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E D I T O R I A L C O M M E N TA R Y
Ebola Virus Ecology
Joseph B. McCormick
University of Texas Health Science Center at Houston School of Public Health, Brownsville Regional Campus, Brownsville
(See the article by Leroy et al., on pages 1895–9.)
It has been nearly 30 years since Ebola
virus was identified during 2 outbreaks in
the Democratic Republic of Congo (DRC)
and Sudan [1, 2], and it has been closer
to 40 years since Marburg virus, the first
identified member of the filovirus family,
was discovered [3, 4]. Despite investigators’ considerable effort, the ecology of the
filoviruses remains arguably as obscure today as it was after these first outbreaks.
The article by Leroy et al. [5] makes a
small step toward a better understanding
of this ecology. Their study supports what
many have suspected: that the filoviruses
circulate widely in the central African rain
forests and that they can infect humans
and many nonhuman primates, including
some previously undocumented members, such as mandrills and baboons (previously infected only in the laboratory).
Although the recent outbreaks of Ebola in
chimps and gorillas have created substantial additional concern for these already
endangered species [6], the data in the
Leroy et al. article show that the virus has
been circulating in these populations, perhaps on a regular basis. The authors claim
that Ebola is not necessarily lethal in these
primates, but the infecting Ebola virus
Received 16 August 2004; accepted 16 August 2004;
electronically published 3 November 2004.
Reprints or correspondence: Dr. Joseph McCormick,
Brownsville Regional Campus, UT Health Science Center at
Houston, 80 Fort Brown, Brownsville, TX 78520 (jbmccormick
@utb.edu).
The Journal of Infectious Diseases 2004; 190:1893–4
2004 by the Infectious Diseases Society of America. All
rights reserved.
0022-1899/2004/19011-0001$15.00
strain and its virulence remain unclear. We
have known since the original Marburg
outbreak that filoviruses could infect primates, because Marburg virus was first
discovered in infected Circopithecus aethiops monkeys shipped from Uganda [7].
We also know that Marburg infections in
humans have been seen from central to
southern Africa and are possibly ongoing
in eastern DRC [8–12], but we know virtually nothing of the ecology of the Marburg or Ebola strains in that or any other
geographic area.
In 1990, the scientific world was surprised by the appearance of another member of the filovirus family, this one occurring in the United States, in Reston,
VA, in infected cynomolgous monkeys
from the Philippines. The tenuous evidence that we have suggests that this lesspathogenic filovirus is from the dense rain
forests of the infected animals’ country of
origin [13]. Unlike the other members of
its family, Reston virus causes no disease
in humans [14], and careful laboratory
studies that used virus seed free of contamination by simian hemorrhagic-fever
virus demonstrated that Reston virus,
compared with the lethal African filoviruses, caused milder or no disease in primates [15, 16].
The geographic distribution of the filoviruses is far from distinct. Previously,
we knew only that these viruses originate
in tropical rain forests near the equator,
where they can infect monkeys and humans, apparently primarily with lethal dis-
ease. Leroy et al. found that infection rates
in chimpanzees in Cameroon was 12.9%
and inferred that the infections were
caused by the same virus strain that circulates in forest areas farther east and
south, where human and nonhuman-primate outbreaks of Ebola have been occurring with regularity in recent years. The
Cameroon forest is also on the same latitude as southern Sudan, where the lessvirulent Sudan strain of Ebola virus circulates. We do know that some humans
with high-titer antibody to Ebola virus
survive infection during known outbreaks
or single infections [17–22]. The Cameroon chimpanzees might, therefore, be survivors of an unknown local or regional
epizootic. It is also plausible, however,
that, as in the Philippines, a less-virulent
member of the filovirus family is circulating in Cameroon, a situation that would
account for the lack of local human cases
and/or observed epizootics.
Antibodies to Ebola and Marburg viruses have been found in humans living
in the same geographic areas of Africa.
Antibodies to Ebola and Marburg viruses
do not cross-react in any test, but no published results of antibody assays have yet
distinguished between antibodies to any
of the known Ebola virus strains, regardless of their origin or pathogenicity. The
data presented in the Leroy et al. article
are based on assays using only antigens
from the Zaire strain of the Ebola virus,
previously confined to the DRC, Gabon,
and the Republic of Congo. Despite the
EDITORIAL COMMENTARY
• JID 2004:190 (1 December) • 1893
improved specificity of the ELISA assays
used in the Leroy et al. study, no antigens
specific to other Ebola virus strains were
included in the assay, so it is impossible
to say with certainty that a given reaction
reflects infection with a particular Ebola
virus strain—rather than with a related
virus, known or unknown—or even with
some confounding antigen. The odds of
finding other filoviruses in this vast, remote, and highly biodiverse geographic
area are high, and diagnosis of human or
primate symptomatic disease in specific
areas may not be sufficient to allow one
to delineate the ecological range of each
virus. Perhaps Cameroon is a good place
to start a geographic survey of filovirus ranges.
Thus, until the ecologies of the Ebola
virus strains are determined through careful investigations defining their distributions and possibly their primary reservoir,
data based solely on antibody assays are
insufficient to determine the distribution
of these viruses. Some novel experiments
have been conducted on potential reservoirs of filoviruses [23], but neither these
nor extensive ecological studies at several
sites have led to the identification of the
primary reservoir, which remains elusive.
We do know that the Sudan strain of the
Ebola virus, which is closely related to the
Zaire strain, infects humans in southern
Sudan (adjacent to both the area in northern DRC with Ebola outbreaks and to
regions in the DRC and Uganda with Marburg outbreaks), but we have no data on
the ecological distribution of the Zaire or
Sudan strain or on nonhuman-primate infections [24]. What Leroy et al. do confirm
is that Ebola viruses circulate in the forests
of central Africa, even in areas where human cases (not necessarily infections) or
epizootics have not been observed. However, the identities of the filoviruses that
circulate in the entire equatorial region remain an important—and, in my view, an
open—question.
Leroy et al. conclude that their data best
support a multiple-introduction hypoth-
esis for the Zaire strain of the Ebola virus.
This hypothesis supports the idea that infections in humans and nonhuman primates are less rare than we had thought
but that they must originate from ecological foci that we cannot identify. Another
acceptable hypothesis is that there are
multiple point sources for infection but
that the ranges and origins of the viruses
are unknown.
The study by Leroy et al. reminds us of
the challenge of understanding the ecological origin of filovirus infections in humans and nonhuman primates in the wild.
In Africa, the resources available in Gabon
are unparalleled for providing opportunities for studies of the ecology of the filoviruses. Cautiously interpreted serological studies in nonhuman primates, such
as that by Leroy et al., along with virological studies and more-extensive human
epidemiological studies, are likely to be the
key to the eventual understanding of the
ecology of the filoviruses.
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