Thesis (Ph.D.)--University of Nebraska-Lincoln, 2006. / Title from title screen (site viewed May 23, 2007). PDF text: iv, 165 p. : ill. (some col.) ; 1.95Mb UMI publication number: AAT 3237062. Includes bibliographical references. Also available in microfilm and microfiche formats.

The part of RNA2 genome segment of several isolates of Radish mosaic virus (RaMV) including capsid protein genes was sequenced. Variability of capsid protein genes among the isolates of Radish mosaic virus was studied.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 5 uppsatser.

The aim of this study was to examine the effect of tick infection with tick-borne encephalitis virus on its behaviour and development. The effect of infection on feeding performance, metamorphosis, locomotion or phototaxis was analysed. Despite the fact that we were not able to demonstrate any significant effect of infection on tick behaviour, the obtained results contribute to understanding transmission dynamics of the virus during tick life cycle including co-feeding and transovarial transmission.

An influenza is an illness annually affecting 5-15 percent of the world population. During the influenza pandemy 40-50 percent of world population can be affected and millions of people can die.The measures resulting from the pandemic plans help to limit the influenza virus spreading, to reduce morbidity and mortality. In April 2009 the first cases of the flue pandemic caused by Pandemic A (H1N1) 2009 virus occurred on the American continent, in the Czech Republic there was the first case registered in May, in the Pilsen region in July. Based on these facts I decided to assess the pandemic plans at the level of the Pilsen region and to analyse the course of the pandemy in the Pilsen region too. Having studied the Pandemic plan of the Pilsen region and the Pandemic plan of the Regional Hygiene Station of the Pilsen Region I got to the conclusion that in case of the pandemy caused by the highly virulent tribe of the influenza it would not be possible to use up the pandemic plans efficiently. The disadvantages concern mainly the way of the distribution of the pandemic vaccine and antivirotics. The other disadvantage is the absence of a parenteral form of antivirotics. A bad awarness of the inhabitants also came out effecting mass rejection of vaccination by the pandemic vaccine and preventative taking antivirotics. The analyse of the course of the pandemy in the Pilsen region proved that at many patients with the flue pandemic there was present a risky factor of more serious course of the influenza in the anamnesis. If these patients had been vaccinated by the pandemic vaccine they had been entitled for, they could have been protected against this illness, for some of them the vaccination might have meant life-saving. It was also proved that originally the pandemic tribe of Pandemic A (H1N1) 2009 virus became the causer of the common seasonal influenza in the season of 2010-2011.

