Steroids what is your experience, do they have a place in hiv treatment

[bimazek]

"Steroids, which are known to down-regulate CD62L and retard
lymph node homing, have been shown to stop reduction of CD4
cells in the blood of patients "
 
The hallmark of HIV-1 disease is the
gradual disappearance of CD4
T cells from the
blood. The mechanism of this depletion, however,
is still unclear. Evidence suggests that lymphocytes
die in lymph nodes, not in blood, and that uninfected
bystander cells are the predominant cells
dying. Our and others’ previous studies showed
that the lymph node homing receptor, CD62 ligand
(CD62L), and Fas are up-regulated on resting
CD4
T cells after HIV-1 binding and that these
cells home to lymph nodes at an enhanced rate.
During the homing process, signals are induced
through various homing receptors, which in turn,
induced many of the cells to undergo apoptosis
after they entered the lymph nodes.

laymens interpretation and the science articles below ......
already in 2007 new INFO cd4 cells die in the lymph nodes not in the blood specifically in the gut
but the loss in the gut lymph nodes is not mirrored in the blood or other lymph nodes
which explains why blood cd4 counts do not give a whole picture of the person and what he is facing
 
also strangely uninfected nearby bystander cd4 cells die --- not the hiv infected ones

FasL anti-body would block this prcess - sounds like breakthrough to me

only one cd4 cell in 1,000,000 is producing virus, very few of them is infected --
 
this is a disease of the homing of the cd4s back to the nodes to be distroyed, the body thinks it has cleared the infecton after the 2 week initial burst and then cytokines that home the cds back to the nodes are relesased this tricks the cd4s to go back and some other molecule kills the un-infected cd4s in the nodes
 
A HOMING RECEPTOR ON OUTSIDE OF UNINFECTED CD4 CELLS GETS TURNED ON BY BEING CLOSE TO OR TOUCHING AN HIV PARTICLE (BUT NOT INFECTED BY IT)
THIS CAUSES THE CD4 TO HOME BACK TO THE LYMPH NODE TO KILL ITSELF CALLED APOSISOS...
 
so the disease is actually a disease of the
 
"i am not stopping but i have to stop so i have to go home now and stop attacking the infection and go by by"
 
kind of an i love lucy disease... do you get it...
the cd4s that are dying ARE NOT INFECTED
we loose cd4s that are not even infected!!!
this is interesting if you ask me...

and very different than how they tell you it works when the simplify it for the patient
 
sure
 
when you get a flu there is that awful giant wave of immune response and all those terrible chemicals cytokines and bugs being killed off
then the immune system pulls back and says, did i get it all, and then it hits with another wave, then pulls back, and then
says ok i finished and i have to put away all the tanks and big guns and rifles...
that means...
 
that is the period called homing back to the lymph nodes
 
so something wierd is happening in hiv disease because the body thinks the infection has been dealt with then
it calls back the cd4s into the nodes and because they have touched or recieved a signal -=BUT ARE NOT INFECTED OR NOR WILL THEY BE INFECTED-
THEY do aposisos and they die and that is why cd4s deplete
 
it is not the infected ones that die off!!!!
 
also this explains why all those weird alternative therapies though they dont stop it can have some minor effects
 
anything that disrupts the homing of the uninfected cd4s back to the node to aposisos or self die.
 
it all has to do with the FasL --- some chemical in immunte system
CD62L is also involved
 
the cool thing is with a anti-FasL monoclonal antibody... which is big time expeimental stuff real complicated to create
they can stop the FasL induced death of the cd4s
 
listen they just figured out which and how the cd4s where dying off a few weeks ago.. before they thought the infected ones were dying
 
now they find out the truth
 
only the CD62L receptor tells the poor uninfected cd4 cell to go home
but it may be that CD62L and a few other receptor switches get turned on once in the node and the poor cell is told to die off
your job is done
 
it reminds me of
 
lucy in the chocolate factory
 
with all the candies on the conviewer belt

HERE IS THE ACTUAL SCIENCE BEHIND THIS...
 
http://www.jleukbio.org/cgi/rapidpdf/jlb.0506338v1.pdf
 
"Steroids, which are known to down-regulate CD62L and retard
lymph node homing, have been shown to stop reduction of CD4
cells in the blood of patients "
 
The hallmark of HIV-1 disease is the
gradual disappearance of CD4
T cells from the
blood. The mechanism of this depletion, however,
is still unclear. Evidence suggests that lymphocytes
die in lymph nodes, not in blood, and that uninfected
bystander cells are the predominant cells
dying. Our and others’ previous studies showed
that the lymph node homing receptor, CD62 ligand
(CD62L), and Fas are up-regulated on resting
CD4
T cells after HIV-1 binding and that these
cells home to lymph nodes at an enhanced rate.
During the homing process, signals are induced
through various homing receptors, which in turn,
induced many of the cells to undergo apoptosis
after they entered the lymph nodes. The purpose of
this study was to determine how the homing process
induces apoptosis in HIV-1-exposed, resting
CD4
T cells. We found that signaling through
CD62L up-regulated FasL. This resulted in apoptosis
of only HIV-1-presignaled, resting CD4
T
cells, not normal CD4
T cells. This homing receptor-
induced apoptosis could be blocked by anti-
FasL antibodies or soluble Fas, demonstrating that
the Fas-FasL interaction caused the apoptotic
event. J. Leukoc. Biol. 81: 000–000; 2007.
 
