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Virus Spread (virus + spread)
Selected AbstractsEpidemiology of Plum pox virus strain M in GreeceEPPO BULLETIN, Issue 2 2006C. Varveri Plum pox virus has been endemic in Greece since 1967 causing important losses in apricot and to a lesser extent in peach crops. A survey undertaken in 1992 in public and private mother-tree plantations to estimate its incidence revealed that the virus was absent in isolated areas far from commercial stone-fruit crops. Virus titers decrease significantly during the hot months in the infected trees but re-increase in October,November permitting reliable detection. It is virulent M-type isolates which are effectively transmitted by aphids that are mostly recovered. Aphis gossypii and Hyalopterus pruni were the most abundant virus vectors captured during the small scale monitoring undertaken in apricot orchards in 1999 and 2000. Virus spread was monitored in two apricot orchards from 1996 to 2000 and analysed. Initial infections followed a completely random spatial pattern, while loose clusters appeared in succeeding years, to finally reach a uniform distribution representing high infection levels. The nearby ecological conditions greatly affected the rate of disease development. [source] A new and efficient method for inhibition of RNA viruses by DNA interferenceFEBS JOURNAL, Issue 16 2009Monika Nowak We report here a new method for inhibition of RNA viruses induced by dsDNA. We demonstrated that both long dsDNA molecules and short interfering DNA with a sequence complementary to that of viral RNA inhibited tobacco mosaic virus expression and prevented virus spread. Also, the expression of the HIV-1 gp41 gene in HeLa cells was inhibited by complementary short interfering DNA. We showed that Dicer processed dsDNA, which suggests activation of the cellular machinery involved in silencing of RNA. For the silencing of viral RNA effected with dsDNA, we coined the term DNA interference technology. [source] Interferon regulatory factor-3 activation, hepatic interferon-stimulated gene expression, and immune cell infiltration in hepatitis C virus patients,HEPATOLOGY, Issue 3 2008Daryl T.-Y. Interferon regulatory factor-3 (IRF-3) activation directs ,/, interferon production and interferon-stimulated gene (ISG) expression, which limits virus infection. Here, we examined the distribution of hepatitis C virus (HCV) nonstructural 3 protein, the status of IRF-3 activation, and expression of IRF-3 target genes and ISGs during asynchronous HCV infection in vitro and in liver biopsies from patients with chronic HCV infection, using confocal microscopy and functional genomics approaches. In general, asynchronous infection with HCV stimulated a low-frequency and transient IRF-3 activation within responsive cells in vitro that was associated with cell-to-cell virus spread. Similarly, a subset of HCV patients exhibited the nuclear, active form of IRF-3 in hepatocytes and an associated increase in IRF-3 target gene expression in hepatic tissue. Moreover, ISG expression profiles formed disease-specific clusters for HCV and control nonalcoholic fatty liver disease patients, with increased ISG expression among the HCV patients. We identified the presence of T cell and plasmacytoid dendritic cell infiltrates within all biopsy specimens, suggesting they could be a source of hepatic interferon in the setting of hepatitis C and chronic inflammatory condition. Conclusion: These results indicate that HCV can transiently trigger IRF-3 activation during virus spread and that in chronic HCV, IRF-3 activation within infected hepatocytes occurs but is limited. (HEPATOLOGY 2007.) [source] Combining adenoviral oncolysis with temozolomide improves cell killing of melanoma cellsINTERNATIONAL JOURNAL OF CANCER, Issue 12 2007Christina Quirin Abstract Oncolytic Adenoviruses are emerging agents for treatment of cancer by tumor-restricted virus replication, cell lysis and virus spread. Clinical studies with first generation oncolytic adenoviruses have revealed that an increased potency is warranted in order to achieve therapeutic efficacy. One approach towards this end is to combine adenoviral oncolysis with chemotherapy. Here, a fundamental requirement is that chemotherapy does not interfere with adenovirus replication in cancer cells. We have previously developed a melanoma-targeted oncolytic adenovirus, Ad5/3.2xTyr, which features tyrosinase promoter regulated replication and enhanced cell entry into melanoma cells. In this study, we investigated a combination treatment of melanoma cells with Ad5/3.2xTyr and temozolomide (TMZ), which produces the same active metabolite as