Infection through subterfuge
- From: "dali" <borgersbrent@xxxxxxxxx>
- Date: 1 Nov 2005 10:44:14 -0800
Has everyone been aware of these genes? I've read at least 4 different
articles stating totally different ways borrelia can beat/evade the
immune sytem.
I'll post them when I get a chance.
Researchers reveal how Lyme disease bacteria hide from immune systems
Paul Tadich
Thursday, June 02, 2005
In the sci-fi classic Invasion of the Body Snatchers, an alien plague
silently commandeers the bodies of its unsuspecting victims. Now, a
group of researchers has shown how a real-life parasite multiplies
undetected in infected people by cleverly subverting the body's immune
system.
Seppo Meri, a professor of immunology at the University of Helsinki,
has discovered why nearly one-third of people with Lyme disease do not
show any symptoms until the bacteria that cause it have colonized the
entire body. "These bacteria are able to spread all the way to the
brain," he said in interviews.
Lyme disease, contracted by approximately 10,000 North Americans each
year, is caused by ticks harbouring a type of bacteria called Borellia.
Most victims of tick bites who become infected break out in a telltale
ring-shaped rash. But 30% of victims suffer no symptoms until the
bacteria have multiplied out of control. Acute arthritis and facial
paralysis can result. A course of antibiotics can usually set things
right, but in about 10% of cases these symptoms are irreversible.
Professor Meri's team, working in Sweden and Finland, studied the
behaviour of Borellia to figure out how it avoids getting gobbled up by
the body's defences once it has established a beachhead underneath the
skin.
In most cases, white blood cells -- also called leukocytes --rush to
the site of an infection to do battle with foreign bacteria. But when
Borellia is the culprit, leukocytes are often nowhere to be seen.
Prof. Meri's team found that when Borellia enters the body it activates
the expression of two genes, OstE and Crasp1. The proteins generated by
these genes stick out from the surface of the bacteria like the
bristles on a kiwi.
The bloodstream is filled with a protein called complement factor H,
which normally binds to the surface of foreign bugs, acting as a beacon
for leukocytes to attack. But OstE and Crasp1 neutralize this protein,
making Borellia invisible to the white blood cells. Then the real
trouble begins.
"In the second phase," said Prof. Meri, "the bacteria very silently
spread around the body -- they go to the blood and then they spread to
joints, the eye, the brain and the skin. Then there is the third phase,
where the bacteria multiply in organs and cause their destruction."
What most surprised Prof. Meri was Borellia's cleverness in adapting to
its environment. "These bacteria behave very dynamically," he said.
"When we grow them in the lab in cultures, they lose the protective
molecules. As soon as they are in the human [body], they up-regulate
the protective molecules." Borellia is also smart enough not to waste
energy manufacturing OstE and Crasp1 when it's living in the tick gut.
Prof. Meri hypothesizes that OstE and Crasp1 genes are turned on and
off depending on the temperature. In the lab dish and in the tick gut
it's relatively cold, so the genes are silenced. In the body, however,
things get hot enough to trigger their expression.
So it's hardly surprising that these ingenious bacteria have evolved a
sophisticated "conjugation" mechanism to share their clever genes with
the entire community -- otherwise known as sex.
Like humans, Borellia bacteria store their hereditary information on
strands of DNA, organized into chromosomes. But unlike us, bacteria
often contain tiny pieces of circular DNA -- called plasmids -- that
are separate from the chromosomes. The OstE and Crasp1 genes are
located on one of these plasmids. By joining together, bacteria can
transfer these plasmids from one individual to another, a process
analogous to a sperm entering an egg.
Because there are several strains of Borellia bacteria -- different
variants are prevalent in Europe and North America, for example -- it's
likely one strain first evolved these genes and then passed them around
to other types of Borellia through bouts of bacterial intercourse.
.
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