Plenary Lectures

Plenary 1

 

Balbir Singh

 

Faculty of Medicine and Health Sciences, UNIMAS, Sarawak Malaysia

PLASMODIUM KNOWLESI: PAST, PRESENT AND FUTURE

Abstract


For a considerable period, malaria in humans was thought to be caused by four species of Plasmodium: P. falciparum, P. vivax, P. malariae and P. ovale. Naturally acquired human infections with simian malaria parasites were thought to be extremely rare, until the use of molecular tools lead to the discovery of a large focus of human P. knowlesi infections in 2004 in the Kapit Division of Sarawak, Malaysian Borneo. Human knowlesi malaria cases have since been described throughout Southeast Asia, although Malaysia has reported the highest incidence to date with 7,745 cases in 2017 and 2018. The widespread distribution of human cases, with some resulting in fatal outcomes, underscore the public health importance of human P. knowlesi infections in this region. The talk will begin with a description of the pioneering work of Dr. Knowles and Dr. Das Gupta in India, following their isolation of P. knowlesi from a long-tailed macaque in 1931, and of other early studies leading to the discovery of the large focus of human infections in Sarawak in 2004. More recent epidemiological and entomological data will be presented, together with whole genome-sequencing and other molecular data of P. knowlesi isolates derived from humans and macaques, which indicate that knowlesi malaria is primarily a zoonosis, and that there are at least 3 sub-populations of P. knowlesi. It remains to be seen whether P. knowlesi continues to cause zoonotic infections or whether the loss of the natural habitat of monkeys due to deforestation, coupled with changes in mosquito abundance and feeding behavior, and an increase in the human population, result in P. knowlesi switching to humans as the preferred host.





Plenary 2

 

Patrick Tan

Singhealth Duke-NUS Institute of Precision Medicine (PRISM) DUKE-NUS Medical School, Singapore

GENOMIC AND EPIGENOMIC PROFILES OF ASIAN ENDEMIC MALIGNANICES

Abstract


Autophagy is a major degradation system in the cell. Intracellular components are sequestered by autophagosomes and then degraded upon fusion with lysosomes. Yeast genetic studies have identified more than 40 autophagy-related (ATG) genes. Many of these genes are conserved in higher eukaryotes, which brought about an exponential expansion of autophagy research in various organisms including mammals. The 2016 Nobel Prize in Physiology or Medicine was eventually awarded to the scientist who spearheaded the rapid development of the field, Dr. Yoshinori Ohsumi. However, there remain many fundamental questions in the autophagy field regarding its physiological roles and molecular mechanisms. For example, selective autophagy has become a hot topic but its precise mechanisms and physiological roles are still under investigation. We recently identified a novel receptor for autophagy of endoplasmic reticulum (ER-phagy). Also, it is now well appreciated that some ATG proteins have autophagy-independent functions or have made interesting evolution. We found that Plasmodium and Toxoplasma have a unique set of ATG proteins that contains a non-covalent type of the ATG12 system instead of the covalent type found in most eukaryotes. In this lecture, these novel findings made in vertebrates and parasites will be discussed.





Abstract


For a considerable period, malaria in humans was thought to be caused by four species of Plasmodium: P. falciparum, P. vivax, P. malariae and P. ovale. Naturally acquired human infections with simian malaria parasites were thought to be extremely rare, until the use of molecular tools lead to the discovery of a large focus of human P. knowlesi infections in 2004 in the Kapit Division of Sarawak, Malaysian Borneo. Human knowlesi malaria cases have since been described throughout Southeast Asia, although Malaysia has reported the highest incidence to date with 7,745 cases in 2017 and 2018. The widespread distribution of human cases, with some resulting in fatal outcomes, underscore the public health importance of human P. knowlesi infections in this region. The talk will begin with a description of the pioneering work of Dr. Knowles and Dr. Das Gupta in India, following their isolation of P. knowlesi from a long-tailed macaque in 1931, and of other early studies leading to the discovery of the large focus of human infections in Sarawak in 2004. More recent epidemiological and entomological data will be presented, together with whole genome-sequencing and other molecular data of P. knowlesi isolates derived from humans and macaques, which indicate that knowlesi malaria is primarily a zoonosis, and that there are at least 3 sub-populations of P. knowlesi. It remains to be seen whether P. knowlesi continues to cause zoonotic infections or whether the loss of the natural habitat of monkeys due to deforestation, coupled with changes in mosquito abundance and feeding behavior, and an increase in the human population, result in P. knowlesi switching to humans as the preferred host.