 
 
 
 

One of the
major observations in this study is that apoptosis of HIV-1-
exposed, resting CD4
T cells, in which CD62L was crosslinked,
could be inhibited significantly by blocking anti-FasL
antibodies or sFas (Fig. 4). This indicated that apoptosis of
HIV-1-exposed, resting CD4
T cells, subsequently signaled
through the homing receptor, is Fas-FasL-mediated. It is interesting
that apoptosis was detected in resting CD4
T cells
exposed with X4 virus strain (HIV-1213) or R5 virus (HIV-1BaL)
strain, subsequently signaled by XLCD62L, indicating that this
is a common property of HIV-1 (Fig. 2). Furthermore, such
effect seems to be independent of HIV-1 replication, as UVinactivated,
HIV-1-exposed, resting CD4
T cells, upon
XLCD62L, underwent apoptosis as well (data not shown).
 

Based on
our data, we proposed that in vivo, CD4
T cells are infected
with HIV in Peyer’s patches, where they may get the signals for
homing fast and up-regulated Fas and get the further signals,
such as FasL, through interaction between homing receptors
and their ligand on lamina propria and finally, undergo apoptosis
in lamina propria. We are currently working on the
effects of HIV on gut homing receptor  4
7 and consequence
of cross-linking of  4
7 on the HIV-exposed CD4
T cells
 
 
 
With respect to the in vivo relevance of our findings in the
context of HIV-1 pathogenesis, our data implicate the following
scenario to be operative in vivo and may act as a mechanism for
the death of uninfected CD4
cells. Resting CD4
lymphocytes
in lymphoid tissues (in gut, lymph nodes, etc.), coming
into contact with HIV-1 virions, productively infected cells, or
HIV-1-coated, follicular dendritic cells, result in induction of
a partially activated phenotype, including up-regulation of
homing receptors and Fas. Because of normal lymph node/
blood circulation, in which most lymphocytes in lymphoid
tissues migrate back to the blood within 2 days [56], many of
these cells will end up back in the blood at the time of
maximum-induced expression of homing receptors. These cells
would then home rapidly to peripheral lymph nodes or gutassociated,
lymphatic tissue, dependent on the type of homing
receptors (e.g., CD62L for peripheral lymph nodes;  4
7 for
gut). Following transendothelial migration, these CD4
T cells
receive signals through homing receptors, resulting in induction
of FasL expression on some of the cells and rapid susceptibility
 

Consequently, together
with the increased Fas expression within the same
CD4
T cell population, approximately one-third of them
would be depleted, and they do not produce HIV-1 [18]. In
support of this review, features that are characteristically associated
with HIV-1 infection include the following. As CD4
lymphocytes disappear in the blood, their numbers do not drop,
and the CD4/CD8 ratios do not invert in lymph nodes until late
in disease [57]; there is increased apoptosis of uninfected cells,
mainly localized in lymph nodes or gut-associated lymphatic
tissue [6, 45, 58] but not in the blood [59, 60]; there is
increased FasL-expressing cells with the morphology of macrophages
and lymphocytes, and the degree of FasL in vivo has
been shown to be correlated with the degree of apoptosis [61].
 
Steroids, which are known to down-regulate CD62L and retard
lymph node homing, have been shown to stop reduction of CD4
cells in the blood of patients [62]. This may be the consequence
as control of aberrant homing signals for the marked
reduction in apoptosis. Future studies, testing whether inhibition
of lymph node homing or homing receptor induction of
apoptosis would prevent depletion of CD4
cells in patients,
are needed.
ACKNOWLEDGMENTS
 
Steroids, which are known to down-regulate CD62L and retard
lymph node homing, have been shown to stop reduction of CD4
cells in the blood of patients [
 
Steroids, which are known to down-regulate CD62L and retard
lymph node homing, have been shown to stop reduction of CD4
cells in the blood of patients
 
Infection with HIV-1 is usually characterized by a gradual and
inexorable depletion of CD4
T lymphocytes. The importance
of the loss of these cells in the development of AIDS is
unquestioned, as it correlates with the loss of immune capabilities
and the consequent occurrence and severity of opportunistic
infections and HIV-1-associated neoplasms. However,
understanding the mechanisms by which HIV-1 causes CD4

