I am currently Professor Emeritus of Preventive Medicine and of Medicine at the
University of Kansas Medical Center. My entire career has focused on infectious
diseases and epidemiology. Even when I was in high school, I had already developed
an interest in microbial agents. This was stimulated by the scientists at the Rocky
Mountain Laboratory in Hamilton, Montana, particularly Drs. Herald R. Cox, William
Jellison and Edward Steinhaus. Respiratory virus infections have been one of my research interests for many years. How I got interested in influenza in the first place, however, is somewhat vague in my memory. I probably got interested in this disease during my medical school years at the University of Michigan Medical School at Ann Arbor, Michigan. I do remember vividly my first attack of influenza during the fall of 1943 when I was a first year medical student. I had a fever, headache, malaise, myalgia, and just felt lousy. I must have looked so terrible and uncomfortable that my histology lab
teacher "ordered" me to go home. Undoubtedly my interest had been "influenzed" by
Dr. Thomas Francis, Jr., who taught us communicable diseases. He and Magill
independently discovered influenza virus type B in 1940, and he and Jonas Salk
reported on their studies of inactivated influenza vaccine in 1945. In 1960 he
proposed the "Doctrine of Original Antigenic Sin", a phenomenon of immunological
fingerprinting conferred on a person by prior influenza virus infections. When a
person is infected with a current epidemic strain of influenza virus, antibody
response is elicited for the previously infected strains as well as the current
strain. That is, there is heterotypic as well as homotypic antibody response.
I had read all about the seriousness of the Spanish flu pandemic of 1918-1919.
But I did not have any professional experience with influenza until July of 1957
when I was asked by Alexander D. Langmuir, Founder of the Epidemic Intelligence
Service of CDC, to investigate an outbreak of influenza at Grinnell, Iowa, where a
conference was being held. Cases of influenza suddenly appeared shortly after
arrival of the participants by train from California. This outbreak was the source
from which influenza spread to various parts of the United States by the participants
returning to their homes. A number of outbreaks occurring in different parts of the
United States were traced to the infected participants. During that winter my CDC
colleagues and I investigated an epidemic of Asian flu in Southwest High School in
Kansas City, Missouri. The investigation yielded some very important data on how the
virus affected the students and their families. When Hong Kong influenza hit the
Kansas City Metropolitan Area again during the winter of 1968, we decided to do a
study in the same high school. These studies had provided us an opportunity to
compare the epidemiological characteristics of the two pandemics of influenza
occurring 11 years apart.
Among the viral respiratory infections, I consider influenza most intriguing.
It has caused major pandemics from time to time, probably as early as 1510, and the
virus tends to mutate every 2-3 years to cause epidemics. Besides the attack of
influenza I had in 1943, I had experienced clinical influenza (either laboratory
confirmed or severe influenza-like illness) at least three other times in my life.
The second time was in 1953 during my military duty in Korea, and the third time in
1968 when an explosive outbreak of influenza occurred among the attendees of an
international conference being held in Tehran. The last attack of typical clinical
influenza I had was in 1977. The influenza vaccines that I have taken the last
several years undoubtedly have either protected me against influenza or have modified
the illness. When will I come down with another bout of influenza is unpredictable.
Neither is pandemic influenza predictable. The vagaries of the influenza virus
continue to kindle my fascination and imagination. Aquatic birds have been identified
primary reservoirs of influenza viruses in nature, and pigs are considered as
intermediate hosts. Presumably, new human influenza viruses emerge as a result of
mixed influenza virus infections in pigs. Exactly how these newly emerged viruses
become human pathogens and cause widespread epidemics in human populations is still a
puzzle. Much remains to be learned.
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