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Ebola virus

Ebola Virus

Ebola virus, a member of the Filoviridae, burst from obscurity with spectacular
outbreaks of severe, haemorrhagic fever. It was first associated with an
outbreak of 318 cases and a case-fatality rate of 90% in Zaire and caused 150
deaths among 250 cases in Sudan. Smaller outbreaks continue to appear
periodically, particularly in East, Central and southern Africa. In 1989, a
haemorrhagic disease was recognized among cynomolgus macaques imported into the

United States from the Philippines. Strains of Ebola virus were isolated from
these monkeys. Serologic studies in the Philippines and elsewhere in Southeast

Asia indicated that Ebola virus is a prevalent cause of infection among macaques
(Manson 1989). These threadlike polymorphic viruses are highly variable in
length apparently owing to concatemerization. However, the average length of an
infectious virion appears to be 920 nm. The virions are 80 nm in diameter with a
helical nucleocapsid, a membrane made of 10 nm projections, and host cell
membrane. They contain a unique single-stranded molecule of noninfectious
(negative sense ) RNA. The virus is composed of 7 polypeptides, a nucleoprotein,
a glycoprotein, a polymerase and 4 other undesignated proteins. Proteins are
produced from polyadenylated monocistronic mRNA species transcribed from virus

RNA. The replication in and destruction of the host cell is rapid and produces a
large number of viruses budding from the cell membrane. Epidemics have resulted
from person to person transmission, nosocomial spread or laboratory infections.

The mode of primary infection and the natural ecology of these viruses are
unknown. Association with bats has been implicated directly in at least 2
episodes when individuals entered the same bat-filled cave in Eastern Kenya.

Ebola infections in Sudan in 1976 and 1979 occurred in workers of a cotton
factory containing thousands of bats in the roof. However, in all instances,
study of antibody in bats failed to detect evidence of infection, and no virus
was isolated form bat tissue. The index case in 1976 was never identified, but
this large outbreak resulted in 280 deaths of 318 infections. The outbreak was
primarily the result of person to person spread and transmission by contaminated
needles in outpatient and inpatient departments of a hospital and subsequent
person to person spread in surrounding villages. In serosurveys in Zaire,
antibody prevalence to Ebola virus has been 3 to 7%. The incubation period for
needle- transmitted Ebola virus is 5 to 7 days and that for person to person
transmitted disease is 6 to 12 days. The virus spreads through the blood and is
replicated in many organs. The histopathologic change is focal necrosis in these
organs, including the liver, lymphatic organs, kidneys, ovaries and testes. The
central lesions appear to be those affecting the vascular endothelium and the
platelets. The resulting manifestations are bleeding, especially in the mucosa,
abdomen, pericardium and vagina. Capillary leakage appears to lead to loss of
intravascular volume, bleeding, shock and the acute respiratory disorder seen in
fatal cases. Patients die of intractable shock. Those with severe illness often
have sustained high fevers and are delirious, combative and difficult to
control. EBOLA SEROLOGY The serologic method used in the discovery of Ebola was
the direct immunofluorescent assay. The test is performed on a monolayer of
infected and uninfected cells fixed on a microscopic slide. IgG- or IgM-specific
immunoglobulin assays are performed. These tests may then be confirmed by using
western blot or radioimmunoprecipitation. Virus isolation is also a highly
useful diagnostic method, and is performed on suitably preserved serum, blood or
tissue specimens stored at -70oC or freshly collected. TREATMENT OF EBOLA No
specific antiviral therapy presently exists against Ebola virus, nor does
interferon have any effect. Past recommendations for isolation of the patient in
a plastic isolator have given way to the more moderate recommendation of strict
barrier isolation with body fluid precautions. This presents no excess risk to
the hospital personnel and allows substantially better patient care, as shown in

Table 2. The major factor in nosocomial transmission is the combination of the
unawareness of the possibility of the disease by a worker who is also
inattentive to the requirements of effective barrier nursing. after diagnosis,
the risk of nosocomial transmission is small. PREVENTION AND CONTROL OF EBOLA

The basic method of prevention and control is the interruption of person to
person spread of the virus. However, in rural areas, this may be difficult
because families are often reluctant to admit members to the hospital because of
limited resources and the culturally unacceptable separation of sick or dying
patients from the care of their family. Experience with human disease and
primate infection suggests that a vaccine inducing a strong cell- mediated
response will be necessary for virus clearance and adequate protection.

Neutralizing antibodies are not observed in convalescent patients nor do they
occur in primates inoculated with killed vaccine. A vaccine expressing the
glycoprotein in vaccinia is being prepared for laboratory evaluation. SELECTIVE

PRESSURES AND CONSTRAINTS It is of interest to determine, what, if any, limits
are placed on virus variation. Despite high mutation rates and opportunities for
genetic reassortment, many factors act to minimize emergence of new influenza A
epidemics (Morse and Schluederberg 1988). even though avian and human influenza
viruses are widespread (in humans an estimated 100 million infections yearly),
pandemic influenza viruses emerge infrequently (every 10-40 years). Powerful
constraints appear to exist since pandemic human influenza strains vary in their

H gene, whereas the neuraminidase and most other genes are conserved. These
constraints on viral evolution are not surprising when one considers the
selective pressures imposed by the host at each stage of the virus life cycle.

