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Burnet, Frank Macfarlane


(b. Traralgon, Australia, 3 September 1899; d. Port Fairy, Australia, 31 August 1985)

virology, immunology, microbiology, tumor biology, gerontology.

Burnet was a leading virologist and immunologist of the twentieth century. He contributed to the understanding of the complexity of host-parasite interactions through his studies of various microbial infections, including the bacteriophage phenomenon, Q fever, poliomyelitis, influenza, psittacosis, and herpes. With the insight gained from these studies, he proposed in 1949 the theory of the “self” and “not-self” distinction and immune “tolerance,” which was confirmed by the team of British scientist Peter B. Medawar. For this achievement, Burnet and Medawar shared the Nobel Prize in Physiology or Medicine in 1960. Burnet’s other major contribution to immunology was his clonal selection theory of 1957, which hypothesized that the antibody is produced through a Darwinian natural selection process among immunocompetent cells, which became one of the central doctrines of modern immunology.

Early Life and Education. Burnet was born in Traralgon, Australia, the second child of a family of Scottish descent.

As a boy he was interested in beetle collecting, and in 1913, he entered Geelong College in Victoria, from which he graduated in 1916. He then enrolled in the University of Melbourne as a medical student, and successfully completed coursework in 1922, standing second in his class. Although he initially hoped to be a clinical neurologist after finishing his medical education, he eventually decided to pursue a career of laboratory research and entered the Walter and Eliza Hall Institute in Melbourne to study pathology and microbiology. In 1924, he received his MD from the University of Melbourne and published his first research papers on typhoid fever.

In 1925, a chance to broaden his perspective came when he went to the Lister Institute of Preventive Medicine in London as an assistant curator of the National Collection of Type Cultures. There he studied phage-bacterium interaction with leading British microbiologists and enrolled in the University of London for his graduate degree. His PhD dissertation (1928) interpreted the appearance of a specific strain of Salmonella in the presence of particular types of phages as the result of selective proliferation of the strain due to its resistance to the phages, rather than the transformation of the bacterium from one strain to another under their influence. In 1927, he returned to the Hall Institute as an assistant director, and in 1928, he married Edith Linda Marston Druce, an Australian he had met in 1923.

Host-Parasite Interaction and Infectious Disease. While staying at London, Burnet was influenced by his supervisors J. C. G. Ledingham and J. A. Arkwright, who studied bacterial variation and the problems of healthy carriers of infectious diseases. From them, Burnet learned a new direction in infectious diseases research, which began to depart from the previous paradigm established by the German bacteriologist Robert Koch and his colleagues. While Koch generally thought that a particular disease was caused by a specific germ strain, which—he assumed—hardly changed its character, Ledingham and Arkwright began to study the variation of bacteria and wrote a book on the healthy-carrier state, which showed that the occurrence of infectious diseases was dependent on numerous constitutional and environmental factors of the host that the earlier germ theorists had ignored. Healthy carriers were those who did not develop symptoms of disease due to these various factors, despite the presence of infectious agents in their body. Burnet’s research after returning to Melbourne followed this new direction.

The first case Burnet investigated with the insight gained in London was “the Bundaberg tragedy,” an incident involving the death of twelve children among the twenty-one who had been inoculated with diphtheria vaccine at Bundaberg, Queensland, in 1928. Although he found that the vaccine was contaminated with a strain of Staphylococcus, he did not attribute the cause of the tragedy to the mere presence of the bacterium within the body, because it was a common germ found on healthy human skin. How could such a normal bacterium cause death? For him, the real problem was that a large number of the bacteria had been suddenly injected into a blood vessel, which was not their natural habitat. Two factors, the number of the bacteria and their place within the body, were thus responsible for such an extreme and unnatural case of host-parasite interaction—the death of the twelve children.

