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Deca Durabolin and T Cells

millgirl

New member
Thought I would post some findings on HIV and steroid usage, The benefits your doctor wont tell you...

The Importance of CD8 T Cells


Note that studies (and doctor's anecdotes) on HIV and rheumatoid
arthritis have shown that some anabolic steroids, including Deca
Durabolin,1 and Anadrol,2 and testosterone3 can promote an
increase in CD8 T cells, immune function cells that may be critically
important for healthy long-term survival in HIV. Some studies
have supported the hypothesis that CD8's may be more important
than CD4's for overall health and longevity in HIV.4


EMBARGOED FOR RELEASE: 27 MARCH 2000 AT 17:00 ET US
Contact: Richard Merritt
[email protected]
919-684-4148
Duke University Medical Center

………………………………....

Duke Researchers Discover Potent Ability
of Specific Immune System Cell Against HIV.

DURHAM, N.C. - Scientists have long known that immune system cells
known as "killer CD8" cells attack the AIDS virus after it enters the body

by killing virus-infected cells. They also have known that CD8 cells can
stop the virus from infecting new cells. Researchers now have found that
CD8 cells continue to fight the virus after it enters another kind of
immune system cell and begins to reproduce.

In fact, Duke University Medical Center researchers have discovered that
CD8 cells can stop human immunodeficiency virus (HIV) in its tracks even
when they are added to the immune cells known as CD4 cells, which are
cousins of CD8 cells in the T-cell family, after HIV has already entered
the cells.

Previous work has suggested that the potency of virus suppression or
number of suppressive CD8 cells could determine how quickly symptoms of
AIDS develop. The new findings, reported in the March 28 issue of the
Proceedings of the National Academy of Science, might point to novel
protective strategies, the researchers say.

"We have known that CD8 cells are important in controlling the level of
virus in the bloodstream and keeping some patients in an asymptomatic
state," said Dr. Michael Greenberg of the Duke University Center for
AIDS Research.

"Now for the first time, we have shown that CD8 suppressive activity
also works later in the infection process, at the stage of gene
expression during virus replication. Furthermore, this ability is
independent of the HIV protective envelope protein.

"Stimulating the production of these virus-suppressive CD8 cells, by a
vaccine or other means, could be a novel way to keep the spread of the
virus under control," he said.

The Duke team's research was supported by numerous grants from the
National Institute of Allergy and Infectious Diseases, part of the
National Institutes of Health (NIH).

An experimental system developed by a young investigator on Greenberg's
team, Dr. Georgia Tomaras, was employed to provide a clearer timeline of
what actually happens during an HIV infection.

After HIV enters the human body, it infects helper CD4 immune system
cells because the viral envelope protein - called the gp120 glycoprotein
- has a special affinity for the CD4 receptor found on these cells.
Once inside a CD4 cell, the virus' genetic material is copied into DNA
and enters the nucleus, where it integrates into the host cell's DNA.
From here the virus takes over the genetic machinery of the cell,
directing it to produce many copies of HIV that eventually flood into
the bloodstream to infect other CD4 cells. As a result of the
destructive nature of HIV, the number of CD4 cells in the blood drops.
However, not all people who are infected with HIV react the same way to
the virus, and much of the variability may depend on the activity of
these CD8 cells.

"HIV can act very differently from person to person - some people
progress to full-blown disease in a relatively short period of time,
while others remain asymptomatic for many years after infection,"
Greenberg said. "In many of these asymptomatic patients, there appears
to be strong CD8 activity. Similarly, patients who progress quickly to
AIDS have very little CD8 activity."

In their experiments, the Duke researchers used blood samples taken from
asymptomatic patients from Duke's Infectious Disease Clinic. The
researchers developed a unique laboratory analysis that allowed them to
follow in minute detail a single cycle of infection in individual CD4
cells.

In asymptomatic patients, CD8 cells can identify infected CD4 cells,
latch on to them, and release compounds that cause the infected cell to
burst, killing it. This cytolytic, or cell-killing, ability has been
well documented.

