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PubMed2002

Serological evidence of herpesvirus infection in gibbons.

BACKGROUND: Herpesviruses are not only infectious agents of worldwide distribution in humans, but have also been demonstrated in various non-human primates as well. Seventy-eight gibbons were subjected to serological tests by ELISA for herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), Epstein-Barr virus (EBV) and cytomegalovirus (CMV). RESULTS: The prevalence of IgG antibodies against HSV-1, HSV-2, EBV and CMV was 28.2%, 28.2%, 14.1% and 17.9%, respectively. CONCLUSIONS: Antigenic cross-reactivity is expected to exist between the human herpesviruses and gibbon herpesviruses. Gibbons have antibodies to human herpesviruses that may reflect zoonotic infection with human herpesviruses or infection with indigenous gibbon herpesviruses. Therefore, it is difficult to draw concrete conclusions from serological studies alone. Identification should be based on further isolation and molecular characterization of viruses from seropositive animals.

Animals↗
PubMed2005

Ultrastructural features of herpesvirus-infected cells in epidermal lesions in larvae of the Japanese flounder Paralichthys olivaceus.

An electron microscopic study (EM) was performed on herpesvirus-infected cells in epidermal lesions of larvae of the Japanese flounder Paralichthys olivaceus to document the ultrastructure of the lesions. Epithelial cells were the primary cell type infected with the herpesvirus, and showed nuclei containing nucleocapsids, vesicles containing enveloped virions in the cytoplasm, and the release of enveloped virions through the cell membrane. Herpesvirus-infected cells were highly vacuolated and necrotic showing fragmented nuclei while these cells retained firm desmosomes to prevent separation from neighboring necrotic cells, which caused cellular aggregation in the upper layer of the epidermis. Based on EM results, the definitive pathological change was necrosis of epithelial cells infected with the flounder herpesvirus; therefore, the name Viral Epidermal Necrosis (VEdN) is appropriate for this herpesvirus infection.

Animals↗
PubMed1980

Visceral herpesvirus infections in leukemic patients receiving cytarabine.

Autopsy evidence of herpesvirus infection was found in visceral organs of four leukemic patients who had received large doses of cytarabine (cytosine arabinoside; Ara-C) shortly before their death. In three of these patients the infection was clinically unsuspected; in the fourth, cutaneous herpes zoster developed after administration of 300 mg of cytarabine daily for the preceding five days. Although cytarabine exhibits pronounced in vitro virucidal activity against herpes viruses and has been successfully used in clinical treatment of severe herpesvirus infections, the present findings and a review of the recent literature cast doubt on the antiviral effectiveness of this drug, particularly in already immunosuppressed patients, and suggest instead that such patients actually have an increased risk for development of disseminated herpesvirus infection owing to further depression of host defenses by the drug.

Adult↗
PubMed2002

Subclinical herpesvirus infection in farmed turbot Scophthalmus maximus.

Subclinical infections with a herpesvirus were detected by light and electron microscopic examination of juvenile turbot collected during a national surveillance programme. Virions detected in the epidermis of skin and in the epithelium of gills had a morphology consistent with those of Herpesvirus scophthalmi described from turbot in the United Kingdom and Denmark. This is the first report of herpesvirus infection in turbot in Norway.

Animals↗
PubMedDate not supplied

Herpesvirus infections in childhood: 1.

Infections due to herpesviruses have received increasing attention over the past decade, culminating in the isolation in 1986 of human herpesvirus 6. We examine the clinical spectrum of acquired herpesvirus infections in children and review developments in our understanding of their molecular biology, pathogenesis, treatment and prevention.

Acyclovir↗
PubMed2001

Potential for immunotherapy in the treatment of herpesvirus infections.

The concept of using immunotherapy to treat recurrent herpesvirus infections dates back to the 1930s, although many of the initial studies were seriously flawed. Since the late-1980s, however, the use of the guinea pig model of genital herpes has allowed investigators to evaluate carefully several vaccine and immunomodulatory strategies for the control of recurrent herpesvirus infections. These investigations have clearly shown that both approaches can significantly decrease recurrence rates of genital herpes, and the most effective routes, adjuvants and treatment regimens have been identified. Similar strategies have also been shown to decrease herpes simplex virus (HSV)-1 recurrences in animal models of ocular infection. To date, only moderate success has been reported for human trials, although the optimum strategies that were identified in the animal models have not yet been evaluated.

Animals↗
PubMed1981

Mortalities associated with herpesvirus infection in captive macropods.

Fatal cases of herpesvirus infection in a quokka (Setonix brachyurus), eight grey dorcopsis wallabies (Dorcopsis muelleri luctuosa) in two separate outbreaks, as well as presumptive fatal herpesvirus infection in a western grey kangaroo (Macropus fuliginosus) are described. All were captive animals and deaths were preceded by a period of stress. Lesions occurred most often in alimentary tract epithelium, respiratory tract, skin, genital epithelium, conjunctivae, liver and adrenal cortex. Herpesviruses were recovered from the quokka and a grey dorcopsis wallaby from each outbreaks. The implications, particularly concerning certain apparently susceptible species, for those responsible for the health of macropod collections are discussed.