Burnet’s research on the bacteriophage led him to another example of the diversity of interactions between hosts and parasites. Although he studied various aspects of the bacteriophage, including its serological properties used for classification, his most pressing concern was its biological identity. On this issue, he was familiar with the controversy between the French-Canadian microbiologist Félix d’Herelle and the Belgian immunologist Jules Bordet. Burnet supported the former’s view that the phage was a bacterial virus, rather than the latter’s argument that it was merely a microbial metabolic product. Agreeing with d’Herelle, Burnet argued that lysogeny—a phenomenon that would later be known as a state in which a phage’s genes were integrated into a bacterium’s genome—was a sort of “symbiosis” between the bacterium and phage that had coevolved for a long time (Burnet, 1932, p. 859). In this respect, lysogeny was similar to the healthy-carrier states that his supervisors were studying, because in both cases, the parasite maintained a coexistence with its hosts, rather than destroying them. Burnet thus began to understand host-parasite interactions from an ecological and evolutionary viewpoint.

His study of psittacosis strengthened this view. During the 1930s, he found that many healthy-looking Australian parrots carried in their body the pathogen of psittacosis, which was assumed to be a kind of virus. They developed the symptoms of the disease only when they were kept in a stressful environment such as a cage, which disturbed the “equilibrium” between them and the pathogen. In the wild state, however, the host and parasite could maintain a harmonious cohabitation.

Burnet found another case of this cohabitation in his research on rickettsial diseases, particularly Q-fever. What was interesting in this case was the relationship between rickettsias and their “intermediate hosts,” such as mites, ticks, and lice. While previous researchers had seldom asked why intermediate hosts did not develop diseases to which humans were susceptible, Burnet became interested in this question during his investigations into the Q-fever pathogen, especially its morphology, growth patterns, natural vectors,

and relation to other rickettsial diseases. With these studies and others’ research on similar subjects, he argued in 1942 that the rickettsia’s intermediate hosts were actually its “natural” hosts that had maintained a peaceful relationship with it through their long coevolution, in which humans were not a part. The fever in human rickettsial infection was only an unnatural case of host-parasite interaction caused by the accidental invasion of humans into the peaceful world of the rickettsia and its natural hosts.

Burnet’s poliovirus research during the 1930s led to a similar conclusion. Although his immediate concern was the experimental study of its properties such as serological differences between Australian and American strains, he was also interested in larger evolutionary issues. Through his experiments on the routes of poliovirus infection and other scholars’ studies of its epidemiological changes in history, he found that the disease had originally been a mild infection affecting only the pharyngeal region till the early twentieth century. The severe poliomyelitis characterized by neuronal damage was caused by variant forms of the virus that had evolved in an overly improved hygienic environment of twentieth-century Western countries. While the virus tended to reduce its virulence

to promote the survival of both hosts and parasites in its natural states, these developed countries blocked this usual pathway of the virus’s evolution and made it search for other ways that promoted its survival at the cost of its host.

Self, Not-Self, and Tolerance. While Burnet had mainly been interested in virology and microbiology during the 1930s, after 1940 he began to investigate immunological problems as well. But one of his most important contributions to immunology, the theory of “self” and “tolerance,” grew from his studies of host-parasite interactions. He was also influenced by the ecological and evolutionary view articulated in H. G. Wells, Julian Huxley, and G. P. Wells’s The Science of Life(1929).

Burnet published his first account of “self” and “tolerance” in Biological Aspects of Infectious Disease (1940), in which he summarized contemporary knowledge on microbial diseases. In this book, he argued that every organism was both a predator and prey in the food chain and was able to maintain the boundary of its “self” during predation processes in the wild. Indeed, the predator could destroy its prey in digestive organs without sacrificing its own body. But the “prey” could also evade the predator’s destruction system and eventually overwhelm it. If the prey was a microbe, it would then become an agent causing an infectious disease. As Burnet had observed in his previous research, however, the interaction between two organisms did not always bring about such a destructive consequence. Rather, continued infection of one organism by another during their evolution often resulted in mutual “tolerance,” because it would benefit both species by allowing their survival and further proliferation.