Scientists have also known, since the discovery by Drs. Christopher
Walker, Jay Levy, and colleagues at the University of California-San
Francisco in the mid-1980s, that CD8 cells also possess a non-cytolytic
weapon as well. However, what scientists did not know was how this non-
cytolytic weapon worked to stop HIV replication.

"Experiments have shown that when the cytolytic action of CD8 cells has
been blocked experimentally, viral replication is still suppressed, so
the CD8 cells are still doing something," Greenberg said.

Important work by Dr. Robert Gallo's group at the University of
Maryland-Baltimore demonstrated that CD8 cells release beta-chemokines
that can block entry of HIV into cells. However, work by Dr. Anthony

Fauci at NIH, as well as work by Levy and Greenberg, have shown that CD8
cells can also suppress HIV replication by other means. Until now, it
was not known how CD8 cells accomplished this.

Greenberg's new experiments show that CD8 cells affect the virus after
it has already entered the CD4 cell, which is very different from the
way beta-chemokines work. The CD8 cells somehow stopped HIV from
hijacking the CD4 cell's genetic machinery to reproduce itself.

To further prove this case, the Duke researchers used a system where the
genetic material of HIV was encased with an envelope protein taken from
a very different virus. The CD8 activity was just as strong against this
"pseudotyped virus," Greenberg said, indicating that CD8's action was
independent of the HIV envelope and specific to the HIV genetic
material.

"These experiments are the first to show that the viral suppression
occurs well after the virus enters the cell and is independent of the
entry process," Greenberg explained.

The exact mechanism by which CD8 cells are able to non-cytolytically
suppress viral replication is not known. According to Greenberg, the
agent could be a soluble factor or a molecule on the surface of CD8
cells that transmits a biochemical signal to the CD4 cells, or a
combination of both. For the first time researchers now know where in
the virus life cycle to look for it, Greenberg said.

This single-cycle experimental system also yielded a rough timeline of
what happens to a cell infected by HIV, and when the non-cytolytic
activity of CD8 occurs. Prior experiments used systems with multiple
replication cycles, making it difficult to follow actions within a
single round of infection. The Duke researchers were interested in
following a single life cycle.

They found that within the first two to six hours, HIV entry into CD4
cells has already been completed. Secondly, reverse transcription of the
viral genetic material was finished by 10 to 14 hours. Finally,
expression of early HIV genes occurs mostly between 14 to 48 hours.

With this life cycle chronology understood, the researchers could
determine when during the infection process the non-cytolytic activity
of the CD8 cells took place. They found if CD8 cells were added from the
time of infection up to six hours after infection, viral replication was
completely halted, and even after 24 hours, could achieve a significant
reduction in replication.

"These experiments demonstrate that the suppressive activity of CD8
occurs later in the virus life cycle - after the virus inserts its
genetic material into the genome of the target cell, but before it is
completely expressed," Greenberg said. "These findings have clarified
the protective role of CD8 cells."

The Duke team hopes that these findings will open new doors for
scientists working on developing novel therapeutics and vaccines for
HIV.

Greenberg's colleagues in the study include, from Duke, Charlene
McDanal, Guido Ferrari and Kent Weinhold. Also part of the team is Simon
Lacey, from the City of Hope, Duarte, Calif.
 
Interesting read. Testosterone and anavar are both known immune system enhancers. They are actually commonly prescribed to people with HIV and muscle wasting diseases like cancer.
 
It isn't that steroids directly improve the immune system, they simply make you stronger, which in turn, helps you ward off illness.
 
I've written for years that certain AAS boost immune system.

Nelson has a point that being strong leads to stronger immune system, but it isn't 'strong' as in being able to bench 400 pounds.. it is strong as in a strong and healthy body .. tren will make you stronger in the gym, but it will weaken your organs where it hurts the immune system.

compounds like deca, a little test, primo will strength the immune system cause they are mild .. that is why AIDS doctors want primo FDA approved for use with that disease

I actually recommend guys use primo with their tren for this reason
 
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