Plenary 3

 

M Madan Babu

MRC Laboratory of Molecular Biology

Francis Crick Avenue, Cambridge Biomedical Campus

Cambridge CB2 0QH, UK

UNDERSTANDING VARIATION IN THE GPCR SIGNALLING SYSTEM

Abstract


Plasmodium falciparum is the most virulent of the human malaria parasites, causing ~440,000 deaths per year. Moreover, emergence of resistance to the first-line antimalarial drug, artemisinin, is looming as a major global health crisis. New therapeutic strategies are needed to prevent disease and to overcome drug resistance. My laboratory employs a suite of technologies to study P. falciparum – ranging from protein chemistry to drug development, from molecular genetics to cell biology, and from advanced imaging to structural biology techniques. The lecture will explore how pioneering imagining modalities such as Super-Resolution Optical Microscopy, Block-Face Scanning Electron Microscopy and single particle Cryo Electron Microscopy can provide insights into the workings of P. falciparum and in particular, the molecular basis of virulence. I will discuss the molecular mechanism of resistance to the front-line antimalarial drug family, the artemisinins, and describe our efforts to develop new antimalarial drugs that target protein homeostasis.





Plenary 4

 

Leann Tilley

Department of Biochemistry and Molecular Biology, Bio21 Institute , The University of Melbourne,  Australia

NEW TECHNOLOGIES THAT PROVIDE INSIGHTS INTO MALARIA PARASITE VIRULENCE AND ANTIMALARIAL DRUG DESIGN

Abstract


Plasmodium falciparum is the most virulent of the human malaria parasites, causing ~440,000 deaths per year. Moreover, emergence of resistance to the first-line antimalarial drug, artemisinin, is looming as a major global health crisis. New therapeutic strategies are needed to prevent disease and to overcome drug resistance. My laboratory employs a suite of technologies to study P. falciparum – ranging from protein chemistry to drug development, from molecular genetics to cell biology, and from advanced imaging to structural biology techniques. The lecture will explore how pioneering imagining modalities such as Super-Resolution Optical Microscopy, Block-Face Scanning Electron Microscopy and single particle Cryo Electron Microscopy can provide insights into the workings of P. falciparum and in particular, the molecular basis of virulence. I will discuss the molecular mechanism of resistance to the front-line antimalarial drug family, the artemisinins, and describe our efforts to develop new antimalarial drugs that target protein homeostasis.





Plenary 5

 

Noboru Mizushima

Department of Biochemistry and Molecular Biology Graduate School of Medicine, The University of Tokyo, Tokyo , Japan

PHYSIOLOGICAL ROLES AND MOLECULAR MECHANISMS OF AUTOPHAGY

Abstract


Autophagy is a major degradation system in the cell. Intracellular components are sequestered by autophagosomes and then degraded upon fusion with lysosomes. Yeast genetic studies have identified more than 40 autophagy-related (ATG) genes. Many of these genes are conserved in higher eukaryotes, which brought about an exponential expansion of autophagy research in various organisms including mammals. The 2016 Nobel Prize in Physiology or Medicine was eventually awarded to the scientist who spearheaded the rapid development of the field, Dr. Yoshinori Ohsumi. However, there remain many fundamental questions in the autophagy field regarding its physiological roles and molecular mechanisms. For example, selective autophagy has become a hot topic but its precise mechanisms and physiological roles are still under investigation. We recently identified a novel receptor for autophagy of endoplasmic reticulum (ER-phagy). Also, it is now well appreciated that some ATG proteins have autophagy-independent functions or have made interesting evolution. We found that Plasmodium and Toxoplasma have a unique set of ATG proteins that contains a non-covalent type of the ATG12 system instead of the covalent type found in most eukaryotes. In this lecture, these novel findings made in vertebrates and parasites will be discussed.





Plenary 6

 

Brad Nelson

Co-Director, Immunotherapy Program

BC Cancer, Victoria BC, Canada

DECIPHERING AND RE-ENGINEERING THE IMMUNE RESPONSE TO CANCER

Abstract


Autophagy is a major degradation system in the cell. Intracellular components are sequestered by autophagosomes and then degraded upon fusion with lysosomes. Yeast genetic studies have identified more than 40 autophagy-related (ATG) genes. Many of these genes are conserved in higher eukaryotes, which brought about an exponential expansion of autophagy research in various organisms including mammals. The 2016 Nobel Prize in Physiology or Medicine was eventually awarded to the scientist who spearheaded the rapid development of the field, Dr. Yoshinori Ohsumi. However, there remain many fundamental questions in the autophagy field regarding its physiological roles and molecular mechanisms. For example, selective autophagy has become a hot topic but its precise mechanisms and physiological roles are still under investigation. We recently identified a novel receptor for autophagy of endoplasmic reticulum (ER-phagy). Also, it is now well appreciated that some ATG proteins have autophagy-independent functions or have made interesting evolution. We found that Plasmodium and Toxoplasma have a unique set of ATG proteins that contains a non-covalent type of the ATG12 system instead of the covalent type found in most eukaryotes. In this lecture, these novel findings made in vertebrates and parasites will be discussed.





Enquiries:

    

    Conference Secretariat 

    faobmbkl2019@gmail.com

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© 2017 by Malaysian Society for Biochemistry & Molecular Biology (MSBMB)