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Virus Induction (virus + induction)
Selected AbstractsMaternal environment affects endogenous virus induction in the offspring of type 1 diabetes model non-obese diabetic miceCONGENITAL ANOMALIES, Issue 3 2005Yukiko Kagohashi ABSTRACT Type 1 diabetes results from the destruction of pancreatic b-cells (insulitis). It is a multifactorial disease involving genetic and environmental factors, including the maternal environment. Viruses have also been implicated in the pathogenesis of human type 1 diabetes as well as in its model non-obese diabetic (NOD) mice during the perinatal period, as endogenous viruses and/or as infectious agents vertically transmitted from mothers. However, the role of virus as genetic or environmental factor and its interaction with other maternal factors remain unclear. In a series of experiments, we transplanted preimplantation-stage NOD embryos into the uterus of recipient Institute of Cancer Research (ICR) mice, which are without diabetic genetic predisposition, and NOD mice, which did not exhibit overt diabetes during the experiment, and designated offspring as NOD/ICR and NOD/NOD, respectively. We previously observed that NOD/ICR offspring developed insulitis significantly earlier than NOD/NOD offspring. To assess the role of viruses in the development of insulitis, we examined the appearance of viral particles and expression of retroviruses between NOD/ICR and NOD/NOD. NOD/ICR showed earlier expression of env region of the xenotropic type C retrovirus by polymerase chain reaction analysis than NOD/NOD, while the retrovirus-like particles were observed in the islet b-cells similarly in both groups by electron microscopy. Serum corticosterone level, which is suggested to enhance retroviral induction, was significantly higher in the ICR than in the NOD surrogate mothers. These findings suggest that the observed virus is endogenous and that maternal environmental factors, including hormone levels, affect the induction of endogenous viruses and cause the earlier onset of insulitis. [source] Respiratory virus induction of alpha-, beta- and lambda-interferons in bronchial epithelial cells and peripheral blood mononuclear cellsALLERGY, Issue 3 2009M. R. Khaitov Background:, Respiratory viruses, predominantly rhinoviruses are the major cause of asthma exacerbations. Impaired production of interferon-, in rhinovirus infected bronchial epithelial cells (BECs) and of the newly discovered interferon-,s in both BECs and bronchoalveolar lavage cells, is implicated in asthma exacerbation pathogenesis. Thus replacement of deficient interferon is a candidate new therapy for asthma exacerbations. Rhinoviruses and other respiratory viruses infect both BECs and macrophages, but their relative capacities for ,-, ,- and ,-interferon production are unknown. Methods:, To provide guidance regarding which interferon type is the best candidate for development for treatment/prevention of asthma exacerbations we investigated respiratory virus induction of ,-, ,- and ,-interferons in BECs and peripheral blood mononuclear cells (PBMCs) by reverse transferase-polymerase chain reaction and enzyme-linked immunosorbent assay. Results:, Rhinovirus infection of BEAS-2B BECs induced interferon-, mRNA expression transiently at 8 h and interferon-, later at 24 h while induction of interferon-, was strongly induced at both time points. At 24 h, interferon-, protein was not detected, interferon-, was weakly induced while interferon-, was strongly induced. Similar patterns of mRNA induction were observed in primary BECs, in response to both rhinovirus and influenza A virus infection, though protein levels were below assay detection limits. In PBMCs interferon-,, interferon-, and interferon-, mRNAs were all strongly induced by rhinovirus at both 8 and 24 h and proteins were induced: interferon-,>-,>-,. Thus respiratory viruses induced expression of ,-, ,- and ,-interferons in BECs and PBMCs. In PBMCs interferon-,>-,>-, while in BECs, interferon-,>-,>-,. Conclusions:, We conclude that interferon-,s are likely the principal interferons produced during innate responses to respiratory viruses in BECs and interferon-,s in PBMCs, while interferon-, is produced by both cell types. [source] Everyone comes from somewhere: Systemic lupus erythematosus and Epstein-Barr virus induction of host interferon and humoral anti,Epstein-Barr nuclear antigen 1 immunityARTHRITIS & RHEUMATISM, Issue 6 2010John B. Harley First page of article [source] | ||||||||||