A review of schistosomiasis in immigrants in Western Australia, demonstrating the unusual longevity of Schistosoma mansoni

Harris, Arthur R. C.; Russell, Robert John; Charters, Alan

doi:10.1016/0035-9203(84)90129-9

Cited by 83 publications

(50 citation statements)

References 7 publications

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“…The ramifications of MEG diversity in the context of immune evasion are a subject for future work. Individual schistosomes can survive in the bloodstream for >30 yr (Harris et al 1984) and do not possess intracellular stages that would be protected from host immune attack. It would be expected that strategies to ensure long-term immune evasion by using protein variation in schistosomes would not be the same of those observed in protozoan parasites, where need for long-term immune evasion is less imperative since either elimination of the infection or death of the host occurs on a much shorter time span.…”

Section: Protein Variation Generated By Micro-exon Genesmentioning

confidence: 99%

Protein variation in blood-dwelling schistosome worms generated by differential splicing of micro-exon gene transcripts

DeMarco¹,

Mathieson²,

Manuel³

et al. 2010

Genome Res.

162

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Schistosoma mansoni is a well-adapted blood-dwelling parasitic helminth, persisting for decades in its human host despite being continually exposed to potential immune attack. Here, we describe in detail micro-exon genes (MEG) in S. mansoni, some present in multiple copies, which represent a novel molecular system for creating protein variation through the alternate splicing of short (#36 bp) symmetric exons organized in tandem. Analysis of three closely related copies of one MEG family allowed us to trace several evolutionary events and propose a mechanism for micro-exon generation and diversification. Microarray experiments show that the majority of MEGs are up-regulated in life cycle stages associated with establishment in the mammalian host after skin penetration. Sequencing of RT-PCR products allowed the description of several alternate splice forms of micro-exon genes, highlighting the potential use of these transcripts to generate a complex pool of protein variants. We obtained direct evidence for the existence of such pools by proteomic analysis of secretions from migrating schistosomula and mature eggs. Whole-mount in situ hybridization and immunolocalization showed that MEG transcripts and proteins were restricted to glands or epithelia exposed to the external environment. The ability of schistosomes to produce a complex pool of variant proteins aligns them with the other major groups of blood parasites, but using a completely different mechanism. We believe that our data open a new chapter in the study of immune evasion by schistosomes, and their ability to generate variant proteins could represent a significant obstacle to vaccine development.

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Section: Protein Variation Generated By Micro-exon Genesmentioning

confidence: 99%

Protein variation in blood-dwelling schistosome worms generated by differential splicing of micro-exon gene transcripts

DeMarco¹,

Mathieson²,

Manuel³

et al. 2010

Genome Res.

162

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“…A proportion of these pass through the tissue and reach the gut lumen to continue the life cycle, whereas others are washed downstream to the liver where they initiate the granulomatous inflammation that characterizes the disease. That schistosomes can survive for 30 -40 years in humans (2) attests to their possession of an effective immune evasion strategy.…”

