Andrew Read | |
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 Andrew Read in 2015, portrait via the Royal Society | |
| Born | Andrew Fraser Read |
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| Thesis | Comparative analyses of reproductive tactics (1989) |
| Doctoral advisor | Paul H. Harvey |
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Andrew Fraser Read FRS [1] is Evan Pugh professor of biology and entomology at Pennsylvania State University and the Director of the Huck Institutes of the Life Sciences. [2] [3] [4] [5] [6] [7] [8]
Read was educated at the University of Otago where he was awarded a Bachelor of Science degree in 1984. [9] He moved on to the University of Oxford where he was awarded a Doctor of Philosophy degree in 1989 for research supervised by Paul H. Harvey. [10]
Read was elected a Fellow of the Royal Society (FRS) in 2015. His certificate of election reads:
Andrew Read's work has revealed the evolutionary forces that shape pathogen virulence, infectivity, vaccine escape and drug resistance in a number of significant human infections. His work on malaria has provided a substantial body of experimental evidence to show that within-host selective pressures drive the evolution of both virulence and drug resistance. Integrating mathematical models with his experimental evidence, he proposed the controversial hypothesis that some vaccines can prompt evolution of more virulent pathogen strains. Recently he confirmed this hypothesis by evolving rodent malaria parasites in mice immunised with a candidate human malaria vaccine and showing virulence increased as predicted. He also developed both the theory and the proof of principle for the production of evolution-proof insecticides and provided the critical experimental evidence that animals have genetic variation in tolerance, a host defence mechanism which complements the more conventionally studied resistance. [1]
Staphylococcus aureus is a Gram-positive spherically shaped bacterium, a member of the Bacillota, and is a usual member of the microbiota of the body, frequently found in the upper respiratory tract and on the skin. It is often positive for catalase and nitrate reduction and is a facultative anaerobe that can grow without the need for oxygen. Although S. aureus usually acts as a commensal of the human microbiota, it can also become an opportunistic pathogen, being a common cause of skin infections including abscesses, respiratory infections such as sinusitis, and food poisoning. Pathogenic strains often promote infections by producing virulence factors such as potent protein toxins, and the expression of a cell-surface protein that binds and inactivates antibodies. S. aureus is one of the leading pathogens for deaths associated with antimicrobial resistance and the emergence of antibiotic-resistant strains, such as methicillin-resistant S. aureus (MRSA), is a worldwide problem in clinical medicine. Despite much research and development, no vaccine for S. aureus has been approved.
Theobald Smith FRS(For) HFRSE was a pioneering epidemiologist, bacteriologist, pathologist and professor. Smith is widely considered to be America's first internationally-significant medical research scientist.
Viral evolution is a subfield of evolutionary biology and virology that is specifically concerned with the evolution of viruses. Viruses have short generation times, and many—in particular RNA viruses—have relatively high mutation rates. Although most viral mutations confer no benefit and often even prove deleterious to viruses, the rapid rate of viral mutation combined with natural selection allows viruses to quickly adapt to changes in their host environment. In addition, because viruses typically produce many copies in an infected host, mutated genes can be passed on to many offspring quickly. Although the chance of mutations and evolution can change depending on the type of virus, viruses overall have high chances for mutations.
Serial passage is the process of growing bacteria or a virus in iterations. For instance, a virus may be grown in one environment, and then a portion of that virus population can be removed and put into a new environment. This process is repeated with as many stages as desired, and then the final product is studied, often in comparison with the original virus.
Paul W. Ewald is an evolutionary biologist, specializing in the evolutionary ecology of parasitism, evolutionary medicine, agonistic behavior, and pollination biology. He is the author of Evolution of Infectious Disease (1994) and Plague Time: The New Germ Theory of Disease (2002), and is currently director of the program in Evolutionary Medicine at the Biology Department of the University of Louisville.
Pseudomonas aeruginosa is a common encapsulated, gram-negative, aerobic–facultatively anaerobic, rod-shaped bacterium that can cause disease in plants and animals, including humans. A species of considerable medical importance, P. aeruginosa is a multidrug resistant pathogen recognized for its ubiquity, its intrinsically advanced antibiotic resistance mechanisms, and its association with serious illnesses – hospital-acquired infections such as ventilator-associated pneumonia and various sepsis syndromes.
Optimal virulence is a concept relating to the ecology of hosts and parasites. One definition of virulence is the host's parasite-induced loss of fitness. The parasite's fitness is determined by its success in transmitting offspring to other hosts. For about 100 years, the consensus was that virulence decreased and parasitic relationships evolved toward symbiosis. This was even called the law of declining virulence despite being a hypothesis, not even a theory. It has been challenged since the 1980s and has been disproved.
