alpha remained similar, and the level of tumor necrosis factor-alpha was now detectable. Herpes simplex virus infection of keratinocytes in vitro stimulated production of beta chemokines followed by IL-12 and then IL-10, IL-1alpha, IL-1beta, and IL-6, indicating a potential role for these events in early recruitment, activation, and interferon-gamma production of CD4 cells in herpetic lesions.

Adolescent↗
PubMed1983

Interim summary of mortality in herpes simplex encephalitis and neonatal herpes simplex virus infections: vidarabine versus acyclovir.

Herpes simplex encephalitis and neonatal herpes simplex virus infections are important consequences of herpes simplex virus infections of humans. The association of both diseases with significant mortality and morbidity has prompted intensive therapeutic trials designed to improve outcome. The NIAID Collaborative Antiviral Study Group has been able to demonstrate that vidarabine therapy decreases the mortality and improves morbidity for both herpes simplex encephalitis and neonatal herpes simplex virus infections. Nevertheless, mortality for both diseases is about 40% and many survivors are left with significant neurological impairment. With the hope of improving outcome, we initiated comparative trials of vidarabine and acyclovir for these two diseases. This report summarizes the status of these trials, which are still underway, with particular reference to the complexities of studies such as these. Because adequate numbers of patients for definitive statistical analyses have not been entered into the trial, data were assessed according to outcome for the entire group, irrespective of drug administered. The mortality of herpes simplex encephalitis and neonatal herpes simplex virus infections has been reduced to 34 and 30%, respectively, a decrease of approximately 10% for each disease. Further analyses await completion of the trials.

Acyclovir↗
PubMed2001

Famiciclovir therapy (famvir) for herpes simplex and herpes zoster infections.

Genital herpes simplex and herpes zoster infections are common afflictions that are associated with significant morbidity and a decreased quality of life. Famciclovir (Famvir, Novartis) is an orally administered prodrug of the antiviral agent penciclovir. Its unique pharmacokinetic profile makes it an efficacious, convenient and well-tolerated alternative to the traditionally prescribed acyclovir. Famciclovir is used for the acute treatment and suppressive therapy of recurrent genital herpes as well as for herpes zoster and its debilitating comorbidities. Famiciclovir allows patients to manage or prevent symptoms, thereby significantly improving their quality of life. Its favorable safety profile makes it a good treatment choice for the elderly as well as for immunocompromised patients, including those infected with HIV.

2-Aminopurine↗
PubMed1973

Herpes simplex and herpes genitalis viruses in etiology of some human cancers.

The results of complement fixation tests on 202 sera from people without cancer and from patients with cancer in 29 different areas of the body indicated that only those with nine varieties of advanced cancer (lip, mouth, oropharynx, nasopharynx, kidney, urinary bladder, prostate, cervix uteri, and vulva-all of 56 tested) gave positive specific reactions with nonvirion antigens induced by the DNA herpes simplex (HSV 1) and herpes genitalis (HSV 2) viruses. None of 57 people without cancer (including 10 with current and 18 with recurrent HSV 1 or HSV 2 infections), none of 81 patients with 20 other varieties of advanced cancer (gum, tongue, tonsil, salivary gland, accessory sinus, epiglottis, lung-bronchus, stomach, colon, breast, corpus uteri, ovary, testis, liver, thyroid, Wilms' embryonal kidney, melanoma, Hodgkin's disease, acute lymphocytic leukemia, and acute myelocytic leukemia), and none of four women with early malignant changes in the cervix uteri gave positive results. The seven patients with advanced cancer of the lip or oropharynx gave positive reactions with HSV 1 but not with HSV 2 nonvirion antigens (compatible with involvement of only HSV 1), all of the 13 women with advanced cancer of the cervix uteri and the one woman with advanced cancer of the vulva gave positive reactions with both HSV 1 and HSV 2 nonvirion antigens (compatible with involvement of only HSV 2), while among the 35 other positive patients only two (one with cancer of the kidney and one with cancer of the bladder) reacted with HSV 1 and not at all with HSV 2 nonvirion antigens. Positive sera failed to react with cells harvested at different times after high-multiplicity infection with the DNA vaccinia virus. Massive absorption of positive sera with trypsinized, uninfected human embryonic kidney cells failed to remove, or lower the titer of, the HSV 1 and HSV 2 nonvirion antibodies. All of these data taken together are interpreted as indicating that HSV 1 and HSV 2 play an etiologic role in certain human cancers, because they provide the kind of evidence by which virus-free experimental cancers can be proved to have been originally induced by such DNA viruses as polyoma, Simian Virus 40, or certain types of adenovirus.

