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At least 397 records · Page 22Linked to original sources
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↗
PubMed1975

Herpes zoster and recurrent herpes simplex.

87 patients with the clinical diagnosis of herpes zoster were seen during a one-year period in 8 general practices in Glasgow, the rate per 1 000 practice population being approximately 2.4. Of these, 78 (90%) had serological evidence of active infection with herpes zoster. A history of recurrent herpes simplex was obtained in 25 (32%) of the 78 patients with confirmed herpes zoster; 63 (81%) of these 78 had complement-fixing (CF) antibodies to herpes simplex. Thus, latent herpes simplex infection did not prevent herpes zoster nor modify the severity of herpes zoster. In most of the patients CF antibodt to varicella-zoster was not detected within 5 days from appearance of the rash. After the acute phase of the illness CF antibody titres fell fairly rapidly, the geometric mean titre being 189 at 2-4 weeks after the rash, 27 from 3-6 months, and 8 from 12-18 months. The rapid rise and decline in CF antibody after herpes zoster infection compared with the unchanging CF titres associated with recurrent herpes simplex infection suggest that varicella-zoster and herpes simplex virus differ in their mechanism of latency.

Adult↗
PubMed1985

Ultrastructural study of early stage of calcification in herpes simplex encephalitis.

A case of herpes simplex encephalitis was investigated at the ultrastructural level. Herpes simplex virions were observed, both in nuclei and perikarya of degenerated cells in the cerebrum. Needle-shaped mineralized precipitates were also present in the disintegrated cells. These mineralized depositions were confined to mitochondria. This finding suggests that mitochondria serve as initial nidus of calcification in herpes simplex encephalitis.

Adult↗
PubMed1993

Induction of bilateral retinal necrosis in mice by unilateral intracameral inoculation of a glycoprotein-C deficient clinical isolate of herpes simplex virus type 1.

Herpes simplex virus can cause acute retinal necrosis, a blinding retinal disease in man. A unilateral intracameral inoculation of herpes simplex virus type 1 (HSV-1) in mice induces retinal necrosis primarily in the contralateral eye and provides an experimental model for the disease. Previous studies suggested that a major envelope glycoprotein of HSV-1, glycoprotein C (gC), is required for retinal necrosis. We studied HSV-1 strain TN-1, a gC-deficient clinical isolated from a lesion of herpetic keratitis, for its pathogenicity in mice with an intracameral inoculation of the virus and found that TN-1 could induce severe necrotizing retinitis in both inoculated and uninoculated eyes of BALB/c mice. Inoculation with a lower dose of TN-1 resulted in a unilateral necrotizing retinitis in the uninoculated eyes. Tissue virus titration of infected mice killed at various times after inoculation detected an infectious virus in various organs including the eyeballs, trigeminal ganglia, brain and adrenal glands. Anterior chamber-associated immune deviation (ACAID) was observed in TN-1-inoculated mice as well as in mice inoculated with gC-positive laboratory strain KOS 7 days postinoculation. Our findings suggested that gC of HSV-1 is not necessary for either the induction of retinal necrosis, neural spread of the virus, or ACAID.

Adrenal Glands↗
PubMed1997

[Central nervous system infection due to Herpes simplex virus in AIDS].

Infections of the central nervous system by Herpes simplex viruses (Herpes simplex type 1 and Herpes simplex type 2) are uncommon in acquired immune deficiency syndrome and are often clinically and pathologically atypical. We have collected 11 cases of herpes simplex encephalomyelitis in AIDS patients reported in the literature. Only 3 of these cases presented with a typical, necrotizing, limbic encephalitis. Other clinicopathological patterns included ventriculitis, rhombencephalitis and myelitis. Ventriculitis and rhombencephalitis were usually due to infection by HSV-1, whereas myelitis was mostly due to HSV-2 infection. Distinction between the 2 types of virus is often difficult by immunohistochemistry due to frequent cross reactivity and usually requires tissue culture, in situ hybridization, or polymerase chain reaction. Association of HSV encephalomyelitis with productive infection of the central nervous system by the human immunodeficiency virus was only found in one case. In contrast, co-infection with cytomegalovirus was found in 9 of the 11 cases. One case also had had varicella zoster virus vasculitis, and another case also had a cerebral malignant non Hodgkin's lymphoma in which Epstein Barr virus genome was identified. This supports the view that concomitant herpes-virus infections of the central nervous system is a characteristic feature of AIDS.