Burnet maintained his biological view in his next book,The Production of Antibodies (1941). While criticizing contemporary chemical immunologists’ “template theory” of antibody formation—which was the orthodox view at the time—he proposed that the antibody was produced by enzymes, which had lifelike characters such as adaptation and self-synthesis. This idea came from two sources. The first was his research following the Bundaberg tragedy on the antibody response against Staphylococcus toxoid, which led him to postulate that the logarithmic rise of antibody titer during the secondary contact with the toxoid could be explained by the “replication” of some cellular or subcellular entities responsible for antibody production after the first inoculation. The second source was the biochemical investigations at the Rockefeller Institute that showed the adaptability and self-synthesizing capacity of some enzymes.

Based on these sources, Burnet argued that antibodies were produced by the adaptive enzymes, which could proliferate in immune cells and modify their structure to the antigen. The antibody was the enzyme’s “partial replica” released into the serum. This idea was different from that of chemical immunologists such as Friedrich Haurowitz and Stuart Mudd, who claimed that the antigen directly shaped the antibody by physically impressing it as its “template.”

In this 1941 book, Burnet also discussed “tolerance.” He cited James Murphy of the Rockefeller Institute and other researchers who observed that the embryonic animal body “tolerated” foreign cells and molecules without antibody response, although it rejected them as it became older. Burnet himself had begun to use the chick embryo to culture various viruses while he stayed at the National Institute of Medical Research in London from 1932 to 1933. He asked why these young animals did not show immune response to the foreign entity but did after becoming adults. He assumed that they could not do so when they were very young, because they then were immature animals without sufficient “training” in dealing with microbes (Burnet, 1941, p. 46).

Although this explanation was for him only a tentative hypothesis, it reveals that Burnet gradually became interested in the differential immune response of animals according to their age. Indeed, he emphasized that a host body’s age, along with its sex, genetic constitution, and environmental conditions, was important for determining whether it developed a disease after contacting a microbe. While earlier scientists scarcely considered the importance of these various factors, he regarded them as crucial components in the pathogenesis of infectious disease.

Burnet observed a paradoxical phenomenon about age, which he called “the age-incidence of infectious disease” (Burnet, 1940, p. 199). While it had been often thought that younger animals and humans were more susceptible to infectious diseases than adults due to their weak and immature bodies, more recent investigations showed that their survival rates in many infections were higher. He explained this phenomenon by postulating that the overly strong immune response in the adult body could often overwhelm and destroy rather than defend it against germs. Children’s immune response was less strong but quite adequate for protecting their body without threatening it. But the cases of infants and embryos were different, because their weak immune system might allow unrestrained proliferation of microbes in their body and cause disease and death. Yet the recent statistical data showed that even these very young organisms were better survivors in many infections than the adult. What, then, made them different? Since the peculiar characters of young animals’ growing immune system seemed to be responsible for their higher chance of survival, Burnet recognized the need to know more about developmental processes in general in order to understand the growth of a young body’s immunity from broader biological perspectives.

During the 1940s, cytoplasmic inheritance theories of enzymes offered a better explanation of embryogenesis and development than any other theories, especially those based on orthodox genetics. When mainline geneticists, particularly those in the United States, could not satisfactorily explain how nuclear genes directed cell differentiation in embryogenesis, the advocates of cytoplasmic inheritance, such as Tracy Sonneborn and Sol Spiegelman, could do so by postulating the existence of cytoplasmic entities—some of which were enzymes—that were inherited by descendent cells and adapted according to environmental conditions. These advocates thought that gradual hereditary changes of these entities guided cell differentiation during the developmental process as they were influenced by intercellular andintracellular environments.

Burnet began to use cytoplasmic inheritance theories after he returned from his wartime trip to the United States and became the new director of the Hall Institute and professor of experimental medicine at the University of Melbourne in 1944. For him, there were two reasons to use the theories. The first was that they were compatible with the self-replicating adaptive enzyme theory he had proposed in 1941. He wrote that the enzyme was located within the cytoplasm and its adaptation and replication occurred during embryogenesis like the hereditary entities Sonneborn and Spiegelman had proposed. The second and more important reason was that it helped him explain the differential response of the host toward microbes according to its age. Indeed, from the perspective of virology and bacteriology, the embryo of an animal, which cytoplasmic inheritance theorists aimed to understand, was only an extremely young host during whose growth diverse viruses and bacteria could gain entrance.

