Is
Selenium Deficiency Behind Ebola, AIDS and Other Deadly
Infections?
Jack
Challem
12/04/96 The latest Ebola epidemic in Zaire may be over,
but it's probably only a matter of time before this supergerm
returns - and still others emerge.
The
reason: Ebola and other deadly viruses, including the human
immunodeficiency virus-1 (HIV-1), might be stimulated by
deficiencies in the mineral selenium.
And
Zaire - where the Ebola and HIV-1 viruses first appeared
- may be a viral "hot zone" because of low selenium
levels in the soil and widespread selenium deficiencies
among people living off that land.
Too
strange to be true? To the contrary, a similar connection
has been established in China, where a common virus mutates
into a dangerous form when it infects people deficient in
selenium.
Selenium,
an essential mineral, functions as an antioxidant and a
component of another antioxidant, glutathione peroxidase.
Deficiencies of either substance impair the body's immune
system and ability to fight infections.
But if recent research is any indication, the role of selenium
in disease prevention may be much more profound than previously
imagined.
Admittedly,
there's no neat, well-documented association between selenium
deficiency and the Ebola virus, but the evidence strongly
suggests one.
"It
is certainly intriguing that a number of viruses have emerged
from these regions in Africa, which appear to be selenium
deficient," said E.
Will Taylor, Ph.D., a viral researcher at the University
of Georgia, Athens.
Selenium
and Viral Mutations
So
far, there are three pieces to the selenium-virus puzzle.
The
first comes from the recent dramatic discovery that a selenium
deficiency in a person or animal triggers a mutation in
the coxsackievirus.
The common form of this virus is generally benign, causing
symptoms no more serious than a common cold or sore throat.
The coxsackievirus mutation, however, attacks heart tissue,
causing Keshan disease (a type of
cardiomyopathy) and heart failure.
In
China, Keshan disease is known to be associated with selenium
deficiency. But because of the seasonal nature of Keshan
disease, researchers suspected that an infectious microorganism
was also involved.
That's when they turned up the coxsackievirus, which also
infects an estimated 20 million Americans annually.
The
plot twisted last year when Melinda Beck, Ph.D., a virologist
at the University of North Carolina, and Orville Levander,
Ph.D., a nutritional chemist at the USDA's Agricultural
Research Service, described how a run-of-the-mill coxsackievirus
mutated into the deadly, rapidly reproducing strain when
an infected person or animal was deficient in selenium or
vitamin E. The coxsackievirus in animals eating a selenium-rich
diet did not mutate. However, the mutated virus could infect
and be deadly to a person or animal eating adequate selenium.
(Journal of Medical Virology, 1994;43:66-70 and Journal
of Nutrition, 1994;124:345-58.)
Their
research took on greater significance this past May, when
Beck and Levander described the specific genetic changes
that occurred in this coxsackievirus mutation. By comparing
the genetic structure of the benign "parent" coxsackievirus
to that of its virulent descendants, Beck and Levander identified
six specific changes in the genetic structure of the virulent
coxsackievirus strain. Although it's not yet clear whether
one or all of these genetic changes triggered the more aggressive
virus, the genetic evidence provides the scientific proof
needed to link a host's selenium deficiency with a more
dangerous form of the coxsackievirus.
(Nature Medicine, May 1995;1:433-6.)
The
coxsackievirus infection is made worse because selenium
deficiency weakens the host's immunity, preventing the virus
from being effectively challenged by T-cell lymphocytes
or antibodies. As a result, the mutated virus can reproduce
faster than it would in a relatively healthy person. In
addition, the lack of selenium prevents the quenching of
mutation-causing free radicals, so when the virus reproduces,
it also mutates at a faster rate.
Although
Beck and Levander studied only one virus, the implications
are profound. They have already begun looking at whether
other "host"
nutritional deficiencies cause viral mutations as well.
