Documente Academic
Documente Profesional
Documente Cultură
Katy Lunger
April 5, 2009
Ebola virus 2
Table of Contents
Abstract……………………………………………………………………………………………3
Introduction………………………………………………………………………………………..4
Background………………………………………………………………………………………..5
History of Weaponization…………………………………………………………………………9
Weaponization Potential…………………………………………………………………………..9
Countermeasures…………………………………………………………………………………15
Risk Assessment…………………………………………………………………………………18
Conclusion……………………………………………………………………………………….21
References……………………………………………………………………………………….24
Ebola virus 3
Abstract
Ebola virus gained widespread public attention after gruesome reports began to surface
detailing outbreaks in Africa in the 1990s. Ebola virus, a member of the Filoviridae family, has
a high mortality rate (50-90%), and can result in hemorrhaging and necrosis of various biological
tissues. There are unconfirmed reports that Ebola virus has been weaponized, despite the lack of
knowledge of the virus’s natural reservoir or a clear understanding of how the virus is spread.
Several countermeasures are being studied for protection from Ebola virus infection, and though
none are yet approved for human use, there are a few that are showing promise in nonhuman
primates. In light of the “age of terror,” new interest in the potentially devastating effects of
biological and chemical weapons has directed governmental resources toward protection from
Introduction
The events surrounding September 11, 2001 and the subsequent anthrax mailings have
spawned enormous efforts in the United States with regard to national defense from various
threats, including those of biological weapons. Reports from various sources have also shed
light on the reality of the looming threat of biological weapons. According to Alibek and
Handelman (2000), the former Soviet Union conducted massive biological weapons research and
production programs beginning in the 1970s until it dissolved in 1991. Dr. Kenneth Alibek, a
former director of the covert program who defected to the United States in 1992, believes Russia
may still be involved in illegal production and storage of biological weapons, while the vast
quantities of previous weapons stocks have likely been sold to rogue nations and other private
consumers (Alibek & Handelman, 2000). Various cults, terrorist organizations, and enemies of
the United States, such as Aum Shinrikyo, Al Quaeda, and Iraq, are believed to have access to or
Much of the knowledge the United States has acquired regarding biological weapons has
come from scientists who defected from the former Soviet Union (Alibek & Handelman, 2000;
Fong & Alibek, 2005; PBS, 2001). According to a PBS (2001) report with Sergei Popov, a
former top soviet scientist and defector, the Former Soviet Union researched weaponization for
both Ebola virus and Marburg virus, among other pathogens, and his claims have been
corroborated by Ken Alibek (2000). Ebola virus, especially if in a weaponized aerosol form,
could be disseminated in an attack, producing high mortality rates with very low dosage, mass
panic, and economic disruption. There is no treatment or immunization for Ebola virus, it is
highly contagious, has a high mortality rate, and it has been classified as a Category A agent by
Background
The first descriptions of the effects of viral hemorrhagic fevers (VHF) were reported in
1967 when 31 people in Germany and Yugoslavia became infected with Ebola’s close relative,
Marburg virus. The infections were believed to have occurred when individuals came into direct
contact with blood, organs or other tissues of African green monkeys that had been caught in
Uganda (Simpson, 1978). After the Marburg incident, the virus seemed to disappear, until 1975
when a traveler, likely exposed in Zimbabwe, presented with Marburg in Johannesburg, South
Africa (CDC, 2004). According to the Centers for Disease Control and Prevention (2004),
The Ebola and Marburg viruses are the sole members of the Filoviridae family, which
appears to be endemic to Central Africa in an area between the 10th parallel north and the 10th