Le circovirus porcin de type 2 (PCV2) est un pathogène majeur pour l’industrie porcine et est associé à une longue liste de maladies associées au circovirus porcin (MACVP). Les premières tentatives pour reproduire ces maladies ont montré que le virus doit être combiné à d’autres agents pathogènes du porc ou à différents stimulants du système immunitaire. De ces agents, le virus du syndrome reproducteur et respiratoire porcin (VSRRP) est celui qui est le plus souvent co-isolé avec le PCV dans les fermes. Une grande partie des efforts faits pour étudier les interactions entre ces deux virus ont été menés in vivo. Les interactions in vitro ont jusqu’à maintenant été peu étudiées du fait qu’il n’existe pas de modèle cellulaire permettant la réplication efficace des deux virus. L’objectif de ce projet était donc de développer un modèle cellulaire propice à la réplication des deux virus et d’étudier leur interaction en co-infection. Une lignée cellulaire provenant de la trachée d’un porcelet nouveau-né (NPTr), permissive au PCV, a été génétiquement modifiée pour exprimer la protéine CD163, un récepteur majeur du VSRRP. Ce projet a montré que cette nouvelle lignée cellulaire (NPTr-CD163) est permissive au VSRRP ainsi qu’à plusieurs génotypes de PCV (PCV1, PCV2a, PCV2b et PCV1/2a). De plus, les résultats obtenus lors d’infections mixtes suggèrent que la réplication du VSRRP et du PCV conditionne de façon génotype-dépendante celle du PCV puisque la réplication du PCV1 est inhibée en présence de VSRRP, alors que celle du PCV2b est significativement augmentée dans les mêmes conditions. Ni la mortalité cellulaire, ni la réponse cellulaire en cytokines n’a permis d’expliquer ces résultats. La modulation de la réplication du PCV par le VSRRP serait donc liée à un mécanisme spécifique qui demeure inconnu. De plus, cet effet varierait en fonction du génotype de PCV. / Porcine circovirus (PCV) type 2 (PCV2) is a major pathogen in the swine industry and has been described as the causative agent of a long list of conditions under the designation of porcine circovirus-associated diseases (PCVAD). Attempts to replicate PCVAD initially failed, as it was discovered that an immune trigger could facilitate the reproduction of clinical signs, either by co-infecting with other swine pathogens or using immune stimulants. Of these, porcine reproductive and respiratory syndrome virus (PRRSV) is the most frequently co-isolated agent in the field. Most effort has been made to understand this interaction in vivo since most in vitro cellular models lack the ability to efficiently replicate both viruses. To answer the lack of an in vitro model, we developed a cell line that allows the replication of both PRRSV and PCV. A neonate porcine tracheal cell line (NPTr) was genetically modified to stably express CD163 (NPTr-CD163), a major PRRSV receptor. NPTr-CD163 cells were able to replicate all PCV genotypes (PCV1, PCV1/2a, PCV2a and PCV2b) and PRRSV. A significant effect of PRRSV on PCV replication was found to be genotype dependent, as PCV1 replication was down regulated in the presence of PRRSV and PCV2b replication was up regulated in the same conditions. Neither cell mortality assays nor cytokine expression analysis were able to provide an explanation for these results. The effect of PRRSV on PCV1 and PCV2b replication is suggestive of a more specific, yet still unknown, mechanism. Furthermore, this effect is PCV-genotype dependant.

Le circovirus porcin de type 2 (PCV2) est un pathogène majeur pour l’industrie porcine et est associé à une longue liste de maladies associées au circovirus porcin (MACVP). Les premières tentatives pour reproduire ces maladies ont montré que le virus doit être combiné à d’autres agents pathogènes du porc ou à différents stimulants du système immunitaire. De ces agents, le virus du syndrome reproducteur et respiratoire porcin (VSRRP) est celui qui est le plus souvent co-isolé avec le PCV dans les fermes. Une grande partie des efforts faits pour étudier les interactions entre ces deux virus ont été menés in vivo. Les interactions in vitro ont jusqu’à maintenant été peu étudiées du fait qu’il n’existe pas de modèle cellulaire permettant la réplication efficace des deux virus. L’objectif de ce projet était donc de développer un modèle cellulaire propice à la réplication des deux virus et d’étudier leur interaction en co-infection. Une lignée cellulaire provenant de la trachée d’un porcelet nouveau-né (NPTr), permissive au PCV, a été génétiquement modifiée pour exprimer la protéine CD163, un récepteur majeur du VSRRP. Ce projet a montré que cette nouvelle lignée cellulaire (NPTr-CD163) est permissive au VSRRP ainsi qu’à plusieurs génotypes de PCV (PCV1, PCV2a, PCV2b et PCV1/2a). De plus, les résultats obtenus lors d’infections mixtes suggèrent que la réplication du VSRRP et du PCV conditionne de façon génotype-dépendante celle du PCV puisque la réplication du PCV1 est inhibée en présence de VSRRP, alors que celle du PCV2b est significativement augmentée dans les mêmes conditions. Ni la mortalité cellulaire, ni la réponse cellulaire en cytokines n’a permis d’expliquer ces résultats. La modulation de la réplication du PCV par le VSRRP serait donc liée à un mécanisme spécifique qui demeure inconnu. De plus, cet effet varierait en fonction du génotype de PCV. / Porcine circovirus (PCV) type 2 (PCV2) is a major pathogen in the swine industry and has been described as the causative agent of a long list of conditions under the designation of porcine circovirus-associated diseases (PCVAD). Attempts to replicate PCVAD initially failed, as it was discovered that an immune trigger could facilitate the reproduction of clinical signs, either by co-infecting with other swine pathogens or using immune stimulants. Of these, porcine reproductive and respiratory syndrome virus (PRRSV) is the most frequently co-isolated agent in the field. Most effort has been made to understand this interaction in vivo since most in vitro cellular models lack the ability to efficiently replicate both viruses. To answer the lack of an in vitro model, we developed a cell line that allows the replication of both PRRSV and PCV. A neonate porcine tracheal cell line (NPTr) was genetically modified to stably express CD163 (NPTr-CD163), a major PRRSV receptor. NPTr-CD163 cells were able to replicate all PCV genotypes (PCV1, PCV1/2a, PCV2a and PCV2b) and PRRSV. A significant effect of PRRSV on PCV replication was found to be genotype dependent, as PCV1 replication was down regulated in the presence of PRRSV and PCV2b replication was up regulated in the same conditions. Neither cell mortality assays nor cytokine expression analysis were able to provide an explanation for these results. The effect of PRRSV on PCV1 and PCV2b replication is suggestive of a more specific, yet still unknown, mechanism. Furthermore, this effect is PCV-genotype dependant.

