The purpose of this study has been to examine a few Swedish advertisment producers opinions on the subject of viral advertising and especially the ethical aspects of hidden viral advertising. The specified purpose of this paper is to: To clarify the underlying reasons for the use of viral advertising. To clarify the advertising producers ethical views on hidden viral advertising. The essay is based on a qualitive research metod of an abductive nature where the empirical data is derived from interviews with three advertisment producers. Through a stratified selection method we contacted agencies that in one way or another uses digital solutions as an advertisment method. All interviews were conducted via the digital chat room Skype, one of the interviews were conducted with both picture and sound and the other two with audio-only. The following points are the essential conclusions of our study: Hidden viral advertising is seen as a rare promotional method in Sweden today, however, the viral-spread effect is more commonly used. The economic factors together with the spreading capacity of the viral advertising is contributing to one of the biggest reasons behind the use of viral advertising. In addition to these, viral advertising is seen as an effective way to stand out from traditional advertising. Viral advertising where the sender is hidden or unclear is always seen as unethical. It is not seen as unethical to spread advertisements through social media as long as the sender is apparent. To produce viral advertising with the intent of generating effective spread is seen as ethically acceptable as long as the sender is apparent. The openness of the Internet creates an opportunity for the consumer to criticice questionable advertising unimpeded, this means that hidden viral advertisment is not seen as a sustainable approach in the long run.

Viruses represent the most abundant biological entities on earth where, they are able to interact with all kingdoms of life. Yet their diversity, ecology and evolutionary aspects are only beginning to be fully elucidated, mainly due to technical limitations. The vast majority of the microbial world remains elusive to culture; more than 90% of genome sequenced viral isolates infect only 5 of the 54 prokaryotic phyla that are currently recognized. In contrast, viral metagenomics bypasses the need for cultures by directly sequencing fragmented genetic material of environmental viral communities. This dissertation uses viral metagenomics by applying well-tested bioinformatic protocols and expanding them to compare and contrast patterns of diversity, richness and specialization of large viral metagenomic datasets, in both local and global scales. First I demonstrate the utility of a functional-based perspective by adopting the protein cluster environment to estimate global viral diversity. Then, I use this PC approach to analyze metagenomes from two ecologically different environments, which by uncovering local gene specialization showcases the adequacy of a gene-centered workflow. Then I continue to expand upon this PC framework to study the Tara Oceans virome analyses of these data reveal patters of diversity that support a seed bank model. Finally, in search of a more meaningful ecological unit, I move from a gene-centered standpoint towards a population-based frame. We adopted a novel metagenomic technique that allowed me to uncover the discontinuity in the genomic sequence space, thus empirically defining a population. This final contribution will allow to sort and count viral communities, the first step to applying ecological and evolutionary theory.

Chronic viral infection is a significant burden on healthcare systems worldwide. Robust anti-viral immune responses are essential for viral clearance. Persistent viruses use a variety of mechanisms to evade immune surveillance including the upregulation of host immunesuppressive factors. Secreted fibrinogen-like protein 2 (FGL2) has been identified as an inhibitory effector molecule in suppressing immune responses in patients with chronic hepatitis C virus (HCV) and hepatitis B virus (HBV) disease. In a murine model of chronic infection caused by Lymphocytic choriomeningitis virus (LCMV) clone 13, we demonstrate that mice deficient in Fgl2 have increased numbers of mature antigen-presenting cells (APC), improved virus-specific cytotoxic T cell immunity and enhanced viral clearance when compared to wild-type mice. These results highlight the importance of the FGL2 inhibitory pathway in immune evasion and provide a rationale to investigate the effects of blocking FGL2 as a novel immune therapeutic in patients suffering from persistent infections.

Chronic viral infection is a significant burden on healthcare systems worldwide. Robust anti-viral immune responses are essential for viral clearance. Persistent viruses use a variety of mechanisms to evade immune surveillance including the upregulation of host immunesuppressive factors. Secreted fibrinogen-like protein 2 (FGL2) has been identified as an inhibitory effector molecule in suppressing immune responses in patients with chronic hepatitis C virus (HCV) and hepatitis B virus (HBV) disease. In a murine model of chronic infection caused by Lymphocytic choriomeningitis virus (LCMV) clone 13, we demonstrate that mice deficient in Fgl2 have increased numbers of mature antigen-presenting cells (APC), improved virus-specific cytotoxic T cell immunity and enhanced viral clearance when compared to wild-type mice. These results highlight the importance of the FGL2 inhibitory pathway in immune evasion and provide a rationale to investigate the effects of blocking FGL2 as a novel immune therapeutic in patients suffering from persistent infections.

No description available.

