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PubMed1990

Demonstration of herpes simplex virus DNA in CSF cells by in situ hybridization for early diagnosis of herpes encephalitis.

Herpes simplex virus (HSV) was studied by in situ DNA hybridization with a biotinylated cDNA probe in 56 air-dried methanol-fixed cerebrospinal fluid (CSF) cell preparations which had been collected from 12 patients with herpes simplex encephalitis (HSE) during the previous 5 years. In three additional HSE cases, freshly prepared acetone-fixed CSF cell preparations were available. In all cases, CSF cell preparations were obtained by cytocentrifugation. Herpes simplex virus DNA could be demonstrated in 8 of the 12 HSE cases with methanol-fixed cells (66%) and in all 3 cases with fresh acetone-fixed CSF cells. The earliest CSF sample was available at the onset of symptoms and showed positive DNA hybridization. In three cases hybridization was positive after a clinical course of more than 5 weeks but was usually found in the 1st week of illness before the beginning of specific inthrathecal IgG synthesis. In 54 control cases with other acute inflammatory diseases of the CNS, including 14 cases of varicella-zoster meningitis, no positive hybridization was detected. These findings strongly suggest that in situ hybridization in CSF cells is a reliable tool for the early and rapid diagnosis of HSE, especially at the onset of the disease, when no antibodies can be detected.

Adult↗
PubMed1977

Herpes simplex encephalitis: an autopsy case with isolation of type 1 herpes simplex virus.

An adult case of herpes simplex encephalitis was studied after autopsy. Postmortem examination revealed necrotizing encephalitis associated with Cowdry type A intranuclear inclusion bodies in glial cells. Herper simplex virus type 1 was isolated from the removed brain. Herpes simplex virus antigens were detected diffusely in wide areas of the brain by immunofluorescent test and viral particles characteristic to herpes simplex virus were demonstrated by electron microscopy. There was an apparent discrepancy between severity of histological changes and distribution of virus antigen.

Adult↗
PubMed1976

Cell-mediated immunity to herpes simplex virus in man. V. Antibody-mediated cell-dependent immune lysis of herpes virus-infected target cells.

Thirty-four patients, subject to recurrent herpes labialis, have been studied. They have all been shown to have high serum levels of an antibody to HSV1. This antibody has the property of sensitizing HSV1-infected target cells to lysis by nonimmune effector lymphocytes. Of 23 subjects who gave no history of herpes labialis, only four had antibody demonstrable by this technique. The level of antibody remains essentially unchanged despite recrudescenes of herpes labialis in the susceptible subjects. Effector cell activity was present in all of these and other subjects tested except for two who were suffering from chronic lymphatic leukemia. We have positive evidence that the effector cells in this system are neither T cells nor macrophages. Additional evidence suggests that the effector cells may be "null" cells.

Antibody Specificity↗
PubMed1990

Rapid detection of herpes-simplex-virus DNA in cerebrospinal fluid of patients with herpes simplex encephalitis.

Herpes-simplex-virus (HSV) DNA in cerebrospinal fluid was amplified by use of the polymerase chain reaction and identified by hybridisation to a specific oligonucleotide probe. Specimens of cerebrospinal fluid (CSF) from 4 of 4 patients with herpes simplex encephalitis were positive for HSV DNA, whereas CSF specimens from 6 patients with other central-nervous-system infections were negative. This technique may expedite diagnosis of herpes simplex encephalitis.

Adult↗
PubMed1982

Efficacy of (E)-5-(2-bromovinyl)-2'-deoxyuridine against different herpes simplex virus strains in cell culture and against experimental herpes encephalitis in mice.

(E)-5-(2-Bromovinyl-2'-deoxyuridine (BrVUdR) showed strong antiviral activity against different laboratory strains and clinical isolates of herpes simplex virus type 1 (HSV-1) on primary rabbit testes (PRT) cells with a 50% inhibition of plaque formation (ID50) at 0.01-0.02 microM. One laboratory strain (HSV-1-S), however, was completely refractory even at concentrations as high as 100 microM. In contrast, the ID50S for all herpes simplex virus type 2 (HSV-2) strains were about 10(2) - 10(3) times higher (8-25 microM) than for the HSV-1 strains. No toxicity in mice treated with 140 mg BrVUdR/kg/day for 14 days was observed, and successful treatments of herpes encephalitis in mice induced experimentally by intracerebral infection with one laboratory strain (HSV-1-Kupka) and one clinical isolate (HSV-1-64) were achieved. Treatment of encephalitis in mice induced by the strain HSV-1-S insensitive to BrVUdR in cell culture failed to be effective. Similar antibody titers against HSV-1 were found in surviving mice of the control and of the BrVUdR-treated groups.

