Genes parasitism

Essential for induction ofthe/Z-5 gene in inflammatory reactions is the binding site for nuclear factor kappa B (NF-kB). NF-kB responds to cytokines, stress, free radicals, ultraviolet irradiation, and bacterial, viral, or even parasitic antigens [2]. NF-kB stands for a family of subunits, which form homo-, and heterodimers. All NF-kB proteins share a highly conserved DNA-binding/dimerization domain called the Rel homology domain (RHD) consisting of two (3-strand core domains... 

Blaxter, 1998). Once the evolutionary framework is in place, the search for genes and processes unique to or important in parasitism can be taken up in earnest. 

Sukhdeo, S.C., Sukhdeo, M.V.K., Black, M.B. and Vrijenhoek, R.C. (1997) The evolution of tissue migration in parasitic nematodes (Nematoda Strongylida) inferred from a protein-coding mitochondrial gene. Biological Journal of the Linnean Society 61, 281—298. 

Nematode-host interactions are complex and poorly understood. The relationship between cyst nematodes and their hosts appears to have co-evolved, and as a result there are numerous genes for host resistance that are complemented by nematode parasitism genes (Triantaphyllou, 1987). Different alleles of these genes may interact in various combinations to give... 

Sequencing of parasite genes provides a powerful tool for the accurate identification of parasites and for systematic studies (Johnson and Baver-stock, 1989 Reddy, 1995 McManus and Bowles, 1996), and is based on either of the two original protocols (Sanger et al., 1977 Maxam and Gilbert, 1980). Cycle-sequencing (Murray, 1989), a PCR-based modification of the... 

Gasser, R.B. (1997) Mutation scanning methods for the analysis of parasite genes. InternationalJournal for Parasitobgy 27, 1449-1463. 

Four fundamental changes induced in host cells will be discussed initially (i) infection-induced cell cycle re-entry (ii) suspension of host cells in apparent G2/M (iii) repression of host muscle gene expression and (iv) further induction of the infected cell phenotype. A clear understanding of these fundamental changes induced by the infection is critical in elucidating the cellular mechanisms involved and, possibly, the host regulatory factors that are interfered with by parasite products. 

Therefore, it is anticipated that chronic repression of muscle gene expression does not require chronic regulation by the parasite. Rather, this effect is expected to result from chronic suspension of infected cells in a non-Go/Gi gene regulatory environment. A simple hypothesis derived from known characteristics of skeletal muscle cells is that induction of cell cycle re-entry is sufficient to cause both chronic suspension in G2/M and repression of muscle gene expression. This possibility has implications for the number of regulatory points at which the parasite might influence the host cell and possible methods to screen for those products. 

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