My cordial thanks to Shohag bhai, Mumin bhai, Rocy bhai, and especially Nayeem bhai for their continuous advice, encouragement and proper guidance. It might be almost impossible form my part to complete this thesis work without their supreme help. I would like to express my special appreciation to Afjal bhai for his help, suggestion and delightful company. I am thankful to Sajib bhai, Wohid bhai and Farid bhai for their assistance. I would like to thank Rabbani, Arafat, Lamyah, Alvee, Shadlee and Khalid for their help and delightful company.
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This expression of the structural gene is the primary vehicle of virulence regulation. Expression of CT and TCP are coregulated by the ToxR regulatory system, which includes the ToxT protein (20). The three primary participants in the cascade system are the tox genes: toxR, toxS, and toxT. These three genes form a regulon which controls the ctx operon expression. The ToxR gene product is a membrane resident transcriptional activator and DNA binding protein, functioning as inducer of the ctx operon. ToxS is a sensory periplasmic ‘chaperone’ like membraneous protein that assists in dimerization of the ToxR protein, activating it.
ToxT is a cytoplasmic protein whose expression is induced by ToxR; it activates transcription of ctx and tcp operons as needed for the expression of the structural toxin genes and toxin coregulated pilus, controlling a total of about 17 virulence factors. It is clear that the ToxRS regulatory system and the gene clusters encoding cholera toxin and the toxin-coregulated pilus (TCP) are nearly always present in pathogenic strains (15). The capacity for horizontal transfer is by no means limited to loci encoding O-antigen.
The discovery by Waldor and Mekalanos that the genes encoding cholera toxin are carried on the genome of a filamentous phage (CTX?) represents the clearest example of horizontal transfer of virulence genes between V. cholerae strains (21). The receptor for CTX? was shown to be the type IV TCP, which is itself a colonization factor in human and animal models (22, 23). This observation implied a temporal pathway for the evolution of pathogenesis. Acquisition of the TCP cluster followed by infection with CTX? could represent sequential steps in the conversion of a nonpathogenic environmental isolate into a highly virulent strain.
Although filamentous phage had not previously been recognized as being responsible for the lysogenic conversion of bacterial pathogens, they seem quite well suited for this purpose (21). It was previously recognized that TCP are encoded on a 39. 5-kb pathogenicity island, which includes putative integrase and transposase genes. This V. cholerae Introduction Page 9 Introduction pathogenicity island (VPI) is associated with epidemic and pandemic strains, and it clearly bears the markings of a horizontally acquired element. 1. 7 Viruses Viruses constitute a large and heterogeneous group of infectious agents.
Viruses alike in that they are obligate intracellular parasites for the cells of their selected hosts. They are so small that they can pass through the pores of filters, which do not permit the passage of bacteria. Viruses have no capacity for independent metabolism or motility. They reproduce by replication in a host cell and are capable of mutation. Viruses use the cells of plants and animals as well as those of other microorganisms as their hosts. 1. 8 Bacteriophages A bacteriophage (from ‘bacteria’ and Greek phagein, ‘to eat’) is any one of a number of viruses that infect bacteria.