Animals↗
PubMed1994

Placebo-controlled trial of vaccination with recombinant glycoprotein D of herpes simplex virus type 2 for immunotherapy of genital herpes.

Immunotherapy of chronic viral diseases with vaccines is an important but unproven concept. We investigated the effect of a vaccine containing recombinant glycoprotein D (gD2) of herpes simplex virus type 2 (HSV-2) on the frequency of symptomatic outbreaks in patients with genital herpes. 98 patients with documented genital herpes who reported 4-14 recurrences per year were enrolled in a double-blind, placebo-controlled trial. Subjects received injections of either 100 micrograms gD2 in alum or alum alone (placebo) at 0 and 2 months, and recurrences were documented for 1 year. The vaccine was well tolerated. gD2 recipients reported fewer recurrences per month than placebo recipients (mean 0.42 [SE 0.05] vs 0.55 [0.05]; p = 0.055), had fewer virologically confirmed recurrences per month (0.18 [0.03] vs 0.28 [0.03]; p = 0.019), and had a lower median number of recurrences for the study year (4 [range 0-17] vs 6 [0-15]; p = 0.039). Neither genital recurrence nor the placebo vaccine had any discernible effect on HSV-2-specific antibody responses, but gD2 vaccine boosted neutralising antibodies to HSV-2 fourfold and gD2-specific titres sevenfold over baseline levels. These results inspire optimism about the potential use of vaccine for the treatment of chronic, recurring viral diseases.

Adult↗
PubMed1997

Severe genital herpes infections in HIV-infected individuals with impaired herpes simplex virus-specific CD8+ cytotoxic T lymphocyte responses.

The specific mechanisms underlying the varied susceptibility of HIV-infected (HIV+) individuals to opportunistic infections (OI) are still incompletely understood. One hypothesis is that quantitative differences in specific T cell responses to a colonizing organism determine the development of an AIDS-defining OI. We evaluated this hypothesis for herpes simplex virus (HSV) infection, a common OI in HIV+ patients. Using limiting dilution analyses, the frequency of HSV-specific CD8+ cytotoxic T lymphocyte precursors (pCTL) and proliferative precursors were quantitated in peripheral blood mononuclear cells from 20 patients coinfected with HIV and HSV-2. The frequency of HSV-specific CD8+ pCTL in HSV+HIV+ individuals was significantly lower than in HSV+HIV- individuals (1 in 77,000 vs. 1 in 6,000, P = .0005) and was not different than in HSV-HIV- individuals (1 in 100,000, P = .24). HIV+ patients who suffered more severe genital herpes recurrences had significantly lower HSV-specific CD8+ pCTL frequencies than those patients with mild recurrences (1 in 170,000 vs. 1 in 26,000, P = .03). In contrast, no significant difference was seen in proliferative precursor frequencies between those patients with mild vs. severe genital herpes (1 in 3,800 vs. 1 in 6,600, P > .5). Quantitative differences in pCTL frequency to HSV appear to be the most important host factor influencing the frequency and severity of HSV reactivation in HIV+ patients. Studies to reconstitute such immunity, especially in people with acyclovir-resistant HSV, appear warranted.

CD8-Positive T-Lymphocytes↗
PubMed1984

Efficacy of herpes vaccine in a rabbit model following intraocular inoculation of herpes simplex virus.

It has been shown that injection of herpes simplex virus type 1 into the vitreous body of the eye in 18-day-old albino rabbits consistently induced encephalitis caused by herpes simplex virus, with 95% survival. In untreated rabbits the lesions followed a defined anatomic pathway in the central nervous system, and produced a chronic progressive disease with gross pathological features very similar to those seen in the natural human disease. The efficacy of heat-killed herpes vaccine in this animal model was studied by starting immunization four days before or four days after the live challenge. All animals immunized before the challenge were protected. Immunization after the challenge not only did not confer protection, but surprisingly, appeared to enhance the primary disease. The rabbits immunized after the challenge developed weakness of the hind legs that progressed very rapidly to paralysis, and an appreciable proportion (40%) of them died between days 18 and 23 postvaccination.

Animals↗
PubMed1987

Detection of antigen to herpes simplex virus in cerebrospinal fluid from patients with herpes simplex encephalitis.