Vaccinia virus (VV) is a large DNA virus belonging to the Orthopoxvirus family. The viral replicative life cycle takes place solely within the cytoplasm of a mammalian host cell. The VV genome contains 196 open reading frames which are expressed in a highly regulated and temporal fashion in order to bring about the production of a mature virion. In the process of viral replication many VV proteins are synthesized that require posttranslational modifications to become functional. A few of these modifications include, glycosylation, ADP-ribosylation, phosphorylation, fatty acid acylation, and proteolytic processing. This last modification is especially important with regard to the structural proteins of the virus in that they undergo prysis for an infectious virus particle to be formed, a common theme in viral systems. In order to understand these events in more detail, three abundant virion protein constituents 4a, 4b, and 25K were chosen as models for study. The three main questions we wanted to answer were: Is there a cleavage consensus site within the precursors, what protease(s) and/or factors are necessary for the process, and how are the events regulated in vivo? Our approach included development of specific immunological reagents to identify cleavage products as well as to show where these core proteins are located during virion assembly. We have subsequently identified cleavage products by N-terminal microsequence from each of the three structural proteins and this information has elucidated a putative cleavage consensus site of Ala-Gly- X, where cleavage is proposed to take place between the Gly and X and X is usually an aliphatic residue. The immunological reagents were used in conjunction with immunofluorescent and immunogold labeling analyses to identify the location of these core proteins during virion assembly. Core proteins were localized to the virosomes in VV infected cells, to the viroplasm of immature virus particles, and to the center of mature virions. Precursor specific antiserum indicated that the larger molecular weight precursors of core proteins are within immature virions as well. From these results the following conclusions can be made. Identification of a putative cleavage consensus site suggests that proteolytic processing is an endoproteolytic event. The observation that precursor structural proteins were found within immature particles indicates that the proteinase responsible for cleavage is also present. The fact that assembly has to occur before proteolytic processing of VV structural proteins suggests that the cleavage events are dependent upon a specific core protein conformation. However the nature of this conformational requirement is not known. Further research is underway to develop a full understanding of the proteolytic events during virion morphogensis. / Graduation date: 1993

Norovirus (NoV) and Sapovirus (SaV) are major causes of outbreak gastroenteritis worldwide. NoV and SaV are highly infectious, have multiple transmission routes and have a short incubation period, thereby facilitating rapid intercontinental spread of new variants. Consequently, a treatment would be advantageous for controlling them. However, currently little is known about the replication cycle and evolution of human NoV or SaV as neither are culturable. NoV and SaV are RNA viruses of the Caliciviridae family and have great genetic diversity which is thought to facilitate irnmune evasion. Consequently variants of NoV GI1.4 arose in 1996, 2002, 2004 and in 2006 and resulted in pandemics. Therefore, in this study, the role of the two main mechanisms associated with generating viral diversity; recombination, and point mutation were investigated for NoV and SaV. Physiological and kinetic properties of three NoV RdRps (genotypes, Gll.b, Gll.4, Gll.7) and two SaV RdRps (genogroups GI, GII) were also investigated. RNA recombination is a significant driving force in viral evolution. Increased awareness of recombination within the Calicivirus genus Norovirus (NoV) has led to a rise in the identification of NoV recombinants and they are now reported at high frequency. Despite this no classification system exists for recombinant NoVs As a result, there is duplication in reporting novel recombinants and the precise number of novel NoV recombinant types is unknown. Therefore, in order to elucidate thero!e of recombination in NoV evolution, 121 NoV nucleotide sequences, compiled from the GenBank database and published literature, were analysed for recombination events. NoV recombinants and their recombination breakpoint were identified using three methods: phylogenetic analysis, Simplot analysis and the Maximum Chi-Squared method. In total 19 unique NoV recombinant types were identified in circulation across the globe and they had a common recombination point near the ORF1/2 overlap. Recombination at the ORF1/0RF2 overlap could have important implications in NoV evolution as it enables a virus to swap its antigenic determinates (capsid) and thereby avoid immune clearance in an analogous manner to antigenic shift in influenza virus. This study also examined the role of NoV and SaV replication in generating viral diversity by comparing the physiological, kinetic and biochemical properties of five genotypically distinct RdRps from two different genera of the Caliciviridae. Genetically diverse HuCV RdRps were expressed in Escherichia coli and characterised in an in vitro assay designed for this study. The results indicated that despite high sequence variation between the five enzymes (between 6% and 71% amino acid difference) they shared similar physiological properties. Though there was some variation in their template usage and kinetic properties. SaV was able to perform primer dependent replication on homopolymeric A RNA whereas the NoV RdRps were not. Additionally, NoV RdRps had a higher incorporation rate and were more kinetically efficient than the two SaV RdRps. The incorporation fidelity of the five enzymes was similar (between 2.2x10-5 to 8.9x10-4 ), although interestingly the most prevalent strain, Gll.4, had the lowest fidelity of the caliciviruses. Therefore, suggesting that RdRp fidelity has an important role in NoV evolution. Overall, this study illustrated that NoV and SaV generate genetic diversity in a similar fashion to other RNA viruses, that is, a delicate combination of recombination, point mutation and replication efficiency. Understanding the mechanisms involved in viral replication and genomic diversity of the calicivirus RdRps is essential if a successful control strategy for the human caliciviruses is going to be developed.

Thesis (Ph. D.)--University of Hong Kong, 2008. / Also available in print.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Tez (Tıpta Uzmanlık) - Süleyman Demirel Üniversitesi, Tıp Fakültesi, Mikrobiyoloji ve Klinik Mikrobiyoloji Anabilim Dalı, 2002. / Bibliyografya var.