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At least 19 recordsLinked to original sources
PubMed2003

Herpesvirus infections in transplant recipients: current challenges in the clinical management of cytomegalovirus and Epstein-Barr virus infections.

Herpesvirus infections are common causes of morbidity and mortality in solid organ and haematopoietic stem cell transplant recipients. Significant scientific breakthroughs have reduced the incidence of herpesvirus infections during the early post-transplant period, but herpesvirus infections continue to impact significantly on the outcome of transplantation. Widespread and prolonged use of antiviral drugs has not eliminated the risk of cytomegalovirus (CMV) disease, but has changed its natural course by delaying its onset. Moreover, there is now increased recognition of ganciclovir (and other antiviral drug)-resistant CMV infections. By contrast, optimal preventive and treatment strategies for Epstein-Barr virus-related post-transplant lymphoproliferative disorders (PTLD) remain elusive. Recent experimental and clinical data, however, demonstrate a promising role for immunotherapy in preventing and treating PTLD. This review highlights the current challenges in managing CMV and Epstein-Barr virus infections in transplant patients.

Bone Marrow Transplantation↗
PubMed2003

Update on herpesvirus infections.

Herpesviruses are responsible for many illnesses that affect the oral and maxillofacial region. The most common of these are primary or recurrent HSV infection, but knowledge of the manifestations of the eight herpesviruses that cause infections in humans will provide clinicians with a better understanding and basis for diagnosing and managing patients with these diseases. Immunocompromised patients are at greater risk for serious illness: therefore, clinicians treating transplant patients, patients receiving cancer chemotherapy, or HIV-infected individuals should be aware of the various clinical manifestations of infection with herpesviruses.

Dental Care for Chronically Ill↗
PubMed1975

Chemotherapy of herpesvirus infections.

Herpesviruses commonly produce lesions that come to the attention of physicians. Many different chemicals are known to suppress the growth of herpesviruses in vitro, but only a few of these have found application in clinical practice. A critical assessment of the place of some of these forms of chemotherapy was briefly presented.

Female↗
PubMed1984

Antibody-mediated bacterial adhesion to cytomegalovirus-induced Fc receptors. Potential relationship to secondary infections complicating herpesvirus infections.

Cytomegalovirus (CMV) and other viruses within the herpes group have recently been shown to induce Fc receptors in infected monolayers. We have examined the possibility that such receptors might facilitate the adherence of antibody-coated bacteria to CMV-infected cells. To do this, we infected confluent human embryonic lung (HEL) cell monolayers with CMV (strain AD 169) and then used a double radiolabel assay to measure adherence of Escherichia coli 06 to both infected and control monolayers. We examined infected monolayers 48 h after viral seeding, at which time 30-60% of the cells exhibited characteristic cytopathic changes. We compared the adherence of untreated E. coli 06 with the adherence of E. coli 06 that had been preincubated for 1 h at 37 degrees C with either nonimmune or anti-E. coli 06 antiserum. Pretreatment of the E. coli 06 with specific antiserum significantly enhanced its adherence to CMV-infected, but not to control, monolayers (P less than 0.01 by the Mann-Whitney U test). We did not see such enhancement when we used anti-E. coli 06 antiserum to treat a nontypable E. coli. The augmented adherence of antibody-coated E. coli 06 to CMV-infected monolayers was abrogated by pretreating the monolayers with nonimmune serum or purified Fc fragments, but not by pretreating with IgA, IgM, or 1 mM trypan blue. Preincubating HEL cell monolayers with 100 U/ml human leukocyte interferon for 72 h at 37 degrees C did not affect the adherence of antibody-coated E. coli 06 to the monolayers. To determine if antibody-coated bacteria that adhered to the surface of CMV-infected monolayers might themselves act as receptors for microorganisms with Fc binding potential, we compared the adherence of Cowan strain Staphylococcus aureus to CMV-infected and control monolayers that had been preincubated with antibody-coated E. coli 06. The S. aureus adhered significantly better to the former monolayers (P less than 0.001). These results illustrate a previously unrecognized mechanism by which certain herpesviruses might enhance the adherence of secondary pathogens to nonphagocytic cell populations. Such a mechanism, if active in vivo, might facilitate the colonization of mucosal surfaces by these pathogenic microorganisms, and in this way might contribute to both the reported predisposition of CMV-infected patients to secondary infections and to the high prevalence of S. aureus in the vaginal flora of women with histories of genital herpes.

Adhesiveness↗
PubMed1997

Histopathology of peripheral nerves in cutaneous herpesvirus infection.