Animals↗
PubMed1988

Recommended procedures for the diagnosis of persistent active herpesvirus infections.

While reliable tests are available to diagnose acute herpesvirus infections, this does not apply equally well to the identification of chronic active or recurrent infections. Common serology in most cases is not very reliable, unless the antibody response is carefully dissected to determine the response to some early antigens related to viral replication, such as against EA complex in Epstein-Barr virus infections. There are a number of techniques that hold some promise for the future: antigen demonstration by monoclonal antibodies such as in the shell vial assay or in tissue culture cells exposed to body fluids; in situ hybridization for viral DNA and polymerase chain reaction; and antigen assays by combined blotting/monoclonal antibody techniques. In developing meaningful parameters for defining persistent active or reactivated herpesvirus infections, techniques for quantitating virus and/or antigen should be helpful.

Antigens, Viral↗
PubMed1987

Magnetic resonance imaging of the brain in childhood herpesvirus infections.

We used magnetic resonance imaging (MRI) to evaluate nine children with neurologic disorders caused by infections with members of the herpesvirus family. MRI studies were abnormal in eight children and demonstrated a wide range of central nervous system lesions, including cystic encephalomalacia, ventricular enlargement, cerebral atrophy and focal parenchymal lesions. When compared with conventional computed tomographic scanning, MRI was more sensitive in detecting abnormalities of white matter and in defining the extent of parenchymal lesions. These studies indicate that MRI scans are highly useful in children with herpesvirus infections involving the central nervous system.

Brain↗
PubMed1993

Herpesvirus infections of the CNS: MR findings.

Herpesvirus infections of the CNS are prevalent in all segments of the population, and are an important health care issue. The family of herpesviruses consists of a large group of double-stranded DNA viruses that includes herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), cytomegalovirus, Epstein-Barr virus, varicella-zoster virus, B virus, herpesvirus 6, and herpesvirus 7. In addition to producing infection when the host initially acquires the virus, an important property shared by these viruses is the ability to produce latent infection and to be reactivated.

Central Nervous System↗
PubMed1988

Herpesvirus infections in pregnancy: risks to embryo, fetus, and neonate.

Gestational herpesvirus infections can significantly alter the outcome of pregnancy. Potential hazards to the embryo, fetus, or neonate are numerous and depend on several variables, including the specific virus involved, gestational timing of infection, and whether the infection is primary or recurrent in nature. This article reviews the epidemiology and clinical manifestations of maternal, fetal, and neonatal herpesvirus infections, methods for establishing an accurate etiologic diagnosis, and prevention strategies, including prospects for prenatal diagnosis of these infections.

Adult↗
PubMed1976

Herpesvirus infection in the newborn. Its treatment by exchange transfusion and adenosine arabinoside.

A case is reported of herpesvirus infection in the newborn following maternal genital herpesvirus infection. The rationale for treating a newborn infant with signs of disseminated herpesvirus infection by exchange transfusion in addition to adenosine arabinoside is discussed. Because of the lack of data concerning therapy for a disease with a 50 to 100% mortality rate, it is important to present material such as this in order to provide information about possible new therapeutic modalities.

Adult↗
PubMed2001

Gene expression profile of herpesvirus-infected T cells obtained using immunomicroarrays: induction of proinflammatory mechanisms.

Herpesvirus infections can frequently lead to acute inflammation, yet the mechanisms regulating this event remain poorly understood. In order to determine some of the immunological mechanisms regulated by human herpesvirus infections, we studied the gene expression profile of lymphocytes infected with human herpesvirus 6 (HHV-6) by using a novel immunomicroarray. Our nylon-based immunomicroarray contained more than 1,150 immune response-related genes and was highly consistent between experiments. Experimentally, we found that independently of the HHV-6 strain used to infect T cells, multiple proinflammatory genes were increased and anti-inflammatory genes were decreased at the mRNA and protein levels. HHV-6 strains A and B increased expression of the genes for interleukin-18 (IL-18), the IL-2 receptor, members of the tumor necrosis factor alpha superfamily receptors, mitogen-activated protein kinase, and Janus kinase signaling proteins. As reported previously, CD4 protein levels were also increased significantly. Specific type 2 cytokines, including IL-10, its receptor, and IL-14, were downregulated by HHV-6 infection and, interestingly, amyloid precursor proteins and type 1 and 2 presenilins. Thus, T cells respond to HHV-6 infection by inducing a type 1 immune response that may play a significant role in the development and progression of diseases associated with HHV-6, including pediatric, hematologic, transplant, and neurologic disorders.

Base Sequence↗
PubMedDate not supplied

Clinical manifestations of herpesvirus infections in pediatric renal transplant recipients.