Antibodies, Viral↗
PubMed1984

Herpes simplex and herpes zoster. Nervous system involvement.

Mainly discussed are neurologic complications of two neurotropic herpesviruses: herpes simplex viruses types 1 and 2 and varicella-zoster virus. Briefly discussed are cytomegalovirus and Epstein-Barr virus. Treatment of immunosuppressed and nonimmunosuppressed patients is reviewed.

Antiviral Agents↗
PubMed2001

Herpes simplex mimicking herpes zoster in a child immunized with varicella vaccine.

A 5-year-old boy had zosteriform vesicular lesions 4 years after immunization with varicella vaccine. PCR analyses of DNA extracted from the crusts revealed herpes simplex virus type 1 infection. Virologic examinations should be performed before the vesicular lesion is attributed to the varicella-zoster virus vaccine strain.

Chickenpox Vaccine↗
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↗
PubMed2006

The incidence of recurrent herpes simplex and herpes zoster infection during treatment with arsenic trioxide.

We report the incidence of varicella zoster virus (VZV) and herpes simplex virus (HSV) infection in patients with multiple myeloma and colon cancer who were treated with arsenic trioxide for their disease. In this report, we discuss the effects of arsenic on immune system, and suggest arsenic compounds as a possible predisposing factor for viral reactivation in these patients.

Aged↗
PubMed2001

Nested multiplex polymerase chain reaction for the diagnosis of cutaneous herpes simplex and herpes zoster infections and a comparison with electronmicroscopy.

Herpes simplex virus (HSV) and varicella zoster virus (VZV) are common causes of cutaneous and mucocutaneous vesicular eruptions. Laboratory diagnostic techniques include Tzanck smears, electronmicroscopy, antigen detection and viral culture. This paper describes a nested multiplex polymerase chain reaction with respective sensitivities of 0.0001, 0.01 and 0.1 TCID50 for VZV, HSV-1 and HSV-2. The assay was used in (a) a salvage capacity for slides already processed for electronmicroscopy, and (b) as a front-line assay for prospectively processed specimens. Sixty-two glass slides with vesicle lymph/scrapings from 58 patients with suspected cutaneous herpetic lesions were examined. The clinical presentations were described as atypical/not specified (24), VZV (20) or HSV (18), and involved eruptions from diverse anatomical sites, including the genitalia. Of the 62 specimens, 6 and 38 were positive by electronmicroscopy and multiplex PCR respectively, giving a comparative sensitivity of 16% for electronmicroscopy. Nested multiplex PCR identified 15 VZV and 20 HSV-1 infections. Where the clinical details indicated either HSV or VZV (38/62), nested multiplex PCR was statistically likely to be reactive (26/38 vs. 9/24) (chi2 P = 0.000004) whereas electronmicroscopy was not (4/38 vs. 2/24) (chi2 P= 0.77). Where the clinical details indicated VZV (20/62) or HSV (18/62), nested multiplex PCR was statistically more likely to confirm VZV (10/20 vs. 5/42) (chi2 P= 0.001) or HSV (9/18 vs. 11/44) (chi2 P = 0.05) respectively. Two suspected HSV and 6 suspected VZV infections were shown to be VZV and HSV respectively by nested multiplex PCR.

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↗