parallel south of the equator (Feldmann, Wahl-Jensen, Jones & Stroher, 2004). Ebola, like
Marburg, is a highly lethal pathogen that causes hemorrhagic fever syndrome in humans and
nonhuman primates (Sullivan, Yang, & Nabel, 2003). Ebola was first identified in Zaire in 1976,
near the Ebola River during an outbreak. There have been a few sporadic, confirmed outbreaks
in Africa since then, including large epidemics that occurred in Kikwit, Zaire in 1995 and in
Research has yet to determine the natural hosts of filoviruses. Because both nonhuman
primates and humans can become infected with filoviruses, they are regarded as zoonotic, yet a
species that can act as a life-sustaining host and vector for Ebola is elusive. Some current
research has suggested that strains collected during outbreaks have indicated evolution of those
strains in an as-yet unconfirmed reservoir. Zaire Ebola virus (ZEBOV) RNA has been reported
Ebola virus 6
in organ tissues of rodents from Central Africa, however, this possible reservoir has not yet been
confirmed due to difficulty isolating the virus or because of difficulties detecting the virus with
antigens (Feldmann et al., 2004). Because of the nature of the pathology and lack of treatment of
Ebola virus, it is only approved for study in a Biosafety Level 4 (BSL) 4 facility; currently, there
are only 5 BSL 4 labs in the United States, which is one possible limitation that may hamper the
In the lab, researchers have inoculated various species with Ebola virus and found that
fruit and insectivorous bats can essentially act as incubators without showing deleterious health
effects (Feldmann et al., 2004), however, bats haven’t been shown to be actual reservoirs in the
field. Feldmann and colleagues (2004) suggest that the difficulty in locating Ebola virus
reservoirs indicates that reservoirs are either rare species or that transmission within the reservoir
The Ebola virion is generally tubular, and as is common with Filoviridae, it may appear
in many different shapes, including long and branched filaments or short “U” or “6” shaped
configurations (CDC, 2004). The virion is made up of a nucleocapsid, a viral envelope, and an
intracellular matrix between the nucleocapsid and the viral envelope; the viral envelope is
There are four known strains of Ebola, which include the Zaire (ZEBOV), Ivory Coast
(EBO-CI), Sudan (EBO-S), and Reston (EBOR) strains. All but the Reston strain can cause
disease in humans, and all are known to cause disease in nonhuman primates (Sullivan et al.,
2003).
The Ebola virus is a negative-sense RNA virus (Sullivan et al., 2003) with a 19 kb long
Ebola virus 7
genome encoding eight proteins (Puskoor & Zubay, 2000). Sanchez and colleagues (1998)
reported a single coding region responsible for two protein products, secreted glycoprotein
(sGP), and transmembrane virion envelope glycoprotein (GP). GP is an edited version of sGP,
which forms a trimeric complex and binds to endothelial cells (Sanchez et al., 1998), and is
thought to play a key role in Ebola virus’ pathogenesis (Sullivan et al., 2003). Research has
allowing the Ebola virus to spill its contents into the cell (Sullivan et al., 2003). sGP may be
involved in silencing the immune response of the cells while GP, which dot the surface of the
Ebola virus membrane envelope, may be responsible for the hemorrhagic fever symptoms
because it binds to reticuloendothelial cells that line blood vessels (Puskoor & Zubay, 2000;
In addition to GP and sGP, the Ebola virus genome encodes the following proteins:
nucleoprotein (NP), which is responsible for packing the RNA genome; viral protein 35 (VP35),
which is a cofactor in transcription and replication; viral protein 40 (VP40), which is associated
with the membrane, viral assembly and viral budding; viral protein 30 (VP30), which appears to
be involved in transcription and the addition of poly-A tails to mRNA; viral protein 24 (VP24),
which is not homologous to any other known viral proteins; and an RNA polymerase; the
numbers indicate approximate molecular weight of the proteins in kilodaltons (Puskoor &
Zubay, 2000).