Cutaneous herpesvirus infection is a common viral disorder manifest by epidermal and/or mucosal vesicle formation. Though it is believed that the virus most likely resides in regional sensory ganglia following primary infection and that cutaneous involvement represents reactivation of a latent infection, the histopathology of cutaneous nerves in sites of disease has not been well characterized. In order to assess and characterize the pathologic changes of these nerves, we retrospectively examined 54 cases of cutaneous and mucosal herpesvirus infection as defined by the presence of diagnostic multinucleate epithelial giant cells that demonstrated viral cytopathic effect. Dermal nerves were evaluable in 48 of 54 cases. All cases showed perineural inflammation that consisted of a dense mixed lymphocyte-polymorphonuclear cell infiltrate. Twenty-six cases exhibited intraneural infiltrations accompanied by Schwann cell hypertrophy with nuclear eosinophilia and pyknosis. Frank neuronal necrosis was present in 21 cases, with viral cytopathic effect evident within neurons of four cases. The degree of peri- and intraneural inflammation correlated with the severity of the inflammatory response within the dermis in most cases; however, in eight cases there was inflammatory involvement of neurovascular structures distant from and out of proportion to dermal and epidermal changes. Immunoperoxidase staining using a polyvalent antibody to human herpesvirus was performed in two cases and demonstrated viral antigen within nerve twigs. This pattern of peripheral nerve twig inflammation, along with the occurrence of more distant neural involvement, may prove to have diagnostic implications and serve as a clue in the recognition of cutaneous herpesvirus infection, particularly in cases with subtle or absent epidermal alteration. Furthermore, the presence of inflammation within and around nerves as well as degenerative changes suggest that nerve twigs are not passive conduits for viral spread but may be directly involved in infection.

Antigens, Viral↗
PubMed2005

Herpesvirus infection in woodland caribou in Alberta, Canada.

Sera and genital swabs collected from 121 adult woodland caribou (Rangifer tarandus caribou) in five subpopulations in northern Alberta, Canada, between December 1997 and October 1999, were examined for evidence of infection with herpesviruses or pestiviruses. No virus was isolated from sera or swabs, and no antibodies against bovine viral diarrhea virus were detected. However, 63 (52%) of the 121 animals had neutralizing antibody titers against bovine herpesvirus 1. There was sufficient serum from 37 of the 121 caribou to allow parallel testing for antibodies against a new alphaherpesvirus isolated from an elk (Cervus elaphus nelsoni), and 20 animals had antibodies against this virus. Paired sera collected 11 mo apart from 14 caribou showed seroconversion in seven animals, indicating that an active herpesvirus infection was present. Virus neutralization data suggest that these caribou are infected with a distinct alphaherpesvirus.

Alberta↗
PubMed1985

Herpesvirus infection in man.

Herpesviruses which affect man are herpes simplex virus type 1 and type 2, varicella-zoster virus, cytomegalovirus and Epstein-Barr virus. The review deals with the more common clinical manifestations of human herpesvirus infections, which occur ubiquitously in all populations throughout the world. Primary infections most commonly occur in childhood. It is a characteristic feature of herpesvirus that they generally remain in a latent form after clearance of the primary infection. The overall majority of clinical problems are related to activated latent infections, viz. recurrent lesions of herpes simplex, herpes zoster with remaining neuralgia in older patients, and in particular herpesvirus infections and reactivation in immunodeficient individuals. Herpes infection during pregnancy may result in severe generalised infection of the newborn. A possible relationship between herpesvirus and cancer, especially between herpesvirus type 2 and cervical cancer and between Epstein-Barr virus and Burkitt's lymphoma are of major interest today.

Adult↗
PubMed2003

Detection of simultaneous beta-herpesvirus infections in clinical syndromes due to defined cytomegalovirus infection.

Human herpesvirus (HHV)-6 and HHV-7 are increasingly being recognized as emerging pathogens among transplant recipients. Using quantitative polymerase chain reaction assays, we demonstrate the presence of HHV-6 and/or HHV-7 in 18 of 20 episodes of clinically presumed or microbiologically confirmed cytomegalovirus (CMV) infection. Seventeen (89%) of 19 microbiologically confirmed cytomegalovirus (CMV)-infected patients had concomitant HHV-6 variant B (47%) and/or HHV-7 (63%) infection. The degree of HHV-6 coinfection was significantly correlated with hyperbilirubinemia while HHV-7 coinfection demonstrated a non-significant trend toward cytopenias. In one of the 20 episodes described herein, the 'viral syndrome' was due solely to HHV-7 infection; clinical and virological response was observed during intravenous ganciclovir therapy in this patient. While this study emphasizes the significance of HHV-6 and/or HHV-7 coinfection during episodes of CMV infection, it significantly highlights the novel observation of the causal role of HHV-7 (in the absence of HHV-6 and CMV) in a clinical illness presumed to be caused CMV. Thus, HHV-7 (and HHV-6) should be considered as a pathogen (or copathogen) in the viral syndromes following organ transplantation.

