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Among Ugandan mother-child pairs, Epstein-Barr virus was more likely to be shed in saliva than Kaposi sarcoma–associated virus. Child’s sex and parasitic infections influenced viral shedding. Shedding of each virus was inversely related, suggesting an interaction between them.

Background. To date, there is no commercially available vaccine to prevent infectious mononucleosis, a disease frequently induced by Epstein-Barr virus (EBV) infection in adolescents or adults devoid of preexisting immunity to the virus. Methods. A total of 181 EBV-seronegative, healthy, young adult volunteers were randomized in a double-blind fashion to receive either placebo or a recombinant EBV subunit glycoprotein 350 (gp350)/aluminum hydroxide and 3-O-desacyl-4′-monophosphoryl lipid A (AS04) candidate vaccine in a 3-dose regimen. Results. The vaccine had demonstrable efficacy (mean efficacy rate, 78.0% [95% confidence interval {CI}, 1.0%–96.0%]) in preventing the development of infectious mononucleosis induced by EBV infection, but it had no efficacy in preventing asymptomatic EBV infection. One month after receipt of the final dose of gp350 vaccine, 98.7% of subjects showed seroconversion to anti-gp350 antibodies (95% CI, 85.5%–97.9%), and they remained anti-gp350 antibody positive for >18 months. Furthermore, there were no concerns regarding the safety or reactogenicity of the gp350/AS04 vaccine. Conclusion. These data support the clinical feasibility of using an EBV vaccine to prevent infectious mononucleosis. Trial registration. ClinicalTrials.gov identifier: NCT00430534.

Abstract Clinical reactivations of herpes simplex virus or varicella zoster virus occur frequently among patients with malignancies and manifest particularly as herpes simplex stomatitis in patients with acute leukaemia treated with intensive chemotherapy and as herpes zoster in patients with lymphoma or multiple myeloma. In recent years, knowledge on reactivation rates and clinical manifestations has increased for conventional chemotherapeutics as well as for many new antineoplastic agents. This guideline summarizes current evidence on herpesvirus reactivation in patients with solid tumours and hematological malignancies not undergoing allogeneic or autologous hematopoietic stem cell transplantation or other cellular therapy including diagnostic, prophylactic, and therapeutic aspects. Particularly, strategies of risk adapted pharmacological prophylaxis and vaccination are outlined for different patient groups. This guideline updates the guidelines of the Infectious Diseases Working Party (AGIHO) of the German Society for Hematology and Medical Oncology (DGHO) from 2015 “Antiviral prophylaxis in patients with solid tumours and haematological malignancies” focusing on herpes simplex virus and varicella zoster virus.

Genital herpes is the main cause of genital ulcers worldwide; the prevalence of herpes simplex virus (HSV) type 2 infections in the general population ranges from 10% to 60%. Most genital herpes is caused by HSV-2, although HSV-1 accounts for about half of new cases in developed countries. The risk of HIV acquisition is three times higher in people with HSV-2. Neonatal herpes is an uncommon but serious complication of genital herpes. Most genital HSV-2 infections are unrecognised and undiagnosed; infected individuals, even with mild symptoms, shed HSV, and can infect sexual partners. Since clinical diagnosis is neither sensitive nor specific, virological and type-specific serological tests should be used routinely. Oral antiviral drugs for HSV infections are safe and effective and can be used both to treat episodes and to prevent recurrences. Antiviral treatment of the infected partners and condom use reduce the risk of sexual transmission of HSV-2.