Ebola virus infection usually occurs after contact with bodily fluids of infected
individuals or accidental needle stick injections, though airborne transmission of viral particles is
a suspected mode of communicability (Groseth, Jones, Artsob, & Feldmann, 2005). There has
also been a case in which a recovered patient transmitted Marburg virus via semen three months
Ebola virus 8
after infection (Leffel & Reed, 2004). Contact between contaminated fingers and the mouth or
eyes may also lead to infection as conjunctivitis has been correlated with Ebola infection
attack, could infect individuals through the inhalational pathway. There is some evidence
indicating natural spread of Ebola virus via aerosol particles as well (Groseth et al., 2005;
After infection, the virus enters an incubation period lasting 2 to 21 days. During this
phase, the virus infects endothelial cells, hepatocytes, monocytes and macrophages, is
transported to the lymph nodes, and begins to replicate at a high rate (Sullivan et al., 2003). The
infected cells leave the lymph nodes to travel throughout the body via the bloodstream.
Ebola’s high rate of viral replication is thought to overwhelm the infected cell and impair
its ability to synthesize proteins to ward off infection (Sullivan et al., 2003). While GP down-
regulates proteins associated with cell adhesion, thereby weakening the cellular network, the cell
wall breaks down and releases the replicated Ebola viruses. Cytokines that were expressed in
response to the invasion of the cell are also released and go on to interact with other cells in a
“cytokine storm,” with the result of an induced state of vascular shock on the cells (Sullivan et
al., 2003). The resulting pathology consists of necrosis of various tissues, including liver, lymph
nodes, kidneys, testes, and ovaries due to the replication of the virus (Puskoor & Zubay, 2000).
The individual displays an abrupt onset of fever after the initial incubation period with a
variety of other symptoms such as skin rash, chills, muscle pain, and/or nausea (Groseth et al.,
2005). Abnormal blood coagulation usually occurs which can lead to bleeding from orifices and
bruising; necrosis of several organs may also occur (Groseth et al., 2005). External
hemorrhaging is usually a rare result of infection, however, internal bleeding is very common
Ebola virus 9
(Groseth et al., 2005). Currently, there are no treatment options for Ebola virus; one only has
hope that their immune system will mount an adequate defense. The mortality rate associated
History of Weaponization
According to a statement made by Dr. Kenneth Alibek before the US Congress Joint
Economic Committee (1998), the Former Soviet Union extensively studied the weaponization of
several viral hemorrhagic fevers, including Ebola virus, both before and after signing the
Biological and Toxin Weapons Convention of 1972. Alibek has divulged that the Russian
government developed techniques and equipment for large-scale cultivation and concentration of
many pathogens (Alibek, 1998). He also claims that extensive research was done on the
smallpox vaccine virus, vaccinia, and that many different experiments were conducted in which
genes from different viruses were inserted into vaccinia’s genome, including genes from Ebola
Aum Shinrikyo has reportedly attempted to obtain Ebola virus during a natural outbreak
in Zaire, however, this report has never been confirmed and there is no evidence of the sect
actually using it (Olson, 1999). Thus far, only faint rumors of weaponized Ebola virus exist;
however, it is highly possible that the virus may be weaponized in the future if it hasn’t already.
Weaponization Potential
Ebola virus has a high potential for weaponization because it is stable at neutral pH, and
can survive for long periods in blood and other body fluids; in proper laboratory media, the virus
could be cultivated (Leffel & Reed, 2004). Leffel and Reed (2004) report that a review of
research on filoviruses shows that they are stable in aerosols and can retain virulence after
lyophilization for long periods of time, however, it should be noted that the referenced studies
Ebola virus 10
were done with Marburg virus, and not with Ebola virus. Experiments have shown aerosolized
Ebola to be lethal in rhesus monkeys (Johnson, Jaax, White, & Jahrling, 1995). The fact that
virtually no cure, antidote, or vaccine exists for Ebola infection makes its use as a weapon highly
viable. Further, public panic and social disruption would likely be high in the even of an Ebola
virus attack. The lack of scientific understanding of reservoirs for Ebola and other viral
Aerosolization of Ebola virus could inflict a massive death toll if dispersed over a large
population of individuals. With a mortality rate between 50-90%, Ebola would pack quite a
punch as a biological weapon. Moreover, it is known to be highly contagious and the longer the
disease progresses the more communicability increases. One slight drawback for someone
interested in weaponizing Ebola might be that by the time an individual was highly contagious
they may have already sought treatment (Borio et al., 2002). On the other hand, individuals who
have mounted an immune defense against the virus have been known to spread active virus
through sexual intercourse months later, infecting unsuspecting individuals, further increasing
Other concerns have been raised about the possible spread of the disease via sweat and
other body fluids (Borio et al., 2002), however, more data is required to confirm these
suspicions. Besides being aerosolized, Ebola virus could be used as a weapon if it could be
spread through the food or water supply, or even through infecting individuals in order to create
an epidemic.