AIDS-Related Opportunistic Infections↗
PubMed1985

Restriction endonuclease digestion analysis of DNA from viruses isolated from different sites of two fatal cases of herpes simplex virus type-1 infection.

Herpes simplex virus (HSV) type-1 was isolated from a fatal case of herpes simplex encephalitis (case 1) and from a fatal case of disseminated herpes simplex (case 2). The virus was isolated from the lip lesion, the frontal lobe and the temporal lobe of the brain in case 1 and from a mesenteric node, myocardium and salivary gland in case 2. Restriction endonuclease digestion analysis showed that each case was infected with different substrains of HSV. The changes in band pattern in isolates from case 1 occurred in the "variable" region of the genome, showing that viruses with such variations can be isolated simultaneously from different tissues. The changes in band patterns in isolates from case 2 indicated the presence of two virus substrains, one in the mesenteric node and salivary gland and a second in the myocardium.

Brain↗
PubMed2003

The role of dendritic cells in immune responses against vaginal infection by herpes simplex virus type 2.

Herpes simplex virus type 2 is a leading cause of genital ulcers that affects more women than men worldwide. Recent evidence indicates that protective immunity can be generated by specialized dendritic cells in the female genital mucosa. This article aims to provide an overview of the effector immunity required for protection from genital herpes, and to discuss the mechanism by which specific subsets of dendritic cells mediate induction of adaptive immunity following genital infection with herpes simplex virus type 2 in vivo.

Animals↗
PubMed1997

The efficacy and safety of Skinner herpes simplex vaccine towards modulation of herpes genitalis; report of a prospective double-blind placebo-controlled trial.

A randomised, placebo-controlled, multi-centre trial of intracellular subunit herpes simplex virus (HSV) type 1 vaccine NFU.Ac.HSV-1(S-)MRC (Skinner vaccine) was conducted at three medical centres in the United States. Subjects with documented herpes genitalis of at least 1-year duration and a history of six or more genital HSV recurrences in the 12 months prior to study entry were randomised to receive vaccine or placebo at 0, 1 and 2 months. Vaccination induced significant neutralising, enzyme-linked immunosorbent assay and lymphocyte transformation response to HSV-1 antigen. The frequency of recurrences was reduced in the vaccinated female patients at both 3 and 6 months following vaccination with an overall reduction in patients of both sexes which did not reach statistical significance. Recurrence severity was reduced as measured by decreased number of lesions and associated symptoms per recurrence (P = 0.04). The data suggest that clinical manifestations of latent HSV genital infection may be modified by therapeutic immunisation.

Adult↗
PubMed1991

Herpes simplex virus infections of the central nervous system. Encephalitis and neonatal herpes.

Herpes simplex virus (HSV) infections are among the most commonly encountered in humans. Fortunately, the resulting diseases are more usually nuisances, such as recurrent fever blisters, rather than life threatening or morbidity inducing. Nevertheless, HSV can result in disease of the central nervous system (CNS) with attendant neurological complications. Examples of the latter include herpes simplex encephalitis (HSE) or neonatal HSV infection. The past decade has witnessed significant advances in our understanding of the pathogenesis of these 2 forms of disease and, even more importantly, their amenability to treatment. This review summarises our current understanding of the natural history, pathogenesis, presentation, and treatment of HSV infections of the CNS. Because of the life-threatening nature of herpes simplex infections of the CNS, particular attention is paid to clinical presentation and differential diagnosis of confounding entities which mimic herpes simplex encephalitis. The controversy of brain biopsy versus alternative noninvasive diagnostic procedures is discussed. Clinical presentation and, importantly, the lack of uniform clinical presentation, as well as the value of intervention with appropriate antiviral drugs such as aciclovir and vidarabine (adenine arabinoside, ara-A), are stressed. The clinical outcome of herpes simplex virus infections of the CNS with therapy is particularly relevant. In spite of early intervention with selective and specific inhibitors of viral replication, return to normal function is not always achieved. At the conclusion of this review, the reader should be aware of the potential value of therapy as well as the problems encountered with diagnosis and management of patients with herpes simplex virus infections of the CNS.

