Open access peer-reviewed Edited Volume

Plasmodium Species and Drug Resistance

Rajeev K. Tyagi

Institute of Microbial Technology

Eminent parasite immunologist, recipient of Global Health Travel Award Funded by Bill & Melinda Gates Foundation, 2010 and Ramalingaswami Reentry Fellowship, 2019.

Covering

Plasmodium Falciparum Plasmodium Vivax Malaria Treatment Artemisinin Chloroquine Amodiaquine Halofantrine Mutation Resistant Gene Chloroquine-Resistance Transporter NGS Microarray

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About the book

Malaria is a disease that spreads through the bite of anopheles female mosquitoes that carry the infection moieties (sporozoites) of the parasite. The Plasmodium falciparum and Plasmodium Vivex parasites are the most dangerous and lethal to humans in terms of morbidity and mortality. Technological advancements in the field of epidemiology and entomology have supported research efforts that have aided in reducing the burden and allowing scientists to go one step further in malaria parasitology. Two major weapons against malaria are vector control and chemoprophylaxis/chemotherapy. Unfortunately, attempts to eradicate the disease based on these methods have had only limited success, due to the widespread development of drug resistance by the parasites and insecticide resistance by the mosquito vector.

There have been antimalarial drugs available to treat human malaria infection, but continuous drug pressure to clear P. falciparum begets the evolution of tolerance to the therapeutic effects of the drugs. Many mechanisms of action parasites may be employed to escape the drug pressure.

Besides known mechanisms for the evolution of resistance through mutations and/or amplification in drug transporters (quinolines) or drug targets (antifolates), P. falciparum reportedly showed a quiescence mechanism allowing it to survive ART treatment. The emergence of resistance against frontline antimalarials and their combinations by P. falciparum is worrisome as it threatens to make malaria practically untreatable in South-East Asia (SEA). This will have severe implications as it would hinder the global endeavors to eliminate this deadliest human disease. A recent series of clinical trials, in vitro, genomics, and transcriptomic studies in SEA have defined in vivo and in vitro phenotypes of artemisinin resistance; identified its causal genetic determinant; explored its molecular mechanism; and assessed its clinical impact. Artemisinin-based combination therapy (ACT) is the only remaining remedy to clear the parasite infection from the periphery thoroughly. However, tolerance shown by the parasite towards the combination of drugs and co-resistance has prompted researchers to address the question of how parasites escape the therapeutic effect of drugs. Therefore, this book will provide collective information about the drug resistance mechanisms and how currently available and new tools can aid in understanding the drug resistance mechanism.

Publishing process

Book initiated and editor appointed

Date completed: November 23rd 2020

Applications to edit the book are assessed and a suitable editor is selected, at which point the process begins.

Chapter proposals submitted and reviewed

Deadline Extended: Open for Submissions

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Approved chapters written in full and submitted

Deadline for full chapters: February 19th 2021

Once approved by the academic editor and publishing review team, chapters are written and submitted according to pre-agreed parameters

Full chapters peer reviewed

Review results due: May 10th 2021

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Book compiled, published and promoted

Expected publication date: July 9th 2021

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About the editor

Rajeev K. Tyagi

Institute of Microbial Technology

Dr. Rajeev K. Tyagi earned Ph.D. degree at Biomedical Parasitology Unit, Institute Pasteur, Paris, France in June 2011 on a very challenging and interesting topic of malaria immunology/parasitology. He developed a long lasting, stable and straightforward laboratory animal model (humanized mouse model: a versatile mouse model). The developed humanized mouse model was deployed to study asexual blood stage infection of P. falciparum and understand biology, physiology and immunology of this human parasite during his doctoral thesis at Pasteur (Tyagi et al, Malaria J 2010, PloS One 2011). As P. falciparum has the potential to evolve extreme artemisinin resistance and more complex patterns of multidrug resistance than anticipated, therefore Dr. Tyagi explored the developed mouse to study the artemisinin resistance (Tyagi et al, BMC Medicine 2018). Dr. Tyagi worked as postdoc fellow in the laboratory of Dr. John Adams, University of South Florida, USA and received training to explore the potential of the developed “humanized mouse” to characterize attenuated asexual blood stage falciparum parasite to understand the innate immune response of the attenuated parasite (growth mutant). Additionally, he developed small laboratory human liver chimeric mice by transplanting the human hepatocytes in transgenic/immunodeficient mice (TK/NOG) at USF, USA to study the least known liver stage infection of P. falciparum (Tyagi et al, 2018 Frontiers in Immunology). Further, discovery of novel dendritic like cell population called “pathogen differentiated dendritic cells (PDDCs)” when incubated with P. gingivalis and tracking of monocyte derived dendritic cells (MoDcs) in a reconstituted immunodeficient NOD.PrkdcscidIl2rg-/- (NSG) mice gave Dr. Tyagi a platform to make the excellent use of his post-Ph.D. training at Augusta University, USA to gain expertise in advanced translational biomedical research aimed at understanding the host-pathogen interaction (Tyagi et al, 2017 Scientific Reports). Dr. Tyagi at the Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition Vanderbilt University Medical Centre (VUMC), USA deployed his efforts to understand the role of IL-23R in the modulation of functioning of regulatory T cells and its role in the pathogenesis of colitis in an experimental humanized mouse (reconstituted with stem cells) as well as IL-23R deficient and sufficient mice (Tyagi et al, 2020, Biochem. Pharmacology). Also, he looked at the role of low-dose IL-2 in expanding Foxp3 regulatory T cells in CD34+ cells reconstituted NSG (NOD-scid IL2Rgammanull) mice and its therapeutic role on the treatment of experimental colitis in these mice. Dr. Tyagi has been leading group at CSIR-Institute of Microbial Technology, Chandigarh and his lab is focused to: 1) develop human-liver chimeric mice for huHep transplantation. The huHep reconstituted TK/NOG transgenic mice by non-invasive Ultra Sound Guided Injection technique through intrasplenic route showing development of human liver “chimeric mouse” to study liver stage infection of P. falciparum and transition to asexual blood stage infection to test antimalarial drugs and vaccine candidates in one host. 2) select highly Artemisinin-resistant asexual blood stage Plasmodium falciparum (ART-R) with Quinine co-resistance under in vitro artesunate pressure. The experimentally selected resistant P. falciparum parasites are being used to find-out the underlying molecular mechanisms that parasite may have been employing to escape and/or cope-up the drug pressure. The engraftment of select ART-R parasites will be grafted in a blood stage humanized mice to complement the in vitro results. 3) Dendritic cells as "therapeutic vaccines" playing a crucial role in translational biomedical research. 4) formulation and characterization of nanoscale drug carriers to deliver methotrexate (MTX) and aceclofenac to address Rheumatoid Arthritis, cancer and other inflammatory diseases (Tygai et al, Nanomedicine, 2016, Int. J. Pharmaceutics, 2016, Acta Biomaterialia, 2015) as well as candidate vaccines (Tyagi et al, vaccine 2015, Human Vacc. Immunothear, 2016). His group is looking at anti-inflammatory effect of methotrexate in breast cancer therapeutics. Dr. Tyagi’s group is funded by DST-SERB, DBT and ICMR, New Delhi. There are grants applications under review with DBT, Wellcome-DBT India Alliance, DST-SERB and BIRAC, New Delhi.

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