Dacarbazine/DTIC, the standard chemotherapy for advanced melanoma. We report that TMZ does not inhibit adenovirus replication in melanoma cells. Additive or synergistic cell killing of melanoma cells, dependent on the cell line used, was observed. Enhanced cell binding was not responsible for synergism of adenoviral oncolysis and TMZ treatment. We rather observed that higher numbers of virus genomes are produced in TMZ-treated cells, which also showed a cell cycle arrest in the G2 phase. Our results have important implications for the clinical implementation of adenoviral oncolysis for treatment of malignant melanoma. It suggests that such studies are feasible in the presence of TMZ or DTIC chemotherapy and recommends the investigation of a viro-chemo combination therapy. © 2007 Wiley-Liss, Inc. [source] Barley yellow dwarf viruses (BYDVs) preserved in herbarium specimens illuminate historical disease ecology of invasive and native grassesJOURNAL OF ECOLOGY, Issue 6 2007CAROLYN M. MALMSTROM Summary 1In plant invasion ecology, viruses and other pathogens are often considered in terms of the enemy release hypothesis, which predicts that plants become invasive in new ranges if they escape pathogens from their home range. However, pathogens may sometimes facilitate host spread rather than hinder it. 2Previously, we hypothesized that apparent competition mediated by barley and cereal yellow dwarf viruses (Luteoviridae: BYDVs, CYDVs) may have facilitated historical grassland invasion in California, USA, where Eurasian grasses displaced native grasses in the 18th and 19th centuries (the disease facilitation hypotheses). However, this could have happened only if the viruses were present during the invasion, which is unknown. 3To investigate the historical ecology of BYDVs in California grasses, we analysed preserved virus infections in herbarium specimens and used the historical virus sequences to determine rough time estimates of relevant phylogenetic events. 4The historical viral RNA sequences we identified in invasive and native grasses date from 1917 and are among the oldest recovered from plants thus far and the oldest from North America. 5Herbarium evidence and phylogenetic analysis suggest that BYDVs were likely to have been present in wild grasses during the California grassland invasion and to have shared some functional characteristics with present-day isolates, supporting the disease facilitation hypothesis. 6We found evidence of virus spread from California to Australia (or, less likely, from Australia to California) in the late 19th century, when much horticultural exchange occurred, as well as potential correspondence in the timing of virus diversification events and the beginning of extensive human exchange between the Old and New Worlds. 7Synthesis. Increasing evidence indicates that viruses are important in the ecology of grasslands and may, in some cases, mediate apparent competition among species. Historical data provide essential insight into plant virus ecology and suggest the need to examine human influence on plant virus diversification and spread within natural ecosystems. [source] The effect of drought stress and temperature on spread of barley yellow dwarf virus (BYDV)AGRICULTURAL AND FOREST ENTOMOLOGY, Issue 3 2000I. N. Smyrnioudis Summary 1 The effect of drought stress and temperature on the dispersal of wingless aphids Rhopalosiphum padi (L.) and the pattern of spread of BYDV (barley yellow dwarf virus) within wheat plants in controlled environment chambers was quantified. Combinations of three different drought stress levels, unstressed, moderate and high stress level, and three different temperatures, 5 ± 1 °C, 10 ± 1 °C, and 15 ± 1 °C, were investigated. 2 With increased temperature there was an increase in the mean distance of visited plants from the point of release and in the number of plants visited and infected with BYDV. Drought stress had no effect on mean distance moved by aphids at any temperature or on plants infected with virus at 10 °C and 5 °C. When plants were drought stressed, the numbers of plants visited and infected were greater at 15 °C than at 10 °C and 5 °C. 3 A greater proportion of plants visited by aphids was infected with BYDV when plants were stressed than when not stressed. At 15 °C a greater proportion of these plants was infected than at lower temperatures. There was no difference between treatments in the numbers of aphids present at the end of the experiment. 