In the second edition of The Production of Antibodies(1949), Burnet proposed a new theory of “self” and “tolerance” based on his thoughts about the role of age and cytoplasmic inheritance in disease causation. Burnet cited two examples of “tolerance” developed in young animals, whose susceptibility to infectious disease was crucial for “the age-incidence of infectious disease”: From 1936 to 1945, Erich Traub at the Rockefeller Institute and Ray Owen at the University of Wisconsin had observed that red cells with different blood types and viruses could be introduced into an embryonic animal that “tolerated” them even after it became an adult.

Burnet explained these observations with cytoplasmic inheritance. He thought that a “self-marker” that existed on every somatic cell was recognized by cytoplasmic adaptive enzymes within phagocytes during embryonic life. Through this recognition process, the adaptive enzymes’ structure was modified according to the shape of the self-marker and inherited by descendant phagocytes till the end of the developmental phase. The adaptive enzymes could then “fit” with the marker on each somatic cell while phagocytes dealt with its normal death occurring in an adult animal.

But a foreign molecule that did not “fit” with the enzyme provoked antibody response by distorting the adaptive enzymes’ shape and making them the “primary units,” whose partial replicas were released as antibodies.Yet even such a “foreign” molecule could be recognized as a part of the organism’s “self” and be “tolerated” thereafter, if it had been introduced during embryogenesis and modified the shape of adaptive enzymes that could thus remember its existence within the body. Hence Burnet argued that “the process by which self-pattern becomes recognizable takes place during the embryonic or immediately post-embryonic stages” (Burnet, 1949, p. 102). This argument was experimentally confirmed in 1953 by Medawar’s British team.

The Influenza Virus. While Burnet’s immunological research was mainly theoretical, his study of the influenza virus was mostly experimental. Although the latter did not make him as famous as the former did, many of his ideas gained from it were important for shaping his immuno-logical theories as well as for the progress of animal virology in general.

Burnet began to be interested in the influenza virus when he saw its experimental pathogenesis during his stay in London in 1933. After returning to Australia, he started his own research and succeeded in culturing the virus within the chick embryo. He also developed the method of “pock counting” as a means of virus titration using the same embryo. Moreover, he attempted to develop during the Second World War a live influenza vaccine for Australians and their army, although it was not very successful.

In the 1940s, Burnet and his team studied viral hemagglutination—the phenomenon in which viruses clumped red blood cells—as a model of virus-cell interaction. Since the red cells treated with the viruses were agglutinated by the sera which had not clumped them before treatment, his team studied more detailed aspects of such an “enzyme-like character” of human influenza viruses and other pathogens with similar characters, such as the mumps virus, the Newcastle disease virus, and the swine influenza virus. Burnet’s team noticed that after being agglutinated by one viral strain, the red cells were not agglutinated by certain other strains. His team also showed that the virus action on red cells could be emulated by cholera vibrio filtrates, which, he thought, contained the receptor-destroying enzyme (RDE) that acted upon the red cell’s surface. But certain kinds of mucins and mucoids had an opposite capacity. They inhibited the activity of the virus, which in turn, along with RDE, could destroy this inhibitory function.

To interpret the results of his influenza virus research, Burnet used orthodox genetics rather than cytoplasmic inheritance theories. In 1943, Burnet wrote that the change of viral character during chick embryo passages was due to the “mutation” of viral genes. During the 1950s, he studied genetic recombination between two viral strains by mixed infections and argued that the influenza genome consisted of many distinct “linkage groups” that replicated independently. This argument, which was confirmed in the late 1960s, reveals his familiarity with and full acceptance of standard genetic theories.

The Clonal Selection Theory. Even though Burnet used orthodox genetics for his clonal selection theory in 1957, he had begun constructing this theory before abandoning cytoplasmic inheritance hypothesis. In the final part of Production of Antibodies (1949), Burnet postulated that there could be various kinds of “primary units”—which, he thought, were cytoplasmic hereditary entities—in an embryo, and some units that bound with “self” molecules were inactivated during development. The units that were not inactivated could then survive after fetal life and would be converted into antibodies when foreign molecules were introduced. But Burnet did not develop this idea further at the time. In Enzyme, Antigen, and Virus(1956), he still maintained his previous standpoint despite some changes of vocabulary.

