WORLD OF MICROBIOLOGY AND IMMUNOLOGY West Nile virus597•
Concurrent with his work with Enders and Robbins,
Weller was named assistant director of the research division of
infectious diseases at Children’s Hospital in 1949. He held this
position until 1954. At the same time, he began teaching at
Harvard in tropical medicine and tropical public health, mov-
ing from instructor to associate professor. In 1953, Weller and
Robbins shared the Mead Johnson Prize for their contributions
to pediatric research. Then, in 1954, Weller was named Richard
Pearson Strong Professor of Tropical Public Health and chair
of the public health department at Harvard. As a consequence,
he moved his research facilities to the Harvard Medical School.
Later, he was appointed director of the Center for Prevention of
Infectious Diseases at the Harvard School of Public Health.
From the end of World War II until 1982, Weller also
continued his research on two types of helminths, trichinella
spiralisand schistosoma mansoni. Helminths are intestinal par-
asites, and these two cause, respectively, trichinosis, which can
also severely affect the human musculature, and schistosomia-
sis. Weller was concerned with the parasites’ basic biology and
performed various diagnostic studies on them. His contribu-
tions to current understanding of these parasites are significant,
advancing an understanding of the ailments they cause.
Weller spent a portion of the same period (1957 to 1973)
establishing the basic available knowledge concerning
cytomegalovirus (commonly known as CMV), which causes
cell enlargement in various organs. Weller’s most important
finding in this area regarded congenital transmission of both
CMV and rubella, a virus also known as German measles. A
pregnant woman infected with either of these viruses may pass
the infection on to her fetus. Weller showed that infected new-
borns excreted viral strains in their feces, providing another
source for the spread of the diseases. His findings became sig-
nificant when it was also learned that children born to infected
mothers often risked birth defects.
In 1962, Weller, along with Franklin Neva, was able to
grow and study German Measles in tissue cultures. These two
also went on to grow and isolate the chickenpox virus.
Subsequently, Weller was the first to show the common origin
of the varicellavirus, which causes chicken pox, and the herpes
zoster virus, which causes shingles. In 1971, Weller was the first
to prove the airborne transmission of pneumocystis carinii, a
form of pneumonia that later appeared as a frequent side effect
of the human immunodeficiency viruscommonly known as HIV.
Weller was elected to the National Academy of Sciences
in 1964. In addition, he served on advisory committees of the
World Health Organization, the Pan American Health
Organization, the Agency for International Development, and
the National Institute of Allergy and Infectious Disease. He
continued his position at Harvard until 1985, when he became
professor emeritus. While at Harvard, he helped establish the
Public Health Department’s international reputation. In 1988,
Weller gave the first John F. Enders Memorial Lecture to the
Infectious Disease Society of America. In addition to his
Nobel Prize, Weller was the recipient of many awards and
honorary degrees during his career.See alsoLaboratory techniques in immunology; Virology;
Virus replication; Viruses and responses to viral infectionWWest Nile virusESTNILE VIRUS
The West Nile virus is a member of the family Flaviviridae, a
virus that has become more prominent in Europe and North
America in the past decade. The virus, which is closely related
to the St. Louis encephalitis virus found in the United States,
causes an encephalitis (swelling of the brain) in domestic ani-
mals (such as horses, dogs, cats), wild animals, and wild birds.
When transferred from an infected animal to a human, the
viral infection can produce encephalitis as well as inflamma-
tionof nerve cells of the spinal cord (meningitis).
In 1937, the virus was isolated from a woman in the
West Nile District of Uganda. This locale was the basis for the
designation of the virus as the West Nile virus. During the
1950s, the ability of the virus to cause the serious and life-
threatening human disease was recognized. In the 1960s, the
virus was established as a cause of equine encephalitis.
Whether the virus has spread geographically from
Uganda, or whether increased surveillance has detected the
virus in hitherto unsuspected regions is not clear. However, the
pattern of detection has been that of a global dissemination.
Long found in humans, animals, and birds in Africa, Eastern
Europe, West Asia, and the Middle East, the virus was first
detected in North America in 1999.
The virus has come to prominent attention in North
America following its 1999 appearance on the continent. That
year, 62 cases of the disease were reported in New York City.
Seven people died. The following year 21 more cases occurred,
and two of the people died. In 1999 and 2000, the West Nile
virus was confined to the northeastern coastal states of the
United States. However, an inexorable spread to other regions
of the country and the continent has begun. In the summer of
2001, dead birds that tested positive for the virus were found as
far north as Toronto, Canada, as far south as the northern por-
tion of Florida, and as far west as Milwaukee, Wisconsin.
Scientists anticipate that the virus will continue to disseminate.
During the summer of 2002, more than 300 cases and at least
14 deaths were reported—with a continued spread of the virus
into the western United States. By August 2002, West Nile
virus was reported in 41 states.
The mosquitoes are the prime vector of the West Nile
virus. When mosquitoes obtain a blood meal from an infected
animal or a bird, they acquire the virus. The virus resides in
the salivary glands of the mosquito, to be passed on to a
human when the mosquito seeks another blood meal. The
cases in New York City, especially those in 2000, are thought
to have been caused by the bite of virus-infected mosquitoes
that survived the cold winter months. The emergence of the
mosquito in the spring can facilitate the re-emergence of the
virus. For example in North America, there were large die-offs
of crow populations due to West Nile virus in the Spring of
2000 and then again in the Spring of 2001.
Upon entry to a host’s bloodstream, multiplication of
the virus in the blood occurs. Then, by a mechanism that is not
yet deciphered, the virus crosses the barrier between the blood
and the brain. Subsequent multiplication of the virus in brain
tissue causes nervous system malfunction and inflammation of
the infected brain tissue.womi_W 5/7/03 10:18 AM Page 597