4 It is concluded that drought stress and temperature are of considerable importance in virus spread. [source] Local expression of enzymatically active class I ,-1, 3-glucanase enhances symptoms of TMV infection in tobaccoTHE PLANT JOURNAL, Issue 3 2001Gregor L. Bucher¶ Summary Mutant tobacco plants deficient for class I ,-1,3-glucanase (GLU I) are decreased in their susceptibility to virus infection. This is correlated with delayed virus spread, a reduction in the size exclusion limit of plasmodesmata and increased cell-wall deposition of the ,-1,3-glucan callose. To further investigate a role of GLU I during cell-to-cell movement of virus infection, we inserted the GLU I coding sequence into TMV for overexpression in infected cells. Compared with the size of local lesions produced on plants infected with virus expressing either an enzymatically inactive GLU I or a frameshift mutant of the gene, the size of local lesions caused by infection with virus expressing active GLU I was consistently increased. Viruses expressing antisense GLU I constructs led to lesions of decreased size. Similar effects were obtained for virus spread using plants grown at 32°C to block the hypersensitive response. Together, these results indicate that enzymatically active GLU I expressed in cells containing replicating virus can increase cell-to-cell movement of virus. This supports the view that GLU I induced locally during infection helps to promote cell-to-cell movement of virus by hydrolyzing callose. Moreover, our results provide the first direct evidence that a biological function of a plant ,-1,3-glucanase depends on its catalytic activity. [source] Breeding for resistance to whitefly-transmitted geminivirusesANNALS OF APPLIED BIOLOGY, Issue 2 2002MOSHE LAPIDOT Summary Geminiviruses comprise a large and diverse family of viruses that infect a wide range of important monocotyledonous and dicotyledonous crop species and cause significant yield losses. The family Geminiviridae is divided into three genera, one of which is Begomovirus. Species of this genus are transmitted by the whitefly Bemisia tabaci in a persistent, circulative manner and infect dicotyledonous plants. Severe population outbreaks of B. tabaci are usually accompanied by a high incidence of begomoviruses. During the last two decades, there has been a worldwide spread of the B biotype of B. tabaci, accompanied by the emergence of whitefly-transmitted geminiviruses. Control measures in infected regions are based mainly on limitation of vector populations, using chemicals or physical barriers. However, under conditions of severe whitefly attack, none of these control measures has sufficed to prevent virus spread. Thus, the best way to reduce geminivirus damage is by breeding crops resistant or tolerant to the virus, either by classical breeding or by genetic engineering. A number of begomoviruses have been the subject of much investigation, due to their severe economic impact. This review considers the most severe viral diseases of four major crops (tomato, bean, cassava and cotton). The approaches taken to breed for resistance to these viral diseases should provide a perspective of the issues involved in breeding for begomovirus resistance in crop plants. [source] Pathogenesis of equine herpesvirus-1 infection in the mouse modelAPMIS, Issue 1 2009GEORG GOSZTONYI Equine herpesvirus-1 (EHV-1) is a major equine pathogen causing respiratory diseases, abortions and severe neurological disorders. The basis of neurological disturbances is, as in other organs, infection of endothelial cells, followed by vasculitis, thrombosis and ischaemic damage of the parenchyma. Here, a murine model was used to explore the mechanism of entry to, and spread within the brain, the cell affinity of the agent and the modulating role of the immune defence, which are all factors governing the pathogenesis of the neurological disease. Because controversial views exist about these mechanisms, we undertook a neuropathological study with intranasally infected adult mice. EHV-1 entered the brain through the olfactory neuroepithelium and along the olfactory nerves, and spread transsynaptically in rostro-caudal direction, using olfactory and limbic neuronal networks. Exclusively neurons were infected. The cellular immune reaction exerted a restraining effect on virus dissemination. Following nasal infection, the olfactory route was the major pathway for virus entry and dissemination, involvement of the trigeminal nerve in virus spread seems much less probable. In the adult mouse brain EHV-1 behaves as a typical neurotropic agent, using, similarly to other herpesviruses, the neuronal networks for dissemination. Vasculitis, the predominant type of lesion in natural infection, and endothelial cell positivity for EHV-1 were detectable only in the lung. Thus, this agent exhibits in the mouse a dual affinity: it is neurotropic in