Burnet’s mature idea of clonal selection was proposed in 1957 after he read the Danish immunologist Niels K. Jerne’s article, “The Natural-Selection Theory of Antibody Formation” (1955). According to Jerne, antibodies against the bodily components were eliminated during embryogenesis and then among the remaining ones those with an affinity to foreign molecules were selectively replicated to attack them.

Although Burnet did not immediately realize the implication of this idea, he eventually found that the antibody in Jerne’s theory could be replaced with the antibody-producing cell, and somatic mutation during embryonic life could be suggested as a probable mechanism for expanding antibody diversity. In a paper published in 1957, Burnet wrote that randomization of antibody repertoire took place through somatic mutations during embryogenesis, and those cells producing antibodies against the body were removed. After the end of development, the remaining immune cells protected the organism from foreign antigens by being selectively stimulated to proliferate by the antigen. This was an application of “population genetics” rather than cytoplasmic inheritance to the problem of antibody production, although an important part of his 1957 idea was already formed in 1949 using the latter theory (Burnet, 1957, p. 68). In 1959, Burnet stated, “Self-not-self recognition means simply that all those clones which would recognize...a self component have been eliminated in embryonic life” (p. 59). David W. Talmage at the University of Chicago independently proposed in 1957 that the replicating unit in Jerne’s theory should be the cell.

Autoimmunity, Cancer, and Aging. In 1965, Burnet retired from the directorship of the Hall Institute and became a professor emeritus of the University of Melbourne. In 1942, he was elected a Fellow of the Royal Society and was knighted in 1951. He served as president of the Australian Academy of Science from 1965 to 1969, and was awarded numerous honors, such as the Copley Medal of the Royal Society (1959) and the Nobel Prize (1960). He also received honorary doctorates from many prestigious institutions, including Cambridge (1946), Harvard (1960), and Oxford (1968). After retirement, he worked for Australian science policy, public health, and education reform as a national scientific leader.

Meanwhile, Burnet kept writing about several important topics in biomedicine, including autoimmunity, aging, and cancer. In 1972, he argued that autoimmune disease was caused by the attack on “self” molecules by the “forbidden clones” of immunocytes that arose from somatic mutation or physiological changes. Aging was another problem that was explained by the failure of the immune system. In 1970, he argued that the weakening of the immune cells that approached the limit of proliferation caused the disturbance of other somatic cells and the senescence of the whole body. From 1973, however, he qualified this argument and claimed that aging resulted from accumulated somatic mutations engendered by the DNA polymerase, whose error rate was determined through evolution. The cause of cancer was similar. After 1957, like many other cancer researchers, he tried to understand how repeated mutations made a somatic cell cancerous, and attempted to conceptualize cancer in relation to immunity and aging. These active theoretical studies were discontinued only when he died of cancer at Port Fairy, Australia, in 1985.



“Bacteriophage Phenomena in Relation to the Antigenic Structure of Bacteria.” PhD diss., University of London, 1928.

“Lysogenicity as a Normal Function of Certain Salmonella Strains.” Journal of Pathology and Bacteriology 35 (1932): 851–863. Biological Aspects of Infectious Disease. Cambridge, U.K.: Cambridge University Press, 1940.

With Mavis Freeman, A. V. Jackson, and Dora Lush. The Production of Antibodies: A Review and a Theoretical Discussion. Melbourne: Macmillan, 1941. 2nd ed. With Frank Fenner. The Production of Antibodies. Melbourne: Macmillan, 1949.

“The Rickettsial Diseases in Australia.” Medical Journal of Australia 2 (1942): 129–134.

With D. R. Bull. “Changes in Influenza Virus Associated with Adaptation to Passage in the Chick Embryo.” Australian Journal of Experimental Biology and Medical Science 21 (1943): 55–69.