Encephalitis↗
PubMed1981

Genital herpes simplex--concepts and treatment.

Genital herpes simplex is an increasingly common venereal disease caused by either herpes simplex virus type 1 or 2. The disease can be manifested in a primary and/or recurrent form, the clinical features and complications of which are reviewed. Potential problems include psychosocial difficulties, neonatal herpes simplex infections, and the possibility of an oncogenic role in cervical cancer. Diagnostic modalities, prophylactic measures, and management technics are discussed.

Animals↗
PubMed2001

Herpes simplex encephalitis--an atypical case.

Herpes simplex virus (HSV) is a common cause of viral encephalitis. Herpes simplex encephalitis (HSE) typically presents with acute neurologic changes and the initial cerebrospinal fluid examination is nearly always abnormal. We report a case of a patient with HSE and normal initial CSF analysis. This resulted in delayed diagnosis and therapy with subsequent severe neurolgical sequelae. Herpes simplex infection should be included in the differential diagnosis of encephalopathic patients and a normal CSF examination.

Anti-Bacterial Agents↗
PubMed2006

ACIDFORM inactivates herpes simplex virus and prevents genital herpes in a mouse model: optimal candidate for microbicide combinations.

The acidic vaginal milieu is presumed to inactivate pathogens but is neutralized by semen. This notion fostered the development of acid-buffering products, such as ACIDFORM (developed by Program for Topical Prevention of Conception and Disease, Rush University, and licensed by Instead), as microbicides. However, the extent and mechanism of protective activity provided by buffering gels is not known. Exposure of herpes simplex virus (HSV) to pH 4.5 or lower irreversibly inactivated HSV and reduced HSV yields by at least 90%; exposure to pH 5.0 had little or no effect. Pretreatment of HSV-2 with pH 3.5-4.5 triggered proteolysis, disrupting the HSV particle and resulting in a reduction in binding and invasion. ACIDFORM protected 21 (81%) of 26 mice from genital herpes, compared with 3 (12%) of 25 mice who received a placebo gel. ACIDFORM retained significant activity if mice were challenged with HSV delivered in seminal fluid. These findings suggest that ACIDFORM offers considerable protection against HSV and may be an optimal candidate for developing combination microbicides.

Animals↗
PubMed1980

The effect of delta-9-tetrahydrocannabinol on herpes simplex virus replication.

Both herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) failed, in an identical fashion to replicate and produce extensive c.p.e. in human cell monolayer cultures which were exposed (8 h before infection, at infection, or 8 h p.i.) to various concentrations of delta-9-tetrahydrocannabinol. Similar results were obtained with a plaque assay utilizing confluent monkey cells. Possible mechanisms for this antiviral activity are discussed.

Animals↗
PubMed1995

Spatial recognition memory deficits without notable CNS pathology in rats following herpes simplex encephalitis.

Survivors of herpes simplex encephalitis (HSE) experience intellectual impairment and an inability to store and recall information. Because the temporal lobes and associated limbic structures are central to storage and retrieval of memories, and are predominantly affected in adult HSE, injury to these areas is postulated to cause behavioral and learning disabilities. A previous study (Beers et al., 1993) demonstrated that intranasal inoculation of Lewis rats with herpes simplex virus type-1 (HSV-1) induced acute partial complex seizures, and hemorrhagic and inflammatory lesions of the hippocampus and entorhinal cortex. Consequently, it was of interest to determine whether rats that had recovered from HSE had limbic system-associated memory impairments. Therefore, rats were evaluated when signs and symptoms of encephalitis were no longer apparent using an eight arm radial maze to assess the acquisition and retention of learned information. An allocentric-spatial location paradigm revealed HSV-1 infected rats performed at chance levels on both acquisition and retention which were statistically different from sham-inoculated controls. However, using an egocentric-spatial left/right discrimination task, infected rats performed statistically similar to sham-inoculated controls. Furthermore, HSV-1 nucleic acids were detected in the nuclei of neurons within the hippocampus and entorhinal cortex using in situ hybridization techniques. Of interest was the observation that rats with learning and memory deficits had no apparent histopathological or immunocytochemical evidence of antecedent CNS infection. This is the first experimental demonstration that HSV-1 can cause behavioral impairments in the absence of obvious inflammatory injury to the temporal lobe memory system.