the brain, and endotheliotropic in visceral organs. Consideration of pathogenetic aspects of equine and experimental murine EHV-1 infections also helps a better understanding of human herpetic brain disease. [source] Non-invasive imaging of mouse hepatitis coronavirus infection reveals determinants of viral replication and spread in vivoCELLULAR MICROBIOLOGY, Issue 5 2009Matthijs Raaben Summary Bioluminescence imaging (BLI) is a powerful new method to study virus dissemination in the live animal. Here we used this method to monitor the spatial and temporal progression of mouse hepatitis coronavirus (MHV) infection in mice using luciferase-expressing viruses. Upon intranasal inoculation, virus replication could initially be observed in the nasal cavity and the cervical lymph nodes, after which the infection spread to the brain and frequently to the eyes. The kinetics of virus spread to and clearance from the brain appeared to depend on the inoculation dose. After intraperitoneal inoculation, virus replication was predominantly observed in the liver and occasionally in the intestines, but interestingly also in the tail and paws. BLI thus elucidated new anatomic locations of virus replication. Furthermore, MHV dissemination was shown to be critically depended on the viral spike protein, but also on the mouse strain used. Widespread dissemination was observed in mice lacking a functional type I interferon response. The importance of the type I interferon system in limiting viral spread was also demonstrated by the administration of type I interferons to mice. Our results provide new insights in coronavirus pathogenesis and demonstrate the potential of BLI to study coronavirus,host interactions in vivo. [source] Antibody response to influenza infection of mice: different patterns for glycoprotein and nucleocapsid antigensIMMUNOLOGY, Issue 4 2003Robert Sealy Summary Our previous studies of C57BL/6 mice intranasally infected with influenza virus (A/PR8) revealed a spike of virus-specific immunoglobulin A (IgA)-secreting antibody-forming cells (AFC) in the mediastinal lymph node (MLN) 7 days post-infection. Here we show that these AFC are directed only against viral glycoprotein, and not nucleocapsid antigens. The early IgA spike associates with a decline in glycoprotein-specific AFC during week 2 post-infection. In contrast to the glycoprotein-specific AFC, nucleocapsid-specific, IgA-secreting AFC develop gradually in the MLN and persist for more than 3 weeks post-infection. As peripheral lymph node reactions wane, the nucleocapsid-specific AFC appear as long-sustained populations in the bone marrow. Microanatomical examination of the respiratory tract in infected mice shows foci of infection established in the lung 2 days post-infection, from which virus spreads to infect the entire lining of the trachea by day 3. At this time, viral haemagglutinin can be seen within the MLN, probably on projections from infected dendritic cells. This feature disappears within a day, though viral antigen expression continues to spread throughout the respiratory tract. Total IgA- and IgG-secreting AFC appear histologically in large numbers during the first week post-infection, significantly preceding the appearance of germinal centres (revealed by peanut agglutinin staining in week 2). To explain these results, we suggest that the initial immunogenic encounter of B cells with viral antigens occurs about 3 days post-infection in the MLN, with antigens transported by dendritic cells from airway mucosa, the only site of viral replication. Viral glycoproteins expressed as integral membrane components on the surface of infected dendritic cells [probably in the absence of cognate T helper (Th) cells] promote members of expanding relevant B-cell clones to undergo an IgA switch and terminal local plasmacytoid differentiation. Anti-glycoprotein specificities are thus selectively depleted from progeny of activated B-cell clones which are channelled to participate in germinal centre formation (perhaps by cognate T helper cells when they become sufficiently frequent). One product of the germinal centre reaction is the long-sustained, bone marrow-resident population, which is accordingly rich in anti-nucleoprotein, but not anti-glycoprotein specificities. Of note, we find that AFC responses toward influenza virus and Sendai virus differ, even though viral replication is limited to the airway mucosa in each case. The response towards Sendai virus exhibits neither the early appearance of anti-glycoprotein AFC expressing IgA in draining lymph nodes, nor the subsequent relative deficit of this specificity from bone marrow AFC populations. [source] | |||||||||||||