Abstract
Endo-parasites that affect humans include Plasmodium, the causative agent of malaria, which remains one of the leading causes of death in human beings. Despite decades of research, vaccines to this and other endo-parasites remain elusive. This is in part due to the hyper-variability of the parasites surface proteins. Generally these surface proteins are encoded by a large family of genes, with only one being dominantly expressed at certain life stages. Another layer of complexity can be introduced through the alternative splicing of these surface proteins. The resulting isoforms may differ from each other with regard to cell localisation, substrate affinities and functions. They may even differ in structure to the extent that they are no longer recognised by the host’s immune system. In many cases this leads to changes in the N terminus of these proteins. The geographical localisation of endo-parasitic infections around the tropics and the highest incidences of HIV-1 infection in the same areas, adds a further layer of complexity as parasitic infections affect the host immune system resulting in higher HIV infection rates, faster disease progression, and an increase in the severity of infections and complications in HIV diagnosis. This review discusses some examples of parasite surface proteins that are alternatively spliced in trypanosomes, Plasmodium and the parasitic worm Schistosoma as well as what role alternate splicing may play in the interaction between HIV and these endo-parasites.
Highlights
The expression of genes can be controlled at many levels, these include transcriptional regulation, post-transcriptional regulation, translational regulation, mRNA degradation, protein degradation and through the actions of inhibitory proteins
The tri snRNP complex U4, U5 and U6 associate with the pre-mRNA, U1 and U4 are ejected from the complex and the activated spliceosome performs the first step where the branch site of the intron carries out a nucleophillic attack of the 5’ splice site
Immune evasion of parasites through antigenic variation is a complex process with a vast amount of literature devoted to it; the vast majority of studies and reviews examine antigenic variation through the expression of different members of a multigene family and not through the alternate splicing of mRNA
Summary
The expression of genes can be controlled at many levels, these include transcriptional regulation, post-transcriptional regulation, translational regulation, mRNA degradation, protein degradation and through the actions of inhibitory proteins. 16 MEG protein products have been detected in secretions or detected in the glands of S. mansoni The transcription of these genes increases during the mammalian stages of the life cycle where the parasite may interact with the host’s immune system, and appear to be associated with host invasion and persistence within the host [67,70]. One of the members of this family SmVAL6 contains four exons of an average size and code for the conserved motifs in the protein family (Figure 9) This is followed by seven small exons, which is similar to the structure of MEGs. As many as 5 isoforms have been identified that occur due to alternate splicing of these smaller exons. The original isoform named CXCR3-A results in an increase in
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