looking back at patients who had died mysteriously before the discovery of HIV. In 1988, for
example, researchers discovered that a Norwegian sailor named Arvid Noe, who died in 1976, had
HIV in his tissues. Reaching back further into HIV’s history was nearly impossible, because many of
its earliest victims lived in poor countries and died without any careful medical tests that would
identify unusual diseases like pneumocystis pneumonia.
It turned out that the viruses replicating in living people offered some powerful clues to the origins
of HIV. Through the 1990s, scientists at Los Alamos National Laboratory amassed a database of
genetic sequences of HIV taken from thousands of patients. They could then use supercomputers to
compare these viruses and figure out which mutations the viruses had acquired since they diverged
from a common ancestor. By adding up these mutations, the researchers found that HIV gradually
acquires mutations at a roughly regular rate. In other words, the mutations piled up like sand in an
hourglass. By measuring how high the sand had piled up, they could estimate how much time had
passed. They estimated that the common ancestor of HIV-1 existed in 1933.
That estimate has been confirmed by the remarkable discovery of HIV preserved in tissues stored
away in hospitals in Kinshasa, the capital of the Democratic Republic of the Congo in central Africa.
In 1998, David Ho and his colleagues at Rockefeller University reported that they had isolated HIV
from a blood sample taken from a patient in Kinshasa in 1959. In 2008, Michael Worobey and his
colleagues at the University of Arizona discovered HIV in a second tissue sample from another
pathology collection in Kinshasa, dating back to 1960. These two samples allowed researchers to
confirm that HIV emerged in the early 1900s.
The molecular clock created by the Los Alamos researchers was accurate enough to predict the age
of the Kinshasa viruses based on their genetic sequence alone. But the two viruses also provide a
surprising glimpse at the diversity of HIV in Kinshasa around 1960. Worobey and his colleagues
found that the old viruses were not closely related to each other. Instead, they were each closely
related to a different branch of HIV-1 found in patients today. Studying the distant kinship of these two
viruses, Worobey and his colleagues concluded that all of the major branches of HIV-1 found in the
world today already existed in 1960. What’s more, they were all probably circulating around
Kinshasa.
All this evidence is now pointing to how HIV-1 got its start. HIV-1-like viruses had been
circulating among populations of chimpanzees throughout Africa. Hunters sometimes killed
chimpanzees for meat, and from time to time they became infected by the viruses. But these hunters,
living in relative isolation, were a dead end for the viruses. In the early 1900s the opportunities for
these viruses changed as colonial settlements in central Africa began to expand to cities of ten
thousand people or more. Commerce along the rivers allowed pathogens to reach the cities from
remote forests. The chimpanzees carrying viruses most closely related to HIV-1 live today in the
jungles of southeast Cameroon. It may be no coincidence that the rivers of that region flow south and
eventually reach Kinshasa.
In the growing city of Kinshasa (then known as Leopoldville), HIV-1 could multiply. Instead of a
few dead ends, it found a population that could sustain it and inside of which it could evolve into new
forms better adapted to humans. By 1960, HIV-1 had bloomed into a wide genetic diversity, although
it probably only infected a few thousand people.