Adult↗
PubMed2001

Current and potential therapies for the treatment of herpesvirus infections.

Human herpesviruses are found worldwide and are among the most frequent causes of viral infections in immunocompetent as well as in immunocompromised patients. During the past decade and a half a better understanding of the replication and disease causing state of herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), and human cytomegalovirus (HCMV) has been achieved due in part to the development of potent antiviral compounds that target these viruses. While some of these antiviral therapies are considered safe and efficacious (acyclovir, penciclovir), some have toxicities associated with them (ganciclovir and foscarnet). In addition, the increased and prolonged use of these compounds in the clinical setting, especially for the treatment of immunocompromised patients, has led to the emergence of viral resistance against most of these drugs. While resistance is not a serious issue for immunocompetent individuals, it is a real concern for immunocompromised patients, especially those with AIDS and the ones that have undergone organ transplantation. All the currently approved treatments target the viral DNA polymerase. It is clear that new drugs that are more efficacious than the present ones, are not toxic, and target a different viral function would be of great use especially for immunocompromised patients. Here, we provide an overview of the diseases caused by the herpesviruses as well as the replication strategy of the better studied members of this family for which treatments are available. We also discuss the various drugs that have been approved for the treatment of some herpesviruses in terms of structure, mechanism of action, and development of resistance. Finally, we present a discussion of viral targets other than the DNA polymerase, for which new antiviral compounds are being considered.

Antiviral Agents↗
PubMed2001

Current and potential therapies for the treatment of herpesvirus infections.

Human herpesviruses are found worldwide and are among the most frequent causes of viral infections in immunocompetent as well as in immunocompromised patients. During the past decade and a half a better understanding of the replication and disease causing state of herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), and human cytomegalovirus (HCMV) has been achieved due in part to the development of potent antiviral compounds that target these viruses. While some of these antiviral therapies are considered safe and efficacious (acyclovir, penciclovir), some have toxicities associated with them (ganciclovir and foscarnet). In addition, the increased and prolonged use of these compounds in the clinical setting, especially for the treatment of immunocompromised patients, has led to the emergence of viral resistance against most of these drugs. While resistance is not a serious issue for immunocompetent individuals, it is a real concern for immunocompromised patients, especially those with AIDS and the ones that have undergone organ transplantation. All the currently approved treatments target the viral DNA polymerase. It is clear that new drugs that are more efficacious than the present ones, are not toxic, and target a different viral function would be of great use especially for immunocompromised patients. Here, we provide an overview of the diseases caused by the herpesviruses as well as the replication strategy of the better studiedmembers of this family for which treatments are available. We also discuss the various drugs that have been approved for the treatment of some herpesviruses in terms of structure, mechanism of action, and development of resistance. Finally, we present a discussion of viral targets other than the DNA polymerase, for which new antiviral compounds are being considered.

Antiviral Agents↗
PubMed2001

Prophylaxis against herpesvirus infections in transplant recipients.

Herpesvirus infections are important after stem cell and organ transplant. During the last decades several antiviral agents have been introduced with efficacy against herpesviruses. These agents are the nucleoside analogues aciclovir, valaciclovir, famciclovir, and ganciclovir; the nucleotide analogue cidofovir; and the pyrophosphate analogue foscarnet. Several studies have been performed with antiviral agents with the aim to reduce morbidity and mortality associated with herpesvirus infections in transplant recipients. Aciclovir and valaciclovir have been examined in randomised, controlled trials in both solid organ and stem cell transplant patients, and were shown to be very effective for the prevention of herpes simplex virus (HSV) and varicella-zoster virus infections. In addition, these drugs were shown to reduce cytomegalovirus (CMV) infection and improve survival in allogenic stem cell transplant patients and to reduce CMV infection, CMV disease (aciclovir and valaciclovir), and acute rejection (valaciclovir) in renal transplant patients. Ganciclovir is very effective for the prevention of CMV infection and disease in both stem cell and solid organ transplant recipients. It can also be used in preemptive strategies in which the aim is to prevent CMV disease in patients who have ongoing CMV infection documented by antigenaemia or detection of CMV DNA. The latter strategy has the advantage of reducing the exposure to the drug and thereby the risk for toxicity. Foscarnet has also been shown to be effective as preemptive therapy for CMV in allogenic stem cell transplant patients and as therapy for aciclovir-resistant HSV infections. Finally cidofovir is an interesting agent with broad spectrum antiherpesvirus efficacy. However, because of the drug's toxicity profile, further studies are needed.

Antibiotic Prophylaxis↗
PubMed2001

A candidate phocid herpesvirus vaccine that provides protection against feline herpesvirus infection.