Most viruses can infect only a reduced range of organisms and an effective replication is possible only in selected hosts. These hosts are called permissive for the virus. Molecular principles of a nonpermissiveness and viral mechanisms of overcoming replication obstacles are still not clearly elucidated. This thesis discusses the molecular causes of the cellular nonpermissiveness against a model retrovirus - Rous sarcoma virus. The research is conducted on duck cells which are semipermis- sive to the subgroup C of Rous sarcoma virus. The virus can enter those cells, but it is not able to produce enough infectious viral progeny. Two blocks of the viral replication cycle in the duck cells are described in the thesis. The first one is the probably not optimal cellular receptor recognition. The second one is in the late phase of the replication cycle when the viral proteins are synthesized. The amount of the envelope glyco- protein coding mRNA is reduced due to the altered splicing ratios, and the virions produced from the duck cells are less infectious. This block is recessive and can be partially omitted by cell fusions with permissive chicken cells; therefore, the block is not caused by specific restriction fac- tors in sensu stricto. Additionally, the influence of mutations in duck adapted Rous...

One of the important tasks of virology and immunology is to explore the species- and cell-barriers preventing virus horizontal transmission and reveal the ways how viruses overcome these barriers and "adapt" to different species. This work is based on a well- established retroviral model - avian Rous sarcoma virus (RSV) and studies virus replication blocks in mammalian cells at both pre- and post-integration level. Interaction of the viral envelope glycoprotein (Env) with a specific cellular receptor mediates virus entry into cells. Although mammalian orthologues of specific chicken receptors do not support RSV entry, it was observed that some RSV strains are able to enter mammalian cells. Several RSV-transformed rodent cells lines were described and analysis of provirus H20- RSV in one these cells lines (hamster H-20 tumor cell line) showed multiple mutations including two crucial amino acid substitutions in different regions of Env. Substitutions D32G and L378S confer virus transmission to hamster, human and also chicken cells lacking the appropriate receptor. Altered conformation of H20-RSV Env is similar to a receptor-primed (activated) state of Env. This observation indicates that virus can circumvent the need of original cell receptor because of spontaneous Env activation caused by single...

This dissertation is a challenge to the Pentecostal churches, particularly, the Apostolic Faith Mission Church in Tumahole, to take an action in meeting the challenges posed by HIV/AIDS. This disease, HIV/AIDS, is the latest enemy to human life that the nations are faced with. In the newspapers like Sowetan, there is an article almost daily about HIV and AIDS. In this dissertation, I have tried to show shocking figures of how this disease is spreading in Africa. The seriousness of the disease, unlike other diseases, is its in curability. The secular organisations are far ahead of the churches in as far as the relevant programmes on combating HIV/AIDS are concerned. Despite these massive programmes, the disease is spreading like the wild fire. Deducing from this background, it is no longer the question of whether the Pentecostal churches have any role to play, but what specific role should the church play in this challenge. In this challenging times, many people look at the church as one of the most important institute that would play a positive role in bringing hope to the hopeless. / Christian Spirituality, Church History and Missiology / M. Th. (Missiology (Urban Ministry))