Background/objectivesB-cells are key players in immune responses and autoimmunity through antibody production, antigen presentation and cytokine production. Fine tuning of B-cell activation depends on convergent signals from the B-cell receptor (BCR) and costimulatory membrane receptors. We studied the expression and function of the recently characterised costimulator HVEM and its receptors, and investigated its role in B-cell activation and differentiation in healthy individuals and patients with systemic lupus erythematosus (SLE).Materials/methodsPeripheral blood mononuclear cells were isolated from healthy volunteers and patients with active SLE. Expression of HVEM and its ligands, BTLA and LIGHT, were assessed by flow cytometry at basal conditions and following activation. Immunomagentically-sorted CD19+total, CD19+CD27-naive, or CD19+CD27+memory B-cells were stimulated with anti-IgM plus or minus IL-21 in presence or not of plate-bound HVEM. Fc chimeric protein to evaluate effects on cell proliferation (CFSE assay), apoptosis (Annexin/7AAD assay), activation (CD80/86, CD40), cytokine production (IL-6) and differentiation (CD38, Ig secretion).ResultsActive SLE patients had significantly higher proportion of circulating HVEM-expressing CD4+T-cells than healthy individuals (95.4 plus or minus 1.3% vs. 85.4 plus or minus 3.9%, p = 0.013). Both patients and controls demonstrated high-level expression of BTLA on freshly isolated peripheral blood B-cells, whereas LIGHT had minimal basal expression and was induced following BCR activation. HVEM. Fc crosslinking on B-cells activated with anti-IgM plus or minus IL-21 led to significantly reduced cell proliferation (by 72 plus or minus 3%) and membrane CD80/CD86 expression (by 29 plus or minus 4%). Notably, in 5-8 days cell cultures, HVEM. Fc induced the differentiation of both CD27- and CD27+ B-cells, as evidenced by the increased expression of CD27/CD38 (CD27+: 27.9% vs. 18.4%; CD38+: 25.0% vs. 21.5%) and CD38/CD138, respectively (CD38+ +: 6.0% vs. 3.8%). This finding was accompanied by strong anti-apoptotic effect of HVEM. Fc treatment. Further experiments are underway to elucidate the molecular mechanisms of HVEM. Fc-mediated effects on B-cells and the potential therapeutic use of HVEM/BTLA manipulation in SLE.ConclusionsHVEM exerts significant B-cell co-stimulatory effects through regulation of proliferation, apoptosis and differentiation. Increased HVEM expression on SLE CD4+T-cells might contribute to enhanced memory and plasma cell differentiation observed in the disease.

Background Equine herpes virus type 1 (EHV‐1) infection in horses is associated with respiratory and neurologic disease, abortion, and neonatal death. Hypothesis Vaccines decrease the occurrence of clinical disease in EHV‐1‐infected horses. Methods A systematic review was performed searching multiple databases to identify relevant studies. Selection criteria were original peer‐reviewed research reports that investigated the in vivo use of vaccines for the prevention of disease caused by EHV‐1 in domesticated horses. Main outcomes of interest included pyrexia, abortion, neurologic disease, viremia, and nasal shedding. We evaluated risk of bias, conducted exploratory meta‐analyses of incidence data for the main outcomes, and performed a GRADE evaluation of the quality of evidence for each vaccine subtype. Results A total of 1018 unique studies were identified, of which 35 met the inclusion criteria. Experimental studies accounted for 31/35 studies, with the remainder being observational studies. Eight vaccine subclasses were identified including commercial (modified‐live, inactivated, mixed) and experimental (modified‐live, inactivated, deletion mutant, DNA, recombinant). Risk of bias was generally moderate, often because of underreporting of research methods, and sample sizes were small leading to imprecision in the estimate of the effect size. Several studies reported either no benefit or minimal vaccine efficacy for the primary outcomes of interest. Meta‐analyses revealed significant heterogeneity was present, and our confidence in the quality of evidence for most outcomes was low to moderate. Conclusions and Clinical Importance Our review indicates that commercial and experimental vaccines minimally reduce the incidence of clinical disease associated with EHV‐1 infection.