Enzyme, Antigen, and Virus: A Study of Macromolecular Pattern in Action. Cambridge, U.K.: Cambridge University Press, 1956.

“Cancer—A Biological Approach.” British Medical Journal 1(1957): 779–847.

“A Modification of Jerne’s Theory of Antibody Production Using the Concept of Clonal Selection.” Australian Journal of Science 20 (1957): 67–69.

Clonal Selection Theory of Acquired Immunity. Nashville, TN:Vanderbilt University Press, 1959.

Changing Patterns: An Atypical Autobiography. Melbourne:William Heinemann, 1968.

“An Immunological Approach to Ageing.” Lancet 2 (1970):358–360.

Auto-immunity and Auto-immune Disease: A Survey for Physician or Biologist. Philadelphia, PA: F. A. Davis Company, 1972.

“A Genetic Interpretation of Ageing.” Lancet 2 (1973): 480–483.


Billingham, R. E., L. Brent, and Peter B. Medawar. “‘Actively Acquired Tolerance’ of Foreign Cells.” Nature 172 (1953): 603–606.

Crist, Eileen, and Alfred I. Tauber. “Selfhood, Immunity, and the Biological Imagination: The Thought of Frank Macfarlane Burnet.” Biology and Philosophy 15 (2000): 509–533.

Fenner, Frank. Sir Macfarlane Burnet: Scientist and Thinker. St. Lucia: University of Queensland Press, 1988. A short description of Burnet’s life and work by his close colleague.

Jerne, Niels K. “The Natural-Selection Theory of Antibody Formation.” Proceedings of the National Academy of Sciences of the United States of America41 (1955): 849–857.

Ledingham, J. C. G., and J. A. Arkwright. The Carrier Problem in Infectious Diseases. London: Edward Arnold, 1912.

Park, Hyung Wook. “Germs, Hosts, and the Origin of Frank Macfarlane Burnet’s Theory of ‘Self’ and ‘Tolerance,’ 1936–1949.”Journal of the History of Medicine and Allied Sciences 61 (2006): 492–534.

Podolsky, Scott H., and Alfred I. Tauber. The Generation of Diversity: Clonal Selection Theory and the Rise of Molecular Immunology. Cambridge, MA: Harvard University Press, 1997.

Sapp, Jan. Beyond the Gene: Cytoplasmic Inheritance and the Struggle for Authority in Genetics. New York: Oxford University Press, 1987.

Sexton, Christopher. The Seeds of Time: The Life of Sir Macfarlane Burnet. Oxford, U.K.: Oxford University Press, 1991. This biography includes Burnet’s complete bibliography.

Talmage, David W. “Allergy and Immunology.” Annual Review of Medicine 8 (1957): 239–256.

Tauber, Alfred I. The Immune Self: Theory or Metaphor Cambridge, U.K.: Cambridge University Press, 1994. This philosophical monograph analyzes the nature and development of modern immunology, including Burnet’s place in it.

Tauber, Alfred I., and Scott H. Podolsky. “Frank Macfarlane Burnet and the Immune Self.” Journal of the History of Biology 27 (1994): 531–573. A good overview of Burnet’s immunology and philosophy from the 1920s to 1959.

Wells, Herbert George, Julian S. Huxley, and George P. Wells. The Science of Life: A Summary of Contemporary Knowledge about Life and Its Possibilities. London: Amalgamated Press, 1929.

Hyung Wook Park

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Burnet, Frank Macfarlane (1899-1985)

Burnet, Frank Macfarlane (1899-1985)

Australian immunologist and virologist

While working at the University of Melbourne's Walter and Eliza Hall Institute for Medical Research in the 1920s, Frank Macfarlane Burnet became interested in the study of viruses and bacteriophage (viruses that attack bacteria ). That interest eventually led to two major and related accomplishments. The first of these was the development of a method for cultivating viruses in chicken embryos, an important technological step forward in the science of virology . The second accomplishment was the development of a theory that explains how an organism's body is able to distinguish between its own cells and those of another organism. For this research, Burnet was awarded a share of the 1960 Nobel Prize for physiology or medicine (with Peter Brian Medawar ).