Current defensive procedures against biological weapons in the United States are still in
their infancy. The Department of Homeland Security (DHS) was created in 2002 under the Bush
Ebola virus 11
administration in response to the terror attacks on September 11, 2001 and the subsequent
anthrax mailings (Center for Democracy & Technology, 2002). The DHS consolidated 22
agencies, and formed four directorates: Information Analysis and Infrastructure Protection,
Science and Technology, Border and Transportation Security, and Emergency and Preparedness
Response (Center for Democracy & Technology, 2002). The Science and Technology (S&T)
Directorate is concerned with “threat awareness, surveillance and detection, response and
recovery, and agro-defense, particularly against foreign animal diseases” (Cohen, 2007). The
S&T collaborates with the Department of Defense (DoD), Department of Health and Human
Services (HHS), the United States Department of Agriculture (USDA), the Department of Justice
(DOJ), the Environmental Protection Agency (EPA), and the Department of State (Cohen, 2007).
The S&T Directorate is required to play the “lead role in conducting assessments of the
evolving biological threat” in order to guide prioritization of investments and research for
biosecurity and biodefense (Cohen, 2007). The S&T Directorate has played a major role in
employing the “BioWatch” aerosol monitoring system (Cohen, 2007). BioWatch is a program in
which at least 31 cities have been equipped with aerosol samplers; the samplers are actually
filters attached to EPA air sampling stations (Shea & Lister, 2003). The filters are tested every
24 hours for the presence of pathogens via DNA extraction and PCR by lab technicians (Shea &
Lister, 2003). Ideally, PCR results would alert authorities to a biological attack before affected
BioWatch has been criticized for several reasons, including the placement of sensors with
EPA stations instead of probable attack areas, the fact that sensor installation and PCR testing of
filters is labor intensive and costly, and that scientific studies have not concluded the efficiency
President Bush signed the Project BioShield Act into law in 2004 with the aim of
weapons of mass destruction (HHS, n.d.). Project BioShield grants the National Institues of
Health the authority to streamline funding awards for projects that will aid in biodefense (HHS,
n.d.). The Biomedical Advanced Research and Development Authority (BARDA) manages
Project BioShield and is directly responsible for the management and integration of vaccines,
drugs, and therapies into the biological defense system of the United States (HHS, n. d.).
The “Select Agent Program” emerged out of the USA Patriot Act after the anthrax
mailings in 2001, and was fully implemented in 2005 (Center for Biosecurity of UPMC, 2009).
The program enforces accountability for those who work with certain pathogens and is run by
the CDC, the USDA’s Animal and Plant Health Inspection Service (APHIS), and the Department
of Justice, which performs background checks on the scientists involved in the program (Center
for Biosecurity of UPMC, 2009). “Select” agents (more than 70 viruses, bacteria, and other
pathogens that are deemed as biological threats) are under regulation of these agencies; and
therefore only certain scientists are legally allowed to study them (Center for Biosecurity of
UPMC, 2009). While APHIS regulates agents that relate to agriculture, the CDC regulates the
human pathogens like Ebola virus (Center for Biosecurity of UPMC, 2009). As of April 2008,
about 14,000 people from 324 government, private, and academic laboratories had been given
clearance by the Department of Justice to work with the special pathogens (Center for
The natural occurrence of “select” agents, including Ebola virus, limits the control the US
government can have over the acquisition and transfer of them; rumors of Aum Shinrikyo’s
attempt to acquire Ebola virus during a natural outbreak highlight the case in point, and this
Ebola virus 13
methodology of culturing pathogens is a very possible one. According to the Center for
Biosecurity at the University of Pittsburgh Medical Center (2009), the Select Agent Program has
order to stay within governmental regulations when further research on the samples could prove
fruitful for understanding how the pathogen harms its host, or for work on vaccines.