Animals↗
PubMed2000

Virological diagnosis of herpes simplex encephalitis.

BACKGROUND: The herpes simplex encephalitis (HSE) represents one of the most severe infectious diseases of the central nervous system. As effective antiviral drugs are available, rapid and reliable diagnosis has become important. OBJECTIVES: To evaluate retrospectively the usefulness of polymerase chain reaction (PCR) as well as serological procedures for the diagnosis of HSE. STUDY DESIGN: 631 cerebrospinal fluids (CSF) from patients with clinical suspicion of encephalitis were tested for type-specific herpes simplex virus (HSV) DNA using PCR. Virus-specific antibodies including their intrathecal synthesis were measured in 624 CSF and 2409 serum samples of 2711 patients suspected of having encephalitis. RESULTS: Positive results were obtained by PCR in eight patients (1. 3%) for HSV-1 and in seven (1.1%) for HSV-2. Intrathecal antibody synthesis was estimated in 24 (3.8%) patients. In general, no intrathecal antibodies could be measured in patients with positive PCR results and vice versa the intrathecal immune response became positive when CSF was cleared from the HSV. Results of the antibody detection in serum specimens revealed an active HSV infection in 268 out of 2367 patients (11.3%). CONCLUSIONS: The detection of HSV-DNA by PCR is the method of choice for diagnosis of HSE in the early phase of the disease. During the later stage, it has to be diagnosed by the estimation of intrathecally synthesized antibodies.

Adolescent↗
PubMed1980

Cutaneous herpes simplex infections and their treatment.

Herpes simplex virus causes many important systemic as well as cutaneous diseases. The most common cutaneous diseases are herpes gingivostomatitis, labialis, and genitalis. Many new treatments for these diseases are proclaimed each year. There are so many treatments that one would believe that either everything works or nothing works. As there is no Federal Drug Administration approved treatment for cutaneous herpes simplex, the latter statement is probably more correct. Regardless of this dilemma, the physician must continue to diagnose and treat many cutaneous herpetic infections. In this paper the basic concepts of the herpes simplex virus will be briefly presented. Additionally, the most common cutaneous herpes infections will be reviewed with emphasis on critical analysis of their proposed methods of treatment.

Adult↗
PubMed1993

Neonatal herpes simplex virus infections.

Neonatal herpes simplex virus infections are a common problem in the United States, occurring at an incidence of one in approximately 3,500 deliveries. In the absence of antiviral therapy significant morbidity and mortality is attendant with disease. Disease manifestations in the newborn include multiorgan involvement (disseminated disease), encephalitis, and/or infection limited to the skin, eye, or mouth. These three broad classifications provide distinctions in severity of disease for evaluation of outcome following antiviral therapy. The availability of antiviral therapy for life-threatening disease, particularly that which is disseminated or involves the brain, has been of particular benefit for children with neonatal herpes. Both acyclovir and vidarabine have proven effective in the management of neonatal herpes simplex virus infection. With current therapeutic modalities, mortality from disease localized to the skin, eye, and mouth is virtually non-existent, yet a few children (approximately 5%) are still at risk for a long-term neurologic sequelae. For babies with encephalitis, the mortality has been reduced to approximately 15% and nearly 50% of survivors develop normally 3 years after treatment. Outcome with disseminated infection is of less value as mortality remains high (50%), but the number of survivors who develop normally is approximately 85%. The introduction of new antivirals with enhanced lipophilicity and, potentially, greater activity in the central nervous system may further improve outcome from this devastating disease.

Acyclovir↗