According to Beck, this propensity to mutate in a selenium-deficient
animal or person might explain why new influenza strains
regularly emerge from China, where selenium deficient soils
are common. The flu virus originates in Chinese ducks, jumps
to pigs, and then infects people.
"The
importance of this finding is not limited to nutritionally
deprived populations," the researchers said in a statement
released by the USDA Agricultural Research Service. "In
theory, it would take only one selenium-deficient person
or animal to produce a new family of virus mutants."
Selenium
and HIV
The
second piece of the Ebola-selenium puzzle comes from Taylor
at the University of Georgia, Athens. Last year, he theorized
that several little-known genes in HIV control the formation
of selenocysteines, proteins with a voracious appetite for
selenium.
When
the virus depletes all of the selenium in an HIV-infected
cell, it reproduces and begins attacking other cells in
search of more selenium. The more selenium the virus uses,
the less that's available for the body's immune system.
Eventually, immunity becomes so weak that AIDS patients
become vulnerable to life-threatening "opportunistic"
infections. (Journal of Medicinal Chemistry, Aug. 19, 1994;37:2637-54.)
If
the theory is correct, supplemental selenium would do two
things, Taylor said in an interview. First, it would provide
what the HIV virus needs so it wouldn't spread throughout,
creating a biochemical stalemate of sorts.
Second, it would help keep the person's overall immune system
functioning, so it could resist the secondary infections
that usually kill HIV patients.
Genetic
evidence and clinical studies using selenium in the treatment
of AIDS suggest that the theory is true. In one ongoing
study, Juliane Sacher, M.D., of Frankfurt, Germany, reported
that selenium-supplemented AIDS patients gain weight, have
a general feeling of well-being, and sometimes benefit from
increases in protective CD4 T-cells. (Chemico-Biological
Interactions, 1994; 91:199-205.) Another study has found
that selenium inhibits the growth of HIV-1 in the test tube.
(Taylor EW, Antiviral Research, 1995;26:A271-86.)
The
Selenium-Ebola Link
The
third piece of the Ebola-selenium puzzle comes from a recent
paper Taylor has submitted for publication. In it, he draws
on his earlier work and that of Beck and Levander to build
a compelling argument that Ebola also contains genes dependent
on selenium. Like HIV, when selenium levels in Ebola-infected
cells drop, or are low to begin with, the virus reproduces
and "escapes" in search of cells with more selenium-spreading
the infection throughout the body.
The
difference is that the genes in the Zaire strain of Ebola
genes appear to need 10 times more selenium than does HIV,
and Ebola's greater dependence on selenium may partly account
for the speed with which it kills. Seventy-five percent
of the people infected with Ebola die within three weeks.
Again,
compounding the infection, normal immune defenses against
to the virus would be handicapped if the host - an animal
or person - were deficient in selenium. "This raises
the possibility that selenium deficiency in host populations
may actually foster viral replication, possibly triggering
outbreaks and perhaps even facilitating the emergence of
more virulent viral strains," explained Taylor.
It's
all very speculative, he admits. But the widespread soil
deficiency of selenium in Zaire, documented by a number
of researchers, would set the stage for vital mutation and
a highly susceptible population, much the way it does in
China.
But
there's still another aspect, Taylor points out. Sulfur
dioxide, a byproduct of the burning of fossil fuels, reacts
with selenium compounds in the soil, making the mineral
more difficult to absorb by plants. "It has long been
suspected that fossil fuel burning and acid rain may be
contributing to a gradual decrease of selenium in the food
chain," Taylor said. "Thus, the deforestation
of jungles and rain forests-exactly what is being done in
Zaire and elsewhere-may also contribute to the emergence
of new viral diseases.
This article originally appeared in the Natural Foods Merchandiser,
published by New Hope Communications. The information provided
by Jack Challem and The Nutrition Reporter newsletter is
strictly educational and not intended as medical advice.
For diagnosis and treatment, consult your physician.