Early-warning systems for biological attacks could potentially improve response time and
recognition of a biological attack, even before physicians know what disease they are dealing
with in the clinic or hospital. Several states already have systems where clinicians input
symptomatic data into an electronic system that sends the information to the CDC; the CDC’s
version is called Early Aberration Reporting System (EARS), and the tool began in New York
City after the September 11, 2001 terror attacks (CDC, 2006). Data in this system is gathered
through a variety of ways, including 911 emergency calls, school and work absenteeism, and
over-the-counter drug sales (CDC, 2006). According to the CDC (2006), there are several US
cities that are currently using EARS as a tool for biological terrorism preparedness. Some
drawbacks, however, include data input that may not actually correlate to an outbreak of a
serious pathogen in the United States. For example, over-the-counter sales of a drug may
increase if the drug is on sale and not because of an epidemic; also, accidents in input coding of
symptomatic data could possibly lead to expensive and unnecessary responses by the CDC, for
Infection with viral hemorrhagic fevers in North America is quite rare, and therefore
physicians may not initially suspect Ebola virus infection if a patient presents with flu-like
Ebola virus 14
symptoms and rash. In the case of an epidemic outbreak, as could be the scenario in the event of
a bioterrorist attack, many severely ill individuals reporting to hospitals and clinics will likely be
who died from Ebola infection. Patients infected with Ebola usually complain about sudden
onset of fever, headache, myalgia, bloody diarrhea, and vomiting; full-blown disease can lead to
shock and bleeding, and eventually death (Leffel & Reed, 2004). Once a clinician suspects
Ebola infection, it must be reported to local and state health departments and to the CDC’s
Special Pathogens Branch (CDC, 2005). Samples should not be taken from the patient without
first consulting the Special Pathogens Branch (CDC, 2005). Because of the high level of toxicity
of Ebola, and the fact that there are currently no treatments available for infection, samples must
be handled extremely carefully, and clinicians should follow all CDC guidelines, including the
According to the CDC (2005), viral hemorrhagic fever should be suspected in patients
that have a fever and that have either 1) traveled to a location where there has been a recent
outbreak; 2) had contact with blood or other body fluids from an infected person or animal; or 3)
were possibly exposed in a laboratory or clinical setting in which viral hemorrhagic fever was
present.
There are only a few public health laboratories that are properly equipped to identify viral
hemorrhagic fever infection (Groseth et al., 2005), and therefore samples must be sent to one
(ELISA) and reverse transcription polymerase chain reaction (RT-PCR) are techniques capable
Ebola virus 15
immunoperoxidase has been used for filovirus identification in infected individuals (Groseth et
al., 2005).
Currently, the United States is ill equipped to handle a biological attack, especially one
with Ebola virus since treatment is mostly supportive and includes very strict isolation and
containment protocols. Once a quarantine facility was arranged to handle a large number of
infected or potentially infected patients, they would likely follow military-type protocols that
include providing supportive medical care in an intensive care facility, the administration of
oxygen, an intravenous route of hydration, ventilation support for severe cases of Ebola
infection, management of pain, and the avoidance of blood-thinning drugs like aspirin (US Army
Countermeasures
Currently there is no cure, vaccine, or antidote for Ebola virus infection. Investigations
into the molecular biology of Ebola virus have offered insight into how the virus attacks its host,
and therefore research has focused on ways in which to defend against the virus’ pathological
offenses. Rodent and nonhuman primate models have been utilized for Ebola virus infection
Mohamadzadeh, 2007).