Phocid herpesvirus type 1 (PhHV-1) causes significant morbidity and mortality among young and immunocompromised harbour seals. Therefore, the availability of an effective PhHV-1 vaccine would be of importance for orphanages and seal rehabilitation centres. Since possibilities to test PhHV-1 candidate vaccines in the target species are limited, a suitable animal model is needed. Given the close genetic and antigenic relationships between PhHV-1 and feline herpesvirus (FHV), the FHV cat system could be considered to test candidate PhHV-1 vaccines. Here we have tested a PhHV-1 based ISCOM vaccine for its protective efficacy against FHV infection in cats. To this end, three groups of cats were vaccinated thrice with ISCOM adjuvanted PhHV-1, FHV, and mock vaccines, respectively. One month after the last vaccination, all cats were challenged with a virulent FHV strain. All PhHV-1 and FHV vaccinated cats were protected from developing severe disease and excreted significantly less FHV than the mock vaccinated cats.

Animals↗
PubMedDate not supplied

Herpesvirus infections in childhood: 2.

Infections due to herpesviruses have received increasing attention over the past decade, culminating in the isolation in 1986 of human herpesvirus-6. This is the second of two articles in which we examine the clinical spectrum of acquired herpesvirus infections in children and review developments in our understanding of the molecular biology, pathogenesis, treatment and prevention of these infections.

Child↗
PubMed2001

The expanding spectrum of herpesvirus infections of the nervous system.

Herpesviruses cause various acute, subacute, and chronic disorders of the central (CNS) and peripheral (PNS) nervous systems in adults and children. Both immunocompetent and immunocompromised individuals may be affected. Zoster (shingles), a result of reactivation of varicella zoster virus (VZV), is the most frequent neurologic complication. Other neurological complications include encephalitis produced by type I herpes simplex virus (HSV-1), and less frequently HSV-2, as well as by VZV and cytomegalovirus (CMV). Acute meningitis is seen with VZV and HSV-2, and benign recurrent meningitis with HSV-2. Combinations of meningitis/ encephalitis and myelitis/radiculitis are associated with Epstein Barr Virus (EBV); myelitis with VZV, CMV, EBV, and HSV-2; and ventriculitis/encephalitis with VZV and CMV. Brainstem encephalitis due to HSV and VZV, and polymyeloradiculitis due to CMV are well documented. HHV-6 produces childhood exanthem subitum (roseola) and febrile convulsions. Immunocompetent and immunocompromised hosts manifest different incidences and patterns of herpesvirus infections. For example, stroke due to VZV-mediated large vessel disease (herpes zoster ophthalmicus) occurs predominantly in immunocompetent hosts, while small vessel disease (leukoencephalitis) and ventriculitis develop almost exclusively in immunocompromised patients. EBV-associated primary CNS lymphomas also are restricted to immunosuppressed individuals. Recent large CSF PCR studies have shown that VZV, EBV, and CMV more frequently produce meningitis, encephalitis, or encephalopathy in immunocompetent hosts than was formerly realized. We review herpesvirus infections of the nervous system and illustrate the expanding spectrum of disease by including examples of a 75-year-old male on steroid treatment for chronic lung disease with fatal HSV-2 meningitis and an 81-year-old male with myasthenia gravis, long-term azathioprine use, and an EBV-associated primary CNS lymphoma.

Adolescent↗
PubMed1983

Correlation between low natural killing of fibroblasts infected with herpes simplex virus type 1 and susceptibility to herpesvirus infections.

Natural killer cells capable of lysing herpes simplex virus type 1 (HSV-1)-infected fibroblasts were studied in three groups of patients unusually susceptible to severe herpes-virus infections. Cord blood was evaluated because of the known susceptibility of neonates to disseminated infections due to herpes simplex virus type 2 at birth. Only 30% of the cord blood specimens tested demonstrated normal lysis of HSV-1-infected fibroblasts and a normal increment in the lysis of infected over uninfected cells. Five out of six patients with Wiskott-Aldrich Syndrome (WAS) also were found to have abnormally low responses by these criteria. The one WAS patient with normal responses had had little difficulty with infections and had survived much longer than usual. Five patients with severe herpesvirus infections and no known primary cellular immunodeficiency had natural killer cell function significantly below normal (P less than 0.001). These data suggest that natural killer cells probably play an important role in human resistance to herpesvirus infection and that deficiencies of this system may result in unusual susceptibility to herpesvirus infections.

Adolescent↗
PubMed1988

Treatment of persistent active herpesvirus infections.

All human herpesviruses cause chronic infections in which latent virus is periodically reactivated. Persistently active infections are uncommon, however, and occur exclusively in individuals whose immune systems fail to control virus multiplication and spread. This paper summarizes the management of these unusual infections.

Antiviral Agents↗