Cerebrospinal fluid (CSF) specimens were obtained from patients with presumed herpes simplex encephalitis who underwent brain biopsy for diagnostic confirmation. Coded CSF specimens were fixed on nitrocellulose filter paper and probed with a pool of monoclonal antibodies directed against four herpes simplex virus glycoproteins (gB, gC, gD, and gE). Herpes simplex virus antigen was detected in 35 of 40 specimens obtained from 26 biopsy-positive patients. In contrast, only three of 25 specimens from 17 biopsy-negative patients gave positive results by this assay. An additional 30 CSF specimens from patients with proven bacterial and fungal infections were all negative by this assay. For all specimens tested, the sensitivity and specificity of the assay were both 88%. However, when results were evaluated by patient, the sensitivity was 92% (24 of 26) with a specificity of 82% (14 of 17). Among specimens collected one week or later after disease onset, the sensitivity was 100%, with a specificity of 93%.

Adult↗
PubMed1994

Quantity of latency-associated transcript produced by herpes simplex virus is not predictive of the frequency of experimental recurrent genital herpes.

The role of the latency-associated transcript (LAT) in control of recurrent herpes simplex virus type 2 (HSV-2) infection was investigated by examining whether LAT concentration in vitro during productive infection or in ganglia during latency correlated with frequency of recurrent genital herpes. Clinical HSV-2 isolates from frequent or infrequent recurrent genital disease produced comparable amounts of glycoprotein D and infected cell polypeptide 0 RNA, but the isolate from frequent disease produced about seven times more LAT. The guinea pig model of genital herpes was used to determine whether the quantity of LAT produced during acute infection in vitro correlated with recurrence phenotype; the frequency of recurrent disease was similar for the 2 clinical isolates. Likewise, there was no correlation between the recurrence phenotype of individual animals and LAT concentration in their ganglia. Thus, while absence of LAT may impair HSV reactivation and recurrence, once a threshold concentration is exceeded, LAT has no further effect on recurrence frequency.

Adult↗
PubMed2007

Trends in herpes simplex virus type 1 and 2 infections among patients diagnosed with genital herpes in a Finnish sexually transmitted disease clinic, 1994-2002.

OBJECTIVE: The objective of this study was to analyze the proportion of herpes simplex virus types 1 and 2 (HSV-1 and -2) in genital infections during a 9-year period (1994-2002) in a Finnish sexually transmitted disease (STD) clinic population. STUDY DESIGN: We analyzed prospectively the proportion of HSV-1- or -2-positive culture samples from our STD clinic patients with genital herpes during years 1994-2002 and compared the proportions of HSV-1 and HSV-2 findings with the age and gender of the patients. RESULTS: The proportion of HSV-1 infections increased from 18.7% (39 of 209) in 1994-1996 to 25.9% (52 of 201) in 2000-2002 (P = 0.032). Female patients with genital herpes and laboratory isolation of HSV-1 were 35.9% of the cohort from 1994-1996 and 67.3% of the cohort from 2000-2002. The mean age of male patients with HSV-1 decreased from 29.3 years in 1994-1996 to 24.1 years in 2000-2002 (P = 0.023). CONCLUSIONS: An increase in the proportion of genital infections caused by HSV-1 was found. The increase was mainly the result of the increase in the number of female patients with HSV-1. Male patients acquire genital HSV-1 infection at a younger age than 10 years ago.

Adult↗
PubMed1997

Prevalence of herpes simplex virus type 1- and 2- specific antibodies among the acute, recurrent, and provoked types of female genital herpes.

Sixty-eight sera from the acute, recurrent, and provoked types of female genital herpes were compared for the seroprevalence of herpes simplex virus (HSV) types 1 and 2 by immunodot assay using HSV glycoprotein G. In the HSV-1-isolated patients, no HSV-2 antibodies were detected, whereas in the HSV-2-isolated patients, HSV-1 seroprevalence was 9% for the acute type, 89% for the provoked type (P < 0.005), and 55% for the recurrent type (P < 0.05). The natural history of female genital herpes and the possible protective role of pre-existing antibodies in preventing the acquisition or clinical manifestation of a subsequent HSV infection are discussed.

Acute Disease↗
PubMed1985

Vaccinia virus recombinant expressing herpes simplex virus type 1 glycoprotein D prevents latent herpes in mice.