Mouse models of Ebola infection are of limited use because mice do not develop
coagulopathy or lymphocyte apoptosis like humans do; guinea pigs show coagulopathy but not
to the level of nonhuman primates (Reed & Mohamadzadeh, 2007). Vaccines that protect guinea
pigs or mice, however, don’t always protect nonhuman primates either (Reed & Mohamadzadeh,
Ebola virus 16
2007). Therefore, nonhuman primates are the most relevant models for human infection with
Ebola; various primates have been used including African green monkeys, rhesus macaques,
cynomolgus macaques, and baboons (Reed & Mohamadzadeh, 2007). While each show
variations of pathology when infected with Ebola, the cynomolgus macaques are thought to be
the most stringent model since the Zaire strain of Ebola is extremely virulent with this species as
According to Reed & Mohamadzadeh (2007), little is known about the pathogenesis of
inhaled filovirus aerosol, and it isn’t thought to be the common route of exposure in natural
outbreaks, though it has been a suspected route of communication. But experimental studies
have shown filoviruses to be stable in aerosol, and therefore more research is necessary in order
Early experimental countermeasures for Ebola were vaccines made with formalin or
gamma-irradiation inactivated virus; but often such a vaccine worked in one animal model but
not another, and therefore that approach has been abandoned (Reed & Mohamadzadeh, 2007).
Several new avenues of research exist for Ebola virus protection. Exploration of DNA vaccines
that express the GP of Marburg and Ebola viruses have shown some promise in guinea pigs
when it was boosted with baculovirus-expressed GP lacking the transmembrane domain (Reed &
Mohamadzadeh, 2007). In 2004, a DNA vaccine construct was successful in protecting guinea
pigs and nonhuman primates from the Zaire strain of Ebola, and began phase I clinical trials
Vector-based vaccines have been utilized in research as well. Genes of interest are
mutated to remove toxicity and then inserted into a vector; ideally the recipient’s immune system
will build antibodies to the gene so that when the real live virus infects, the immune system will
Ebola virus 17
be prepared to attack it. Various issues exist that make the use of vector-based vaccines
problematic. Live viral vectors can be harmful to immunosuppressed individuals, and people
may also be immune to the vector, thereby blocking any potential immunity formation against
Zaire strain Ebola. Sullivan and colleagues (2003) reported a single immunization with
adenovirus vector containing the GP gene from the Zaire strain of Ebola protected cynomolgus
macaques from lethal dose injection of the virus. Reed and Mohamadzadeh (2007) pointed out
that this study used a dose that is much lower than a common accidental needlestick exposure;
still, all control animals were killed. This study used a nonreplicating adenovirus, making it
necessary to receive a very high dose of vaccine; further, pre-existing immunity to the
adenovirus vector in the general population may be an issue; there are reports that as much as
50% of the human population are immune to the adenovirus used by Sullivan and colleagues
Vesicular stomatitis virus (VSV) engineered to express GP of Ebola (Zaire strain) has
protected cynomolgus macaques from challenge, as well as from rechallenge with different
strains of Ebola (Reed & Mohamadzadeh, 2007). Because VSV is a live virus, it was necessary
to test it in immunocompromised models, as live virus vaccines can be dangerous for such
individuals. Geisbert and colleagues (2008) reported a VSV for Ebola that protected against
Virus-like particles (VLP) are viral protein aggregates; they mimic the native protein’s
conformation but do not confer safety concerns as do live viruses. By transfecting 293T cells
with GP and VP40 genes from Ebola, Bavari and colleagues (2002) discovered the cells
Ebola virus 18
produced VLPs that were virtually indistinguishable from Ebola virus particles; therefore the
introduced genes were building VLPs using materials available within the cell, including the
cells lipid membrane. These VLPs may be useful for eliciting immune responses, and therefore
as vaccines for Ebola virus. Guinea pigs that were vaccinated with VLPs have been fully
protected from Zaire strain Ebola as well as Marburg virus (Reed & Mohamadzadeh, 2007).