Any cause that reduces or increases reproductive success in a portion of a population potentially exerts evolutionary pressure, selective pressure or selection pressure, driving natural selection. It is a quantitative description of the amount of change occurring in processes investigated by evolutionary biology, but the formal concept is often extended to other areas of research.
The gene-for-gene relationship was discovered by Harold Henry Flor who was working with rust of flax. Flor showed that the inheritance of both resistance in the host and parasite ability to cause disease is controlled by pairs of matching genes. One is a plant gene called the resistance (R) gene. The other is a parasite gene called the avirulence (Avr) gene. Plants producing a specific R gene product are resistant towards a pathogen that produces the corresponding Avr gene product. Gene-for-gene relationships are a widespread and very important aspect of plant disease resistance. Another example can be seen with Lactuca serriola versus Bremia lactucae.
Antigenic escape, immune escape, immune evasion or escape mutation occurs when the immune system of a host, especially of a human being, is unable to respond to an infectious agent: the host's immune system is no longer able to recognize and eliminate a pathogen, such as a virus. This process can occur in a number of different ways of both a genetic and an environmental nature. Such mechanisms include homologous recombination, and manipulation and resistance of the host's immune responses.
Raymond J. St. Leger is an American mycologist, entomologist, molecular biologist and biotechnologist who currently holds the rank of Distinguished University Professor in the Department of Entomology at the University of Maryland, College Park.
Evolution of Infectious Disease is a 1993 book by the evolutionary biologist Paul W. Ewald. In this book, Ewald contests the traditional view that parasites should evolve toward benign coexistence with their hosts. He draws on various studies that contradict this dogma and asserts his theory based on fundamental evolutionary principles. This book provides one of the first in-depth presentations of insights from evolutionary biology on various fields in health science, including epidemiology and medicine.
Pathogenomics is a field which uses high-throughput screening technology and bioinformatics to study encoded microbe resistance, as well as virulence factors (VFs), which enable a microorganism to infect a host and possibly cause disease. This includes studying genomes of pathogens which cannot be cultured outside of a host. In the past, researchers and medical professionals found it difficult to study and understand pathogenic traits of infectious organisms. With newer technology, pathogen genomes can be identified and sequenced in a much shorter time and at a lower cost, thus improving the ability to diagnose, treat, and even predict and prevent pathogenic infections and disease. It has also allowed researchers to better understand genome evolution events - gene loss, gain, duplication, rearrangement - and how those events impact pathogen resistance and ability to cause disease. This influx of information has created a need for bioinformatics tools and databases to analyze and make the vast amounts of data accessible to researchers, and it has raised ethical questions about the wisdom of reconstructing previously extinct and deadly pathogens in order to better understand virulence.
Host–parasite coevolution is a special case of coevolution, where a host and a parasite continually adapt to each other. This can create an evolutionary arms race between them. A more benign possibility is of an evolutionary trade-off between transmission and virulence in the parasite, as if it kills its host too quickly, the parasite will not be able to reproduce either. Another theory, the Red Queen hypothesis, proposes that since both host and parasite have to keep on evolving to keep up with each other, and since sexual reproduction continually creates new combinations of genes, parasitism favours sexual reproduction in the host.
Bryan Thomas Grenfell is a British population biologist and the Kathryn Briger and Sarah Fenton Professor of Ecology and Evolutionary Biology and Public Affairs at the Princeton School of Public and International Affairs at Princeton University.
In biology, a pathogen in the oldest and broadest sense, is any organism or agent that can produce disease. A pathogen may also be referred to as an infectious agent, or simply a germ.
Julian Parkhill is the Marks & Spencer Professor of Farm Animal Health, Food Science and Safety in the Department of Veterinary Medicine at the University of Cambridge. He previously served as head of pathogen genomics at the Wellcome Sanger Institute.
Silvie Huijben is an evolutionary biologist and Assistant Professor at Arizona State University. The Huijben Lab uses fieldwork, lab experiments, and mathematical modeling to study antimalarial and insecticide resistance in parasites, such as disease-transmitting mosquitoes. Her work is focused on applying evolutionary theory to produce resistance management strategies to best combat malaria.
Andrew Rambaut is a British evolutionary biologist, as of 2020 Professor of molecular evolution at the University of Edinburgh.
Vaccine resistance is the evolutionary adaptation of pathogens to infect and spread through vaccinated individuals, analogous to antimicrobial resistance. It concerns both human and animal vaccines. Although the emergence of a number of vaccine resistant pathogens has been well documented, this phenomenon is nevertheless much more rare and less of a concern than antimicrobial resistance.
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