In humans, herpes simplex virus causes a primary infection and then often a latent ganglionic infection that persists for life. Because these latent infections can recur periodically, vaccines are needed that can protect against both primary and latent herpes simplex infections. Infectious vaccinia virus recombinants that contain the herpes simplex virus type 1 (HSV-1) glycoprotein D gene under control of defined early or late vaccinia virus promoters were constructed. Tissue culture cells infected with these recombinant viruses synthesized a glycosylated protein that had the same mass (60,000 daltons) as the glycoprotein D produced by HSV-1. Immunization of mice with one of these recombinant viruses by intradermal, subcutaneous, or intraperitoneal routes resulted in the production of antibodies that neutralized HSV-1 and protected the mice against subsequent lethal challenge with HSV-1 or HSV-2. Immunization with the recombinant virus also protected the majority of the mice against the development of a latent HSV-1 infection of the trigeminal ganglia. This is the first demonstration that a genetically engineered vaccine can prevent the development of latency.

Animals↗
PubMed1998

Sorivudine versus acyclovir for treatment of dermatomal herpes zoster in human immunodeficiency virus-infected patients: results from a randomized, controlled clinical trial. Collaborative Antiviral Study Group/AIDS Clinical Trials Group, Herpes Zoster Study Group.

The present randomized, double-blind, placebo-controlled, multicenter clinical trial was designed to compare the efficacy and tolerability of sorivudine [1-beta-D-arabinofuranosyl-E-(2-bromovinyl)uracil] and acyclovir for the treatment of dermatomal herpes zoster in human immunodeficiency virus (HIV)-seropositive patients. A total of 170 HIV-seropositive adults presenting with herpes zoster (confirmed by direct fluorescent-antigen testing and/or viral culture) were enrolled and randomized to receive a 10-day course of orally administered sorivudine (40 mg once daily plus acyclovir placebos) or acyclovir (800 mg five times daily plus sorivudine placebo). Patients were monitored daily to document the events of cutaneous healing, pain, zoster-related complications, and drug-related adverse events. Patients were reassessed on days 21 and 28 and then once monthly for 1 year. The primary efficacy endpoint was time to the cessation of new vesicle formation. Secondary efficacy endpoints included times to other events of cutaneous healing, resolution of pain, and frequency of dissemination and zoster recurrence. In a multivariate analysis, sorivudine was superior to acyclovir for reducing the times to the cessation of new vesicle formation (relative risk [RR] = 1.54, 95% confidence interval [CI] = 1.00 to 2.36; P = 0.049) and total lesion crusting (RR = 1.48, 95% CI = 1.07 to 2.04; P = 0.017). In a univariate analysis, there was a trend favoring sorivudine for the cessation of new vesicle formation (median of 3 versus 4 days; P = 0.07) and a significant advantage for time to total lesion crusting (median of 7 versus 8 days; P = 0.02). The time to the resolution of zoster-associated pain, the frequency of dissemination, and the frequency of zoster recurrence were not different between the two treatment groups. Both drugs were well tolerated. Sorivudine is an effective drug for the treatment of herpes zoster in HIV-infected patients and results in accelerated cutaneous healing when compared with acyclovir therapy.

AIDS-Related Opportunistic Infections↗
PubMed2002

Penciclovir susceptibilities of herpes simplex virus isolates from patients using penciclovir cream for treatment of recurrent herpes labialis.

The antiherpesvirus agent penciclovir (PCV) shares an identical activation pathway and a similar mode of action with acyclovir (ACV). However, since PCV represents a relatively recent treatment option, the clinical resistance profile to PCV is less well known. A susceptibility program was established to assess the resistance profile for serial herpes simplex virus isolates from immunocompetent patients with recurrent herpes labialis obtained throughout a 4-day period of treatment with topical PCV (1% cream) or a placebo. Two isolates (2 of 1,035 [0.19%]), representing 0.34% of the patients (2 of 585), were confirmed to be PCV-resistant (Pcv(r)) herpes simplex virus type 1 by a plaque reduction assay in MRC-5 cells. These two viruses were highly resistant to PCV (50% inhibitory concentrations [IC(50)s], >55 micro g/ml) and were isolated less than 17 h after the start of patient-initiated treatment. However, subsequent isolates on days 2 and 3 from these patients were completely susceptible to PCV (IC(50)s, <2.0 micro g/ml). Thus, it is not clear whether the resistance to PCV for these two early-treatment isolates was directly associated with the 17 h of PCV treatment; several possible explanations are discussed. In an analysis of the distribution of IC(50) differences between the first and last isolates, there were three patients with minor IC(50) increases in the PCV-treated population and one in the placebo-treated group, although statistically, only the latter was an outlier. No patients were found to have Pcv(r) virus at the end of acute treatment, regardless of treatment group. Overall, the prevalence of Pcv(r) was found to be similar to the 0.3% Acv(r) reported for immunocompetent, untreated populations.