Risk Assessment
Proof of previous weaponization of Ebola virus has been elusive, despite reports of soviet
defectors (Alibek & Handelman, 2000; PBS, 2001). Because Russian defectors have claimed
such weaponization, and because former Russian President Boris Yeltsin admitted that Russia
covered up biological weapons research performed even after signing the Biological Weapons
Convention treaty in 1972 (Alibek & Handelman, 2000; Fong & Alibek, 2005; PBS, 2001; PBS,
2006), the potential threat of weaponized Ebola virus has been taken seriously by the United
States. Further, the United States has not visited Russian biological research facilities since 1994
(Moodie, 2001), leaving 15 years with which possible weapons could have been created and/or
delivery for a variety of reasons, including the potential to infect large numbers of people (or
other targets, such as livestock or crops) with one delivery of agent. Ebola virus is a highly
lethal agent, with a mortality rate between 50-90% (Groseth et al., 2005). Because there is no
treatment or vaccine available, an attack with Ebola virus would create mass panic and likely
overwhelm health care facilities that are not equipped to contain a BSL 4 virus. It is likely that
infected individuals may present at hospitals with flu-like symptoms, and diagnosis of Ebola
infection may not occur until obvious symptoms arise, at which time the individual may have
Ebola virus 19
Hospitals would only be able to offer supportive care for victims of Ebola, and it is likely
that severe disruption of the healthcare system in the affected area would occur. Hospitals would
likely not accept patients known to be infected with Ebola virus in an effort to protect the
uninfected as quarantine quarters would probably not be available. A separate quarantine facility
would have to be set up as quickly as possible after an attack, and other potentially infected
Humans infected with Ebola virus have been found to contain high titers of virus in their
skin and sweat glands (Borio et al., 2002). While evidence is lacking, it is possible that Ebola
could be spread from person-to-person via touch. More probable would be infection of small
abrasions or cuts from touching an infected person, as several people in the Democratic Republic
of the Congo have contracted Ebola after washing the bodies and cutting the hair and nails of
There has been some evidence for the possibility of transmission of Ebola virus through
small drops of airborne particles, such as those ejected during coughing. Though most evidence
suggests that the virus is not contagious during the incubation period, the evidence is not
conclusive (Groseth et al., 2005). It is possible, though the probability not completely
understood, that if an attack occurred, unsuspecting individuals could spread the virus to others
before the onset of symptoms. In the event that an Ebola virus attack occurred without warning
or suspicion, individuals may not seek help even after the onset of symptoms, increasing the risk
of spreading the disease to others, as the risk of transmission seems to increase with time after
While some individuals infected will mount an effective immune response and overcome
Ebola virus 20
Ebola infection, there is evidence that the virus can persist in body fluids such as semen and
ocular fluids for 12 weeks after the onset of symptoms (Groseth et al, 2005). Individuals,
therefore, may appear quite healthy and active yet still transmit the disease to others.
Not enough evidence exists yet to determine possible vectors, such as mosquitoes or
rodents indigenous to the United States, for transmission of Ebola. Pigs have been infected with
Ebola Reston, however, and therefore infection of livestock as a weapon of terror is possible (Pig
Progress, 2008). Rumors have circulated that the Japanese cult, Aum Shinrikyo, once sent a
group to Zaire during an Ebola outbreak to gather viral samples in order to culture them for
biological weapons (Olson, 1999). It appears, therefore, that the acquisition of virus is highly
possible; weaponization has probably already occurred in Russia; and aerosolization has proven
to be highly lethal in monkeys, with very low doses (400 viral particles) (Leffel & Reed, 2004).