Section: Molecular and Cellular Proteomics 5:347-356 2006mentioning

confidence: 99%

Proteins Exposed at the Adult Schistosome Surface Revealed by Biotinylation

Braschi

Wilson

2006

Molecular & Cellular Proteomics

237

309

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The human blood-dwelling parasite Schistosoma mansoni can survive in the hostile host environment for decades and must therefore display effective strategies to evade the host immune responses. The surface of the adult worm is covered by a living syncytial layer, the tegument, bounded by a complex multilaminate surface. This comprises a normal plasma membrane overlain by a secreted bilayer, the membranocalyx. Recent proteomic studies have identified constituents of the tegument, but their relative locations remain to be established. We labeled the most exposed surface proteins using two impermeant biotinylation reagents that differed only in length. We anticipated that the two reagents would display distinct powers of penetration, thereby producing a differential labeling pattern. The labeled proteins were recovered by streptavidin affinity and identified by tandem mass spectrometry. A total of 28 proteins was identified, 13 labeled by a long form reagent and the same 13 plus a further 15 labeled by a short form reagent. The parasite proteins included membrane enzymes, transporters, and structural proteins. The short form reagent additionally labeled some cytosolic and cytoskeletal proteins, the latter being constituents of the intracellular spines. Only a single secreted protein was labeled, implying a location between the plasma membrane and the membranocalyx or as part of the latter. Four host proteins, three immunoglobulin heavy chains and C3c/C3dg, a fragment of complement C3, were labeled by both reagents indicating their exposed situation. The presence of the degraded complement C3 implicates inhibition of the classical pathway as a major element of the immune evasion strategy, whereas the recovery of only one truly secreted protein points to the membranocalyx acting primarily as an inert protective barrier between the immune system and the tegument plasma membrane. Collectively the labeled parasite proteins merit investigation as potential vaccine candidates. Molecular & Cellular Proteomics 5:347-356, 2006.The trematode Schistosoma mansoni is a long lived parasite of the human hepatic portal system, infecting millions of people in Africa and South and Central America (1). Infection of the mammalian host occurs by direct cercarial penetration through the skin followed by transformation into schistosomula. These then undertake a protracted intravascular migration to the hepatic portal vein where they begin to feed on blood, mature, and pair. The male carries the female up the mesenteric blood vessels to the gut wall where she begins to deposit eggs. A proportion of these pass through the tissue and reach the gut lumen to continue the life cycle, whereas others are washed downstream to the liver where they initiate the granulomatous inflammation that characterizes the disease. That schistosomes can survive for 30 -40 years in humans (2) attests to their possession of an effective immune evasion strategy.The mature worm is covered by a syncytial cytoplasmic layer, the tegument, attached to underlying cell bo...

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“…2 Some infectious diseases may be diagnosed in immigrants living in developed countries as a result of the burden of the disease in their country of origin, exposure during migration, and conditions experienced during resettlement in the host country. [3][4][5] Most undocumented sub-Saharan immigrants take high-risk land and maritime routes to reach Europe. 6 In fact, the prevalence of some of these infections has been estimated to be particularly high among sub-Saharan immigrants, especially among the more vulnerable cases requiring social help.…”

Section: Introductionmentioning

confidence: 99%

Infectious Diseases in Sub-Saharan Immigrants to Spain

Serre-Delcor¹,

Maruri²,

Soriano‐Arandes³

et al. 2016

The American Society of Tropical Medicine and Hygiene

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Abstract. Immigrants may be carriers of infectious diseases because of the prevalence of these diseases in their country of origin, exposure during migration, or conditions during resettlement, with this prevalence being particularly high in sub-Saharan Africans. We performed a retrospective review of 180 sub-Saharan immigrants screened for infectious diseases at an International Health Center from January 2009 to December 2012. At least one pathogenic infectious disease was diagnosed in 72.8% patients: 60.6% latent tuberculosis infection, 36.8% intestinal parasites (intestinal protozoa or helminths), 28.1% helminths, 14.8% hepatitis B surface antigen positive, 1.2% anti-hepatitis C virus positive, 1.2% human immunodeficiency virus-positive, and 1.2% malaria. Coinfections were present in 28.4%. There was significant association between eosinophilia (absolute count or percentage) or hyper-IgE and the presence of helminths (P < 0.001). Relative eosinophilia and hyper-IgE were better indicators of helminth infection than absolute eosinophilia, particularly for schistosomiasis and strongyloidiasis. We found a high prevalence of infectious diseases in sub-Saharan immigrants, which could lead to severe health problems (in the absence of prompt treatment), representing a high cost to the public health system and possible transmission in the host country. Accurate screening and tailored protocols for infectious diseases are recommended in sub-Saharan immigrants.

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A review of schistosomiasis in immigrants in Western Australia, demonstrating the unusual longevity of Schistosoma mansoni

Cited by 83 publications

References 7 publications

Protein variation in blood-dwelling schistosome worms generated by differential splicing of micro-exon gene transcripts

Protein variation in blood-dwelling schistosome worms generated by differential splicing of micro-exon gene transcripts

Proteins Exposed at the Adult Schistosome Surface Revealed by Biotinylation

Infectious Diseases in Sub-Saharan Immigrants to Spain

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