Ashleigh Peck is a third-year PhD Candidate at Murdoch University. Ashleigh has conducted a 2-year surveillance project to map mosquito biodiversity and disease risk across Perth, Western Australia’s metropolitan area. By integrating traditional taxonomy and molecular methods, their research explores the genetic structure of mosquito populations and the ecological drivers (land cover and climate) influencing them. A core focus of this research is the application of xenomonitoring to investigate mosquito-borne pathogens, using PCR and next-generation sequencing to uncover the prevalence and diversity of parasites and viruses within Perth.
Talk title: Mapping Diversity and Vector Associations of Mosquito-Borne Parasites in Western Australia.
Authors: AM Peck(1), A Lymbery(2,3) SL Egan(4), A Ash(1,5).
(1) School of Medical, Molecular and Forensic Sciences, Murdoch University, 90 South Street, Murdoch, Western Australia, 6150, Australia; (2) School of Environmental and Conservation Sciences, Murdoch University, 90 South Street, Murdoch, Western Australia, 6150, Australia;
(3) Centre for Sustainable Aquatic Ecosystems, Harry Butler Institute, Murdoch University, Western Australia; (4) Centre of Computational and Systems Medicine, Murdoch University, 90 South Street, Murdoch, Western Australia, 6150, Australia; (5) Centre for Biosecurity and One Health, Murdoch University, Western Australia
Abstract:
Mosquitoes are the most significant vectors for human and animal diseases. Competent vectors and susceptible vertebrate hosts are required to maintain transmission of mosquito-borne disease (MBD). Therefore, MBD are maintained in a dynamic system shaped by the biodiversity of vectors, hosts, and pathogens, which varies over time and space. Through mosquito surveillance programs, the biodiversity of mosquitoes and blood-borne parasites they carry can be evaluated to uncover local disease transmission risks to humans and animals. Advancements in molecular techniques have enabled researchers to use mosquitoes as proxies to determine the prevalence of mosquito-borne diseases, a practice known as xenomonitoring. Xenomonitoring is a non-invasive, convenient and cost-effective surveillance method. In Western Australia, routine xenomonitoring only screens for mosquito-borne viruses of human importance. Therefore, the prevalence and transmission potential of mosquito-borne parasites, which can impact human and animal health, was previously unknown in Perth, Western Australia. In this presentation, I will discuss recently published results of my 2-year molecular surveillance study aimed at uncovering the diversity of mosquito-borne parasites, including Haemosporida and filarial nematodes, in the Perth region. I will also provide insight into vector species associations, highlighting local transmission dynamics and potential associated risks.
Maria Saeed is a PhD student in the Rogerson Lab at the Peter Doherty Institute, University of Melbourne. Her PhD focused on exploring the role of functional antibodies and their interactions with immune cells in protection against malaria in pregnant women and children. Maria is currently awaiting thesis examination and is open to post-doctoral, research assistant and related job opportunities.
Talk Title: Antibody-dependent neutrophil phagocytosis of Plasmodium falciparum
infected erythrocytes is mediated by FcγRIIa
FcγRIIIb, a glycosylphosphatidylinositol (GPI) linked receptor, is the most abundant FcγR on neutrophils followed by FcγRIIa. There is evidence that antibody dependent neutrophil phagocytosis (ADNP) protects against malaria, but the role of specific FcγRs involved is not clear. To probe the relative importance of FcγRIIIb and FcγRIIa in ADNP of Plasmodium falciparum infected erythrocytes (IEs), purified neutrophils from healthy donors were treated with tumor necrosis factor (TNF) to mobilize the intracellular FcγRIIIb to the surface followed by phosphatidylinositol phospholipase C (PIPLC) treatment to cleave FcγRIIIb. In TNF/PIPLC treated neutrophils, relative gMFI of FcγRIII decreased by 79% while FcγRIIa detection increased by 82%, compared to untreated neutrophils (gMFI = 100%). When opsonised IEs were incubated with TNF/PIPLC treated neutrophils, relative ADNP by FcγRIIIb-depleted neutrophils increased (585%+-108%) compared to untreated neutrophils (100%, p = 0.042). Using FcγR blocking we show that relative to no-blocker (phagocytosis = 100%), ADNP was reduced over five-fold by FcγRIIa blocker alone (~17%+-1.5%, p<0.05) and to the same degree by combined FcγRIIa and FcγRIII blockers (~24% +- 5.5%, p <0.05). We found that FcγRIIa is the main phagocytic receptor mediating ADNP of IEs and FcγRIIIb acts as a decoy receptor.