Conclusion
While Ebola virus can cause devastating and gruesome disease in infected individuals,
proof of its weaponization has not been attained. Dr. Kenneth Alibek, former deputy director of
the Russian agency Biopreparat, is the most notable proponent of the idea of Ebola
weaponization. His credibility is questionable, and therefore, so is the notion that Ebola has been
weaponized. According to an article in the Los Angeles Times, some of Alibek’s research
findings have not withstood peer review; he promotes a nonprescription pill that allegedly
bolsters the immune system; his claims that Iraq definitely had stores of smallpox was never
proven, even after the US invaded after September 11, 2001 (Willman, 2007). Alibek’s claims
have been part of the driving force behind the US government’s biodefense agenda, which has
thus far cost billions of dollars. Nevertheless, the possibility of Ebola virus being used as a
weapon exists and defensive plans have begun to take shape in the United States.
Because of claims that Russia has experimented with deadly pathogens that defy the
Biological and Chemical Weapons Convention that they are party to, inspections of Russian
facilities should be conducted by the United States. Not only should this be done for the safety
of the world, but also as a way to determine Alibek’s credibility. There is virtually no evidence
thus far to prove that Ebola virus has ever been used as a weapon, and no concrete evidence that
Project BioWatch is underway in the United States. The project is ambitious, and it is
just beginning. While it has been criticized for falling short of the ideal of complete protection
of biological and chemical attacks, the project has been a giant stride forward in terms of
biosecurity and biodefense. Refining the detection factors is necessary in order to ensure that
Project BioWatch will move closer and closer toward the goal of complete protection; however,
Ebola virus 22
that goal may be unattainable. The best possible protection will be in prevention of an Ebola
virus attack; however, because that is not completely possible, vaccines and antidotes will be key
such as wind currents, background levels of pathogens, likelihood of attack at location where
sensor is placed, and the re-evaluation of placing BioWatch sensors with EPA sensor sites will
More information must be gathered regarding the weaponization potential of Ebola virus,
including Ebola-specific aerosolization studies to include the ease with which Ebola can be
weaponized as an aerosol. Though some information has shown that Marburg virus can be
aerosolized and can survive for long periods of time on contaminated surfaces, this has not been
proven for Ebola (Leffel & Reed, 2004). There has been a report of the spread of Ebola virus to
uninfected macaques that were housed in the same room as experimentally infected macaques,
and Leffel and Reed (2004) suggest that it was possibility that the spread occurred through
aerosolized particles infected with Ebola during cage cleaning. This theory has not yet been
Much is known about the pathogenesis of Ebola virus infection via injection, but not
much is known about inhalational infection because of a lack of research in this area. An
aerosolized form of Ebola virus would arguably be the most effective method of dissemination
on a target; therefore more research on aerosolized Ebola virus needs to be done. Moreover,
more research should be done on individuals who have mounted immunity to Ebola virus, as
their biochemistry may provide valuable information to scientists in search of protection from
the virus.
Another aspect of an attack with Ebola virus, or any other pathogen, that should be
Ebola virus 23
studied is the possibility of genetic modification which may be done in order to increase
virulence, to add layers of disease by combining genes from another pathogen, for example,
adding a gene from Venezuelan equine encephalitis (VEE) with Ebola virus, or to mask the
identity of the pathogen. Dr. Alibek has made claims that Biopreparat experimented with
chimeras while he was employed there (Alibek & Handelman, 2000). By determining sequences
within the Ebola virus’ genome that can be modified in order for it to maintain its virulence
could help in designing a robust vaccine that could still defend against a modified virus.
Enormous strides have been made in regard to developing protective countermeasures against
Ebola virus. While there is not yet an approved vaccine for humans, one is surely on the
horizon. With Geisbert and colleagues (2008) report detailing a well-tolerated vaccine in
Improvements in all aspects of biological terror preparedness in the United States are
underway, and, while currently little evidence exists for the use of Ebola virus as a weapon,
perhaps governmental vigilance for protecting its citizens may benefit Ebola research. Because
Ebola virus has thus far rarely shown itself in the United States, it has not been considered an
imminent threat; the fact that is must be studied in a BSL-4 facility makes fast progress for Ebola
virus protection difficult when there are only 5 such facilities in the US.
Ebola virus 24
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