Burnet was born in Traralgon, Victoria, Australia. His father was Frank Burnet, manager of the local bank in Traralgon, and his mother was the former Hadassah Pollock MacKay. As a child, Burnet developed an interest in nature, particularly in birds, butterflies, and beetles. He carried over that interest when he entered Geelong College in Geelong, Victoria, where he majored in biology and medicine.

In 1917, Burnet continued his education at Ormond College of the University of Melbourne, from which he received his bachelor of science degree in 1922 and then, a year later, his M.D. degree. Burnet then took concurrent positions as resident pathologist at the Royal Melbourne Hospital and as researcher at the University of Melbourne's Hall Institute for Medical Research. In 1926, Burnet received a Beit fellowship that permitted him to spend a year in residence at the Lister Institute of Preventive Medicine in London. The work on viruses and bacteriophage that he carried out at Lister also earned him a Ph.D. from the University of London in 1927. At the conclusion of his studies in England in 1928, Burnet returned to Australia, where he became assistant director of the Hall Institute. He maintained his association with the institute for the next thirty-seven years, becoming director there in 1944. In the same year, he was appointed professor of experimental medicine at the University of Melbourne.

Burnet's early research covered a somewhat diverse variety of topics in virology. For example, he worked on the classification of viruses and bacteriophage, on the occurrence of psittacosis in Australian parrots, and on the epidemiology of herpes and poliomyelitis . His first major contribution to virology came, however, during his year as a Rockefeller fellow at London's National Institute for Medical Research from 1932 to 1933. There he developed a method for cultivating viruses in chicken embryos. The Burnet technique was an important breakthrough for virologists since viruses had been notoriously difficult to culture and maintain in the laboratory.

Over time, Burnet's work on viruses and bacteriophage led him to a different, but related, field of research, the vertebrate immune system . The fundamental question he attacked is one that had troubled biologists for years: how an organism's body can tell the difference between "self" and "not-self." An organism's immune system is a crucial part of its internal hardware. It provides a mechanism for fighting off invasions by potentially harmfuland sometimes fatalforeign organisms (antigens) such as bacteria, viruses, and fungi . The immune system is so efficient that it even recognizes and fights back against harmless invaders such as pollen and dust, resulting in allergic reactions.

Burnet was attracted to two aspects of the phenomenon of immunity . First, he wondered how an organism's body distinguishes between foreign invaders and components of its own body, the "self" versus "not-self" problem. That distinction is obviously critical, since if the body fails to recognize that difference, it may begin to attack its own cells and actually destroy itself. This phenomenon does, in fact, occur in some cases of autoimmune disorders .

The second question on which Burnet worked was how the immune system develops. The question is complicated by the fact that a healthy immune system is normally able to recognize and respond to an apparently endless variety of antigens, producing a specific chemical (antibody ) to combat each antigen it encounters. According to one theory, these antibodies are present in an organism's body from birth, prior to birth, or an early age. A second theory suggested that antibodies are produced "on the spot" as they are needed and in response to an attack by an antigen.

For more than two decades, Burnet worked on resolving these questions about the immune system. He eventually developed a complete and coherent explanation of the way the system develops in the embryo and beyond, how it develops the ability to recognize its own cells as distinct from foreign cells, and how it carries with it from the very earliest stages the templates from which antibodies are produced. For this work, Burnet was awarded a share of the 1960 Nobel Prize in physiology or medicine. Among the other honors he received were the Royal Medal and the Copley Medal of the Royal Society (1947 and 1959, respectively) and the Order of Merit in 1958. He was elected a fellow of the Royal Society in 1947 and knighted by King George V in 1951.

Burnet retired from the Hall Institute in 1965, but continued his research activities. His late work was in the area of autoimmune disorders, cancer, and aging. He died of cancer in Melbourne in 1985. Burnet was a prolific writer, primarily of books on science and medicine, during his lifetime.

See also Antigens and antibodies; Autoimmune disorders; Bacteriophage and bacteriophage typing; Immunity, cell mediated; Immunity, humoral regulation; Virology; Virus replication; Viruses and responses to viral infection

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