The frequency of central nervous system infections due to herpesvirus have been studied in various populations; however, studies in Mexican mestizo patients are scant. This paper documents the frequency of herpesvirus encephalitis in Mexican mestizo patients from the National Institute of Neurology and Neurosurgery (NINN) of Mexico. To study the frequency of herpetic viral encephalitis at the NINN in the period from 2004 to 2009. We reviewed clinical records from patients with clinically suspected encephalitis; polymerase chain reaction assays were done for detection of herpesviruses in cerebrospinal fluid (CSF) samples. The total number of patients studied was 502; in 59 (12%), the diagnosis of herpetic encephalitis was confirmed by PCR-based testing of CSF. Of them, 21 (36%) were positive for herpes simplex virus type 1, 15 (25%) for Epstein–Barr virus, 10 (17%) for varicella zoster virus, 8 (14%) for cytomegalovirus, 3 (5%) for human herpesvirus 6, and 2 (3%) for herpes simplex virus 2. Our results show a varied frequency of viral encephalitis in mestizo patients due to herpesviruses in a tertiary neurological center and point out the importance of modern molecular technology to reach the etiological diagnosis in cases of encephalitis.

Shortly after the discovery of human herpesvirus 6 (HHV-6), two distinct variants, HHV-6A and HHV-6B, were identified. In 2012, the International Committee on Taxonomy of Viruses (ICTV) classified HHV-6A and HHV-6B as separate viruses. This review outlines several of the documented epidemiological, biological, and immunological distinctions between HHV-6A and HHV-6B, which support the ICTV classification. The utilization of virus-specific clinical and laboratory assays for distinguishing HHV-6A and HHV-6B is now required for further classification. For clarity in biological and clinical distinctions between HHV-6A and HHV-6B, scientists and physicians are herein urged, where possible, to differentiate carefully between HHV-6A and HHV-6B in all future publications.

Background and aimsAcute necrotizing encephalopathy in childhood (ANEC) is a disease characterised by acute encephalopathy and radiological features of bilateral thalamic necrosis. Medium and long term morbidity is not well described. We describe the mortality and morbidity outcomes in our paediatric cohort with this disease.MethodsThis is a retrospective ten-year series. Children aged one month to 18 years diagnosed with 'ANEC' were collated from Neurology and Radiology databases.18 fulfilled clinical criteria of acute encephalopathy. All were scored with Mizuguchi's radiological checklist by two paediatric neurologists and one radiologist. 11 cases scored unlikely were excluded.Data analysis focused on discharge and follow-up outcomes.Results7 patients were analysed. The median age was 3.7 years. All were previously well with normal development. All had impaired consciousness at presentation with preceding fever and prodrome. Typical radiology showed bilateral thalamic involvement with/without areas of haemorrhage and necrosis. Causative organisms included Influenza A H1N1, Human Herpes Virus 6 and Metapneumovirus. All were treated with steroids, immunoglobulin or both.Outcomes were evaluated at discharge and follow-up and divided into good or poor (including death). One passed away from brainstem death. All had neurological deficit at discharge: 50% mildly affected; 50% severely affected. 00% in the former group restored normal neurological function on follow-up. In the latter, two responded well to rehabilitation but one remained severely impaired.ConclusionsANE mortality at our institution is 14%. Morbidity of survivors at discharge is 100%. Long term follow up morbidity however, improves to 50% with half achieving normal neurological function at follow up.

Herpes simplex virus (HSV), a common latent virus in humans, causes certain severe diseases. Extensive use of acyclovir (ACV) results in the development of drug-resistant HSV strains, hence, there is an urgent need to develop new drugs to treat HSV infection. Houttuynia cordata (H. cordata), a natural herbal medicine, has been reported to exhibit anti-HSV effects which is partly NF-κB-dependent. However, the molecular mechanisms by which H. cordata inhibits HSV infection are not elucidated thoroughly. Here, we report that H. cordata water extracts (HCWEs) inhibit the infection of HSV-1, HSV-2, and acyclovir-resistant HSV-1 mainly via blocking viral binding and penetration in the beginning of infection. HCWEs also suppress HSV replication. Furthermore, HCWEs attenuate the first-wave of NF-κB activation, which is essential for viral gene expressions. Further analysis of six compounds in HCWEs revealed that quercetin and isoquercitrin inhibit NF-κB activation and additionally, quercetin also has an inhibitory effect on viral entry. These results indicate that HCWEs can inhibit HSV infection through multiple mechanisms and could be a potential lead for development of new drugs for treating HSV.