Acyclovir↗
PubMed2006

Increase in rates of herpes simplex virus type 1 as a cause of anogenital herpes in western Sydney, Australia, between 1979 and 2003.

BACKGROUND/OBJECTIVE: Recent studies suggest that herpes simplex virus type 1 (HSV-1) is becoming more common as a cause for genital herpes, relative to HSV-2. We aimed to calculate trends in HSV type from isolates and serology samples sent to a reference virology laboratory in New South Wales (NSW), Australia. METHODS: We compared the proportions of HSV-1 and HSV-2 positive samples, adjusting for age and sex of source patient, in three datasets: anogenital isolates from 1979 to 1988; anogenital isolates from 1989 to 2003; and HSV type specific IgM seropositivity from 1994 to 2003. RESULTS: The number of specimens in each analysis was 17 512, 4359, and 497, respectively. There was a progressive rise in the proportions of typed specimens being HSV-1 in all analyses. The proportion of isolates that were HSV-1 ranged from 3% in 1980 to 41% in 2001. Female sex and age under 25 were associated with a greater proportion of HSV-1 isolates in both time periods. In the period 1979-88, comparing the proportions of HSV-1 and HSV-2 gave an odds ratio (OR) per additional year of 1.24 (95% confidence interval (CI) 1.20 to 1.27; p<0.005) after adjustment for age and sex. In the period 1989-2003 there was a steeper rise in the proportion of isolates that were HSV-1 in samples from younger individuals (OR per year 1.17, 1.12 to 1.22) compared to those over 25 (OR per year 1.06, 1.03 to 1.08). The rise in the proportion of IgM seropositive results reactive for HSV-1 compared to HSV-2 gave an OR of 1.36 per year (1.26 to 1.47; p<0.005). CONCLUSIONS: These data suggest that HSV-1 has become more common as a cause of anogenital herpes in NSW.

Age Factors↗
PubMed1982

Confirmation of herpes simplex virus type 2 infections in herpes-like genital lesions by a simple complement-fixation test.

The presence of complement-fixing antibody to an early herpes simplex virus type 2 (HSV-2) antigen (the AG-4 antigen) was correlated with HSV-2 infection in the sera of patients with genital herpes. Eighty-eight per cent of sera taken two weeks after clinical diagnosis of a primary or recurrent herpes infection in patients, confirmed to have HSV-2 by virus isolation and typing, contained the anti-AG-4 complement-fixing antibody. None of the patients with genital HSV-1 had the antibody, and only 9% of controls or patients with facial HSV-1 infection had positive results for the antibody. This correlation was used to identify genital HSV-2 infections when either no virus sample had been taken or when virus isolations had been unsuccessful. Thus, a simple complement-fixation test can confirm an HSV-2 virus infection without isolation of the virus from the herpetic lesion.

Adolescent↗
PubMed1999

British Co-operative Clinical Group national survey on diagnostic issues surrounding genital herpes. MSSVD Special Interest Group on Genital Herpes and the British Co-operative Clinical Group.

OBJECTIVES: To investigate the current use of diagnostic methods for genital herpes simplex virus (HSV) infection, to determine how information from these tests influences clinical practice, and to identify areas for future guideline development within genitourinary medicine (GUM) clinics in the United Kingdom. METHODS: National survey of 173 consultants in UK GUM clinics. RESULTS: Completed questionnaires were returned by 146 (84%) consultants. Cell culture was the first line diagnostic method for 133 (91%) respondents, the remaining 13 (9%) used antigen detection tests. Typing of isolates (HSV-1 or HSV-2) was available in their local laboratory to 109 (75%) clinicians; however, less than two thirds routinely pass this information on to their patients. Although 74 (51%) respondents had access to serological diagnosis, the majority of methods described were non-specific; only three (2%) had access to type specific tests. Only 81 (56%) respondents frequently (> 90% of the time) recommend notification of recent sexual partners of genital herpes patients. CONCLUSIONS: While access to culture based diagnosis is widespread, type specific serology has limited availability. Information on typing of isolates as HSV-1 or 2, although available in three quarters of centres, is underutilized in counselling patients. As HSV type influences both clinical and subclinical reactivation rates and may also affect probability of transmission, this is an important omission. Future guidelines need to address the optimal use of viral typing and new diagnostic tests to optimise health gain; there is also a need for evidence based recommendations about partner notification in genital herpes.

Contact Tracing↗