We report our experience with 29 symptomatic herpesvirus infections occurring during the course of 87 pediatric transplant procedures performed over the 10-year period, 1973 to 1982. The yearly attack rate ranged from 0.05 to 0.40 case per cumulative patient years at risk. A greater proportion (9 of 14) of children who received more than 10 units of whole blood or packed red blood cells prior to transplantation developed a viral infection compared with those given 10 transfusions or fewer (8 of 25) (P = 0.10). Fever occurred in 22 (76%) children, pulmonary disease in 8 (28%), hepatitis in 11 (35%), leukopenia in 7 (24%), thrombocytopenia in 9 (31%) and central nervous system disease in 3 (10%). Herpesvirus infections were responsible for allograft loss in 7 (24%) patients. However, no differences in the actuarial graft survival curves were noted for transplants performed since 1979 in children with and without viral infection. The etiologic viral agents were cytomegalovirus in 19 (65%) episodes, herpes simplex virus in 8 (28%), Epstein-Barr virus in 2 (7%) and varicella-zoster virus in 2 (7%). Cytomegalovirus-infected patients were younger and more commonly developed primary infection compared with children with herpes simplex virus disease who were more likely to have secondary infection and to manifest a mucocutaneous vesicular rash. We conclude that the etiologic agents and clinical features of herpesvirus infections are similar in pediatric and adult renal allograft recipients. Moreover except for distinctive syndromes such as mucocutaneous vesicular eruption or a central nervous system lymphoma, the various herpes-viruses cause clinically indistinguishable illnesses in pediatric transplant patients with similar end organ involvement and untoward renal consequences.

Adolescent↗
PubMed1983

Drug therapy. Treatment of herpesvirus infections.

Guidelines for the prophylaxis or therapy of herpesvirus infections are shown in Table 1. Progress is so rapid in this area that frequent revisions of such guidelines will be necessary. Newer drugs or new formulations of older agents are constantly being developed. Combination therapies--e.g., interferon plus acyclovir--appear promising in laboratory models of herpesvirus infections and will undoubtedly receive clinical investigation in the years ahead. The problem of dealing with latent virus infections still eludes us, and major breakthroughs will be necessary before we can discuss cure of recurrent infections. Nevertheless, important strides have been made in the past few years, and further progress is predictable in the years ahead.

Acyclovir↗
PubMed2004

Diagnosis of herpesvirus infections of the central nervous system.

The International Herpes Management Forum (IHMF) has produced guidelines to promote improved diagnosis of herpesvirus infections of the central nervous system (CNS). Recommendations include using polymerase chain reaction (PCR) analysis of cerebrospinal fluid (CSF) to help diagnose herpes simplex virus (HSV), varicella zoster virus (VZV) and cytomegalovirus (CMV) infections of the CNS. Laboratories routinely using such tests should participate in a proficiency testing programme. For retrospective diagnosis of herpesvirus infections of the CNS, intrathecal antibody detection can be used as an adjunct to PCR, assuming all appropriate controls are utilized. For suspected cases of herpes simplex encephalitis (HSE), a sensitive HSV PCR test of the CSF should be used in preference to other methods. Cultures are not recommended for HSE except as an adjunctive test in suspected neonatal HSV infections. While research continues into the role of PCR with VZV infections of the CNS, studies demonstrate that the technique is useful for diagnosing varicella-associated CNS syndromes but further research is required for its role in zoster-associated syndromes. For CMV CNS infections, PCR represents the most sensitive diagnostic method and can be used in conjunction with virus culture to determine suspected cases of CMV myelitis. For CNS infections with lymphotropic herpesviruses, a positive PCR test is suggestive, but not definitive, evidence of virus encephalitis. PCR analysis of CSF for Epstein-Barr virus can be useful for diagnosing AIDS-associated primary CNS lymphoma. This article presents the current evidence for these and other guidelines for the diagnosis of herpesvirus infections of the CNS.

Central Nervous System Viral Diseases↗
PubMed1993

Impact of herpesvirus infections in the future.

Numerous diverse, often opposing, trends will determine the frequency (and severity) of herpesvirus infections in the future. A major factor is the growing population of iatrogenically immunocompromised patients, accruing especially from large increases in organ and autologous bone marrow transplantation. Of even greater importance is the immense number of human immunodeficiency virus (HIV)-infected patients for whom herpesviruses may: (1) have been a cofactor in acquisition of HIV infection; (2) contribute to in vivo activation of HIV; (3) cause severe infections. Another factor influencing severe herpesvirus infections is the aging of populations in developed countries; this will be associated with a greater prevalence, and more morbid manifestations, of herpes zoster. Sociologic changes will also be important. The consequences of these, such as attempts to influence sexual practices, will be difficult to predict. Other changes, such as more frequent use of early child care facilities, will predictably lead to early acquisition of most herpesviruses, thereby decreasing the incidence of severe disease in adulthood. Factors that will reduce the incidence and/or severity of herpesvirus infections include vaccines (varicella, herpes simplex, cytomegalovirus); prophylactic strategies for immunocompromised hosts (passive immunization, antiviral drugs, blood product selection); more rapid and sensitive diagnostic methods; and suppressive or early antiviral therapy for common infections, such as genital herpes simplex and varicella.(ABSTRACT TRUNCATED AT 250 WORDS)

Forecasting↗