Day 1 :
Cairo University, Egypt
Keynote: Fish Infected With Trematode Encysted Metacercariae and Its Role in Transmitting Parasitic Diseases to Humans and Domestic Animals
Time : 09:30-10:15
Dr Faiza M El Assal is professor of invertebrate zoology and parasitology at the Zoology Department, Faculty of Science, Cairo University. She is interested in the conservation of the freshwater ecosystem and biological control of the snail vectors of parasitic diseases. She published more than 50 papers in international and national journals. She supervised more than 60 M Sc & Ph D theses and was reviewer for many theses. She planned and supervised projects on biological control of schistosomiasis snail vector.
Centre International de Recherche Médicale De Franceville (CIRMF), Gabon
Keynote: Immunological and molecular similarities between human filarial Loa loa and Brugia pahangi antigens
Time : 10:15-11:00
JP Akue has completed his PhD at the University of Liverpool (Liverpool School of Tropical Medicine). He has been a Welcome Trust Fellow in the Department of Veterinary Parasitology from the University of Glasgow and Visiting Scientist at the CDC, Atlanta, GA, USA (infectious diseases). Currently, he is a Senior Researcher at the Franceville (Gabon) International Centre for Medical Research. He has published more than 40 papers in reputed journals and serves as reviewer for several other scientific journals
After long-term, 7-year follow-up, Loa loa-exposed individuals from one village in Gabon were divided into four groups according to parasitological and clinical findings, mainly: endemic controls, amicrofilaraemic, low microfilaraemic and high microfilaraemic individuals. This study carried out using Brugia pahangi adults, microfilariae and L3 antigens compared the level of specific isotypes (IgA, IgE, IgG and IgM) and IgG subclasses in different defined groups of villagers. The study showed that the levels of IgG1 and IgM were significantly higher in amicrofilaraemics compared too high and low microfilaraemics. IgG4 was high in all groups, but there was no significant increase in IgG2 and IgG3. Interestingly, the level of IgG1 was inversely correlated with microfilarial density when using L3 antigen (Spearman’s r= –0.839; p<0.0001). Identification of antigen targets of this response shows several molecules with their molecular weight varying from 8 kDa to 150 kDa. Amplification followed by Southern blot of Loa loa DNA using primers designed from Brugia gp29 confirms the homology between B. pahangi and L. loa genes. The removal of the glycosylated portion of the antigen in the B. pahangi adult did not inhibit the reactivity of the major reacting antibodies IgG1 and IgG4 from the L. loa-infected population, suggesting that the reactivity is linked to the peptide backbone. This study shows that the map of the distribution of lymphatic filarial in L. loa endemic zones should be re-evaluated. The similarities in structural epitopes could be exploited in view of a vaccine strategy designed to control L. loa.
Federal University of Rio de Janeiro, Brazil
Keynote: The interface of the host antiviral response and the infection by Leishmania amazonensis: role of RNA sensors and Phlebovirus coinfection
Time : 11:20-12:05
Ulisses Gazos Lopes is an Associate Professor at the Instituto de Biofísica Carlos Chagas Filho, Federal University of Rio de Janeiro, Brazil. He completed his MSc in Parasitology from the Federal University of Minas Gerais, Brazil and obtained his PhD in Genetics from Federal University of Rio de Janeiro, Brazil. He was a Research Fellow at Harvard School of Public Health, Boston, US, from 1984 to1986. He did his Post-doctoral training from the Dana-Farber Cancer Institute/Harvard Medical School, Boston, US. Currently, he is a Visiting Researcher at Institut Pasteur, Paris, France
PKR (dsRNA activated kinase) activation, a key regulator of the antiviral pathway, occurs in L. amazonensis infection, leading to the expression of IL-10 and IFN1beta and favoring the parasite intracellular growth. Importantly, the immune staining of human cutaneous leishmaniasis lesions revealed impressive high levels of IFN1beta/PKR positive cells from patients with untreatable diffuse cutaneous leishmaniasis. We have investigated whether the endosome dsRNA receptor, TLR3, shared a similar role in L. amazonensis infection. The intracellular growth of the parasites was reduced in TLR3-/- macrophages and this phenomenon was accompanied by significantly reduced levels of IFN1beta and IL-10 and increased levels of IL-12. These data prompted us to test the hypothesis that arboviruses, RNA arthropods transmitted viruses, would interfere with the Leishmania infection. To tackle this hypothesis, we worked with Phlebovirus, a sub group of the Bunyaviridae, which is transmitted by sandflies. We tested a viral isolate of the rodent Nectomys sp., a natural sylvatic reservoir of L. amazonensis from the Amazon region. Leishmania and Phlebovirus coinfection led to high intracellular parasite growth. Importantly, this effect required PKR, TLR3 and IFN1 signaling. L. amazonensis and Phlebovirus synergize the expression of IFN1beta and IL-10. However, the coinfection of L. amazonensis with the ssRNA arbovirus (DENVII) did not induce these effects. Altogether, our data revealed that the classical antiviral cellular responses mediated by PKR and TLR3 are subverted by L. amazonensis. We predict that specific RNA viral coinfections may enhance and sustain the activation of cellular RNA sensors, resulting in the aggravation of the parasite infection.