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Different Viruses (different + viruse)
Selected AbstractsA new look at viruses in type 1 diabetesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 1 2003Hee-Sook Jun Abstract Type 1 diabetes (T1D) results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of T1D, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that nongenetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of T1D. To date, 14 different viruses have been reported to be associated with the development of T1D in humans and animal models. Viruses may be involved in the pathogenesis of T1D in at least two distinct ways: by inducing beta cell-specific autoimmunity, with or without infection of the beta cells, [e.g. Kilham rat virus (KRV)] and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, KRV, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus (EBV) are discussed. With respect to the destruction of beta cells by cytolytic infection, encephalomyocarditis virus, mengovirus and Coxsackie B viruses are discussed. In addition, a review of transgenic animal models for virus-induced autoimmune diabetes is included, particularly with regard to lymphocytic choriomeningitis virus, influenza viral proteins and the Epstein-Barr viral receptor. Finally, the prevention of autoimmune diabetes by infection of viruses such as lymphocytic choriomeningitis virus is discussed. Copyright © 2002 John Wiley & Sons, Ltd. [source] Programmed responses to virus replication in plantsMOLECULAR PLANT PATHOLOGY, Issue 1 2000A. J. Maule Despite their economic importance, we understand very little about the mechanism leading to symptom formation in compatible virus infections. By applying a spatial analysis to advancing infection fronts, we have been able to relate molecular events in small groups of cells to a sequence of virus-induced changes. This sequence starts ahead of the main front of virus replication and virus protein accumulation and lasts beyond the time at which virus replication has ceased. The host changes include alterations in gene expression, physiology and cellular ultrastructure. The relationship between these effects has been analysed in comparative studies between different virus infections in different hosts and abiotic stress. The research points to there being common features for different viruses leading to common effects. Also, although many of the consequences of virus infection are similar to the effects of heat shock, there are sufficient differences to suggest that the two inducers use distinct control pathways. The immediate challenge for the future is to establish synchronous infections of tissues so that the complex relationship between the virus and the host can be investigated using temporal rather than spatial analyses. [source] Viruses and atypical bacteria associated with asthma exacerbations in hospitalized children,PEDIATRIC PULMONOLOGY, Issue 6 2010Alberto F. Maffey MD Abstract Objectives and Working Hypothesis To evaluate the prevalence of respiratory viruses Mycoplasma pneumoniae and Chlamydophila pneumoniae and gain insight into their seasonal circulation pattern in children with acute asthma exacerbations in a temperate southern hemisphere region. Study Design Patients hospitalized between 3 months and 16 years of age were included in a 1-year prospective, observational, cross-sectional study. Respiratory secretions were collected and the presence of different viruses and atypical bacteria analyzed by immunofluorescence and polymerase chain reaction. Results Two hundred nine patients (118 females) aged (mean,±,SD) 4.4,±,4 years were included. A potential causative agent was detected in 78% of the patients. The most frequently detected viruses were respiratory syncytial virus (HRSV) (n,=,85; 40%) and rhinovirus (HRV) (n,=,52; 24.5%); M. pneumoniae and C. pneumoniae were detected in 4.5% and 2% of the cases, respectively. Patients with HRSV (vs. HRV) were hospitalized for a longer time (6.7 vs. 5.2 days, P,=,0.012), required more days of oxygen supply (5.1 vs. 3.4, P,=,0.005), had a longer duration of the exacerbation before hospitalization (3.6 vs. 1.9 days, P,=,0.001) and were younger (3.7 vs. 5.1 years, P,=,0.012). Three peaks of admissions were observed. A first peak (early autumn) caused by HRV, a second peak (winter) caused mainly by HRSV and a third one (spring), caused by HRSV, an increase in HMPV together with a second outbreak of HRV. Conclusions Children with an acute asthma exacerbation presented a high prevalence of respiratory viruses. Most hospitalizations corresponded to seasonal increases in prevalence of HRV and HRSV. Pediatr Pulmonol. 