Tissue tropism determinants, include site of entry, viral attachment proteins,
host cell receptors, tissue- specific genetic elements (for example promoters),
host cell enzymes (like proteinase), host transcription factors, and host
resistance factors such as age, nutrition and immunity. Host factors contribute
significantly: sequences such as hormonally responsive promoter elements and
transcriptional regulatory factors can link viral expression to cell state. The
interaction of virus and host is thus complex but highly ordered, and can be
altered by changing a variety of conditions. Unlike bacterial virulence, which
is largely mediated by bacterial toxins and virulence factors, viral virulence
often depends on host factors, such as cellular enzymes that cleave key viral
molecules. Because virulence is multigenic, defects in almost any viral gene may
attenuate a virus. For example, some reassortments of avian influenza viruses
are less virulent in primates than are either parental strain, indicating that
virulence is multigenic (Treanor and Murphy 1990). Viral and host populations
can exist in equilibrium until changes in environmental conditions shift the
equilibrium and favour rapid evolution (Steinhauer and Holland 1987). It seems
reasonable to expect that new viruses will emerge occasionally, but the
stochastic and multifactorial nature of viral evolution makes it difficult to
predict such events. According to Doolittle, retrovirus evolution is sporadic,
with retroviruses evolving at different rates in different situations. For
instance, the human endogenous retroviral element is shared with chimpanzees,
indicating no change in over 8 million years, whereas strains of HIV have
diverged in mere decades. Endogenous retroviruses carried in the germline evolve
slowly compared with infective retroviruses. Generation of new viral pathogens
is rare, and often possible only because of high mutation rates that permit many
neutral mutations to accumulate before selective pressure forces a change. The
seeming unpredictability of these events ensure that recognition of new
pathogens must await their emergence. CONCLUSION The proposed American fiscal
budget for 1995 allows allocations for the CDC which remain basically the same
as those for past years and the $11.5 billion budget for the National Institutes
of Health includes only a modest increase for non-AIDS infectious and
immunological diseases research (Cassell 1994). In view of the magnitude of the
problem, this budget is unacceptable. Currently, infectious diseases remain the
leading cause of death worldwide. In the United States infectious diseases
directly account for 3 and indirectly account for 5 of the 10 leading causes of
death, AIDS is the ninth leading cause. Infectious diseases account for 25% of
all visits to physicians in the United States. In total, the annual cost of AIDS
and other infectious diseases reached $120 billion in 1992, about 15% of the
nation's total health-care expenditure. The expanding pool of immunodeficient
patients due to the AIDS epidemic, cancer treatment, transplant recipients, and
hemodialysis has caused an explosion of opportunistic infections due to a number
of fungal, parasitic, viral and bacterial agents. According to the Gail H.

Cassel, president of the American Society of Microbiology, the public health
system is not prepared to meet the challenges of new and re-emerging infections.

Perhaps the most obvious defect is inadequate disease surveillance and
reporting. In America, only one-quarter of the states have a professional
position dedicated to surveillance of food-borne and waterborne diseases. In

1992, only $55000 was spent on federal, state and local levels tracking
drug-resistant bacterial and viral infections. In addition, the public health
laboratories are eroding. Overall, CDC's budget for infectious diseases
unrelated to AIDS has declined approximately 20% in the last decade. This is the
case in the developed world of the United States, and we in developing South

Africa are certainly no better off in terms of disease surveillance and
concomitant protection. It should be clear that a mixture of basic and applied
research related to infectious disease is needed. Coupled with this, better
diagnostic techniques, prevention strategies and risk factor analysis is needed.

Finally, enhanced communication among health care professionals and the public
is integral in coming to terms and dealing with this issue. The American

National Institute of Allergy and Infectious Diseases (NIAID) plans to develop a
research and training infrastructure to elucidate the mechanisms of molecular
evolution and drug resistance and to learn more about actual disease
transmission through molecular and environmental studies and to continue their
emphasis on vaccine development. For example, NIAID-funded research has already
led to the creation of a new Haemophilus influenzae type B vaccine which is
expected to save nearly $400 million in health-care costs each year. Similarly,
the NIH spent less than $27 million dollars to find the connection between

Helicobacter pylori and chronic peptic ulcers, yet using antibacterial therapy
for the disease will save $760 million dollars in health care costs annually.

Given the diverse nature of threats from infectious diseases, it is not adequate
merely to face each crisis as it emerges, as this may provide a strategy which
proves to be too little and too late. Instead, a more holistic approach is
required. This must include a global perspective as well as the need to address
the issue of infectious disease within the context of shared environmental
responsibility. Improved health care derived from socioeconomic betterment is
crucial, as are long term policies involving systems thinking as opposed to the
limiting nature of long term over-specialization.


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