http://news.bbc.co.uk/2/hi/health/8435320.

stm

… http://health.yahoo.com/news/ap/us_fda_cancer_drug.html

http://esciencenews.com/dictionary/microbes.and.viruses

…
http://esciencenews.com/articles/2009/08/20/single.host.gene.may.hold.key.treating.both.
ebola.and.anthrax.infections

… http://www.biology-online.org/kb/biology_articles/virology.html

… http://www.biology-online.org/articles/researchers_discover_leukaemia_virus.html

http://www.biology-
online.org/articles/genetically_engineer
ed_poliovirus_fights.html

theory involved, procedure, conclusion. Antibiotics used

assumptions, furtherstudy, comments, suggestons

Single Host Gene May Hold Key to
Treating Both Ebola and
Anthrax Infections
Published: Thursday, August 20, 2009 - 15:21 in Health & Medicine

Research published by Army scientists indicates that a minor reduction in levels of one
particular gene, known as CD45, can provide protection against two divergent microbes:
the virus that causes Ebola hemorrhagic fever and the bacterium that causes anthrax.
Taken together, the results suggest a common host restriction factor and a promising
approach to drug development for treating two completely different infections. Writing in
the August 20 online issue of Cell Host and Microbe, scientists at the U.S. Army Medical
Research Institute of Infectious Diseases (USAMRIID) reported that mice expressing
reduced levels of CD45 (between 11 and 77 percent) were protected against Ebola virus.
In addition to an overall survival rate of 90 to 100 percent, these mice had reduced levels
of virus load in the major organs, and had completely cleared the virus 10 days after
challenge.

In contrast, mice that had naturally occurring levels of CD45—or none at all— failed to
clear the virus and succumbed to infection within 7 to 8 days following challenge.

The protein encoded by CD45 is a member of the protein tyrosine phosphatase (PTP)
family. PTPs are known to be signaling molecules that regulate a variety of cellular
processes, including cell growth, cell division, and the development of malignancies that
can lead to tumor formation.

Scientists created various "knockdown" mice, which expressed reduced levels of CD45,
to determine how those changes may alter the body's immune response to microbial
pathogens such as Ebola virus. According to the researchers, the "knockdown" mice
retained greater control of gene expression and immune cell proliferation following Ebola
virus infection. These factors contributed to enhanced viral clearance, increased
protection against the virus, and a reduction in cell death.

The team's results suggest that host susceptibility to Ebola virus is dependent on the
delicate balance of the body's natural immune system, which can be determined by the
levels of a single regulator gene.

Ebola virus, which causes hemorrhagic fever with human case fatality rates up to 80
percent, is a global health concern and a potential biological threat. Currently there are no
available vaccines or therapies. Scientists at USAMRIID study the Ebola virus to support
development of medical products to prevent and treat infection.
The recently published research work builds upon a related study that appeared in the
Journal of Biological Chemistry in May of this year. That research showed that CD45
also plays a role in protection from Bacillus anthracis, the causative agent of anthrax.
Specifically, the USAMRIID team demonstrated that in mice expressing 62 percent of
the CD45 gene, about 70 percent were protected following exposure to anthrax.

Bacillus anthracis causes three types of disease—cutaneous, gastrointestinal, and

inhalational—depending upon the route of exposure. A licensed vaccine is available, and
is protective if administered before exposure. Inhalational anthrax is difficult to diagnose
early, and despite antibiotic therapy, has a high fatality rate. In addition, because anthrax
spores can remain in the body for extended periods, antibiotic treatment is typically
recommended for 60 days or more following exposure.

"This report demonstrates the critical connection between basic research and the potential
development of medical products," said COL John P. Skvorak, commander of
USAMRIID. "Understanding pathogenesis of disease and host response is critical to the
Department of Defense's investment in broad spectrum countermeasures."

The next step for investigators is to look at the mechanism of action to better understand
how reduced expression of this gene regulates the pathogenesis of both diseases. That
information could one day lead to the identification and discovery of additional
promising compounds for treating Ebola and anthrax infections.