2010; 45:619,625. © 2010 Wiley-Liss, Inc. [source] Detection of human herpesvirus-6 in cerebrospinal fluid of patients with encephalitis,ANNALS OF NEUROLOGY, Issue 3 2009Karen Yao MS Objective Virus infections are the most common causes of encephalitis, a syndrome characterized by acute inflammation of the brain. More than 150 different viruses have been implicated in the pathogenesis of encephalitis; however, because of limitations with diagnostic testing, causative factors of more than half of the cases remain unknown. Methods To investigate whether human herpesvirus-6 (HHV-6) is a causative agent of encephalitis, we examined for evidence of virus infection by determining the presence of viral sequence using polymerase chain reaction and assessed HHV-6 antibody reactivity in the cerebrospinal fluid of encephalitis patients with unknown cause. In a cohort study, we compared virus-specific antibody levels in cerebrospinal fluid samples of patients with encephalitis, relapsing-remitting multiple sclerosis, and other neurological diseases. Results Our results demonstrated increased levels of HHV-6 IgG, as well as IgM levels, in a subset of encephalitis patients compared with other neurological diseases. Moreover, cell-free viral DNA that is indicative of active infection was detected in 40% (14/35) of encephalitis patients, whereas no amplifiable viral sequence was found in either relapsing-remitting MS or other neurological diseases patients. In addition, a significant correlation between polymerase chain reaction detection and anti-HHV-6 antibody response was also demonstrated. Interpretation Collectively, these results suggested HHV-6 as a possible pathogen in a subset of encephalitis cases. Ann Neurol 2009;65:257,267 [source] Virus susceptibility of Chinese hamster ovary (CHO) cells and detection of viral contaminations by adventitious agent testingBIOTECHNOLOGY & BIOENGINEERING, Issue 4 2010Andreas Berting Abstract Biopharmaceuticals are of increasing importance in the treatment of a variety of diseases. A remaining concern associated with their production is the potential introduction of adventitious agents into their manufacturing process, which may compromise the pathogen safety of a product and potentially cause stock-out situations for important medical supplies. To ensure the safety of biological therapeutics, regulatory guidance requires adventitious agent testing (AAT) of the bulk harvest. AAT is a deliberately promiscuous assay procedure which has been developed to indicate, ideally, the presence of any viral contaminant. One of the most important cell lines used in the production of biopharmaceuticals is Chinese hamster ovary (CHO) cells and while viral infections of CHO cells have occurred, a systematic screen of their virus susceptibility has never been published. We investigated the susceptibility of CHO cells to infection by 14 different viruses, including members of 12 families and representatives or the very species that were implicated in previously reported production cell infections. Based on our results, four different infection outcomes were distinguished, based on the possible combinations of the two factors (i) the induction, or not, of a cytopathic effect and (ii) the ability, or not, to replicate in CHO cells. Our results demonstrate that the current AAT is effective for the detection of viruses which are able to replicate in CHO cells. Due to the restricted virus susceptibility of CHO cells and the routine AAT of bulk harvests, our results provide re-assurance for the very high safety margins of CHO cell-derived biopharmaceuticals. Biotechnol. Bioeng. 2010;106: 598,607. © 2010 Wiley Periodicals, Inc. [source] Impaired virus-induced interferon-,2 release in adult asthmatic patientsCLINICAL & EXPERIMENTAL ALLERGY, Issue 3 2006K. Gehlhar Summary Background Interferon-, (IFN-,) not only serves as a first defence line of the immune system against viral attacks but also interacts with T-helper type 1 (Th1)/ T-helper type 2 (Th2) regulation and various other cell types like basophils and monocytes, thereby linking innate and acquired immunity. Recently, we demonstrated that children with allergic asthma produced significantly lower amounts of virus-induced IFN-,2 compared with healthy children or those with intrinsic asthma. Objective In this study, we extend our analysis to examine in a cohort study whether IFN-,2 is also reduced in allergic asthma of adults. Methods Adults with allergic asthma and healthy controls were prospectively recruited. Blood cultures were stimulated with different viruses (respiratory syncytial virus (RSV), newcastle disease virus (NDV)) and analysed for IFN-,2 protein release and gene transcription. Results Virus-induced IFN-,2 release from blood cells of allergic asthmatic patients was significantly reduced compared with healthy controls, independent of the virus used (NDVasthma=221±134 pg/mL, NDVhealthy=555±341 pg/mL, P=0.003 and RSVasthma=46±27 pg/mL, RSVhealthy=108±90 pg/mL, P=0.014). Values=mean±standard deviation). It was not influenced by medication, especially cortico-steroids. IFN-,2 mRNA expression 5 h after NDV stimulation confirmed the ELISA results and correlated well with release data (r=0.397, P=0.033). Conclusion Like children, adults with allergic asthma show impaired virus-induced IFN-,2 release in whole blood, indicating a systemic phenomenon in patients with bronchial asthma and atopic phenotype. Impaired virus-induced IFN-, release could be a marker of inflammation in chronic allergic asthma. [source] | |||||||||||||