Initial symptoms are fever, severe headaches and muscle aches, and loss of appetite;
blood clots and profuse uncontrollable hemorrhaging appear within days, followed by
nausea, vomiting, and diarrhea. Death occurs in 8 – 17 days; fatality rates range from
50% to 90%. There is no known treatment. It takes its name from the Ebola River in
northern Congo (Zaire), where it first emerged in 1976. The virus appears as long
filaments, sometimes branched or intertwined. The virus particle contains one molecule
of RNA. How it attacks cells is unknown. It can be transmitted through contact with
bodily fluids; unsanitary conditions and lack of adequate medical supplies have been
factors in its spread.

An extremely contagious filovirus causing an acute, usually fatal hemorrhagic fever and
spread through contact with bodily fluids of infected persons and by airborne particles.
After the Ebola River in northwest Congo (formerly Zaire), where the disease was first
observed
The incubation period ranges from 2–21 days, although it is generally 5–18 days,[40].
Illness is characterized by the rapid onset of fever, malaise, muscle pain, headache, and
the inflammation of the pharynx. Six days following vomiting and bloody diarrhea,
individuals may develop maculopapular rash with bleeding at needle sites and bodily
orifices.[41]
Being acellular, viruses do not grow through cell division; instead, they use the
machinery and metabolism of a host cell to produce multiple copies of themselves

iloviruses have an unusual morphology, with the virus particle, or virion, appearing as
long thin rods. A filovirus virion is composed of a single species of ribonucleic acid
(RNA) molecule that is bound together with special viral proteins, and this RNA–protein
complex is surrounded by a membrane derived from the outer membrane of infected
cells. Infectious virions are formed when the virus buds from the surface of infected cells
and is released. Spiked structures on the surface of virions project from the virion and
serve to recognize and attach to specific receptor molecules on the surface of susceptible
cells, allowing the virion to penetrate the cell. The genetic information contained in the
RNA molecule directs production of new virus particles by using the cellular machinery
to drive synthesis of new viral proteins and RNA. See also Ribonucleic acid (RNA);
Virus.

Although much is known about the agents of Ebola hemorrhagic fever disease, the
ecology of Ebola viruses remains a mystery. The natural hosts of filoviruses remain
unknown, and there has been little progress at unraveling the events leading to outbreaks
or identifying sources of filoviruses in the wild. Fortunately, the incidence of human
disease is relatively rare and has been limited to persons living in equatorial Africa or
working with the infectious viruses. The virus is spread primarily through close contact
with the body of an infected individual, his or her body fluids, or some other source of
infectious material.

Ebola virus hemorrhagic fever disease in humans begins with an incubation period of 4–
10 days, which is followed by abrupt onset of illness. Fever, headache, weakness, and
other flulike symptoms lead to a rapid deterioration in the condition of the individual. In
severe cases, bleeding and the appearance of small red spots or rashes over the body
indicate that the disease has affected the integrity of the circulatory system. Individuals
with Ebola virus die as a result of a shock syndrome that usually occurs 6–9 days after
the onset of symptoms. This shock is due to the inability to control vascular functions and
the massive injury to body tissues.

It appears that the immune response is impaired and that a strong cellular immune
response is key to surviving infections. This immunosuppression may also be a factor in
death, especially if secondary infections by normal bacterial flora ensue. See also
Immunosuppression.
Outbreaks of Ebola virus disease in humans are controlled by the identification and
isolation of infected individuals, implementation of barrier nursing techniques, and rapid
disinfection of contaminated material. Diagnosis of Ebola virus cases is made by
detecting virus proteins or RNA in blood or tissue specimens, or by detecting antibodies
to the virus in the blood.

Dilute hypochlorite solutions (bleach), 3% phenolic solutions, or simple detergents

(laundry or dish soap) can be used to destroy infectious virions. No known drugs have
been shown to be effective in treating Ebola virus (or Marburg virus) infections, and
protective vaccines against filoviruses have not been developed.

Ebola virus electron micrograph

Structure of Bacillus anthracis.

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