T cell loss remains one of the unanswered questions in the
AIDS field. Many mechanisms have been proposed to explain
how HIV-1 causes depletion of CD4
T cells and the earliest
theorized that virus replication in CD4
T cells resulted in
their death or that virus-specific CTLs killed these infected
cells. However, elimination of productively infected cells could
not explain the significant loss of CD4
T cells [1], as few cells
in vivo are producing virus at any given time (approximately
one in 105 cells) [2, 3]. Recent studies suggest that depletion
of CD4
T cells mainly occurs in lymphoid tissues of the
gastrointestinal tract [4, 5], but the loss of these cells in the gut
is not mirrored in the blood and lymph nodes. In fact, CD4
T
cell depletion occurs in the “effecter area” of gut (lamina
propria) not in the “inductive area” (Peyer’s patches), where
most of the cells producing virus reside. It has also been shown
that increased numbers of CD4
cells are dying in peripheral
lymphoid tissues of HIV-infected subjects, but cells replicating
HIV-1 are not the principal cells dying; uninfected, neighboring
cells are dying [6]. Therefore, most theories about how
HIV-1 depletes CD4
T cells now depict ways uninfected
bystander cells can be eliminated. Some early studies indicated
that HIVgp120 binding to CD4 and CXCR4 receptors
induced apoptosis [7, 8]. All of these studies used transformed
cell lines, and studies using normal CD4 lymphocytes did not
find this phenomenon [7–11]. Also, the apoptosis induced in
cell lines was not Fas/Fas ligand (FasL)-mediated, but other
pathways were [7–9]. Recently, collagen deposition-associated
fibrosis and damaged lymphatic tissues that accompany immune
activation have been shown to be correlated inversely
with blood CD4
T cell count [4, 12]. Some studies suggest
that there is a significant dysregulation of cytokine responses,
which likely, influences T cell susceptibility to apoptosis [13].
Many of these factors may play some roles in CD4
T cell
depletion. However, excessive apoptosis of uninfected CD4
T
cells is thought to be the major reason for depletion of CD4

T cells [13, 14].
Our previous studies showed that HIV-1 binding to resting
CD4
T cells up-regulated the expression of CD62L, the
receptor for homing to lymph nodes, on some cells and enhanced
the homing of these cells from the blood into lymph
nodes [15–17]. Subsequent signaling through various homing
receptors during the homing process on these abortively infected
CD4
T cells induced many of them to undergo apoptosis
[16]. These signaling events occur when the cells transendothelial
migrate into lymph nodes, and it was shown that
CD4
T cells in the blood of HIV-infected people
 
 
 
 
 
 
 

Rapidly progressive periodontitis as an important clinical marker for HIV disease.
    * Levine RA,
    * Glick M.
Albert Einstein Medical Center.
Acquired immunodeficiency syndrome (AIDS) patients are in desperate need of the clinical therapies that can enable them to retain their dentition for the rest of their lives. It is important to weigh the social, clinical-oral, and radiographic assessments with all patients, especially those with undiagnosed human immunodeficiency virus (HIV) infection. Many experience denial and are noncompliant with both medical and dental prevention. Many HIV-infection-related sequelae are first seen intraorally; dentists must be aware of them and consider all patients as HIV carriers until proved otherwise. HIV-associated gingivitis has been demonstrated to progress to HIV-associated periodontitis. Therefore, early recognition and management of HIV-associated gingivitis is essential to prevent the rapid loss of hard and soft periodontal tissues.

[antibody]

does this include Androgel?

if so i can say from my experience with Androgel is that it has given me energy where i had none before. i was diagnosed with low testosterone which left me depressed, fatigued and feeling very ill. within a few weeks of replacement therapy my mood stabilized and my energy level and libido returned so with out it i'm pretty sure i'd be dead by now.

[bimazek]

if you are on steroids please post your experiences

and numbers

thanks

[mark54]

Hi, new to the website with current problem.  is anyone having treatment failure with androgel and any solutions.  found studies which indicated it was occuring at around the three year mark which is about where i am at.  called the company and got the reply that they had noticed the trend.  my endo response was he can't believe it is happening, and of course thanks alot for that.  andorgel had really restored my ability to live a fairly active life and then got zapped.  changed application to 50mg around 9am and 50mg around 11am with some degree of success.  so if anyone is experiencing the problem lets start talking so we don't have to wait 10 years for them to acknowledge the problem like we do for most everything else.  i've been diagnosed since '83 and turned down all treatment programs till i developed aids  11/98 after PH treatments became available.  please poll your friends and try to get them involved with this thread if they are showing up with the problem.

[bimazek]

 when you say.... " is anyone having treatment failure with androgel"

do you mean   treatment failure with HAART, your VL is returning

or

do you mean treatment failure with androgel, the androgel is not working well you dont have energy?

[antibody]

okay. i ahte putting on androgel every morning. it's a pain in the ass. i hate waiting for it to dry before getting dressed and in the winter it sucks putting on cold gel! anyways i was hoping since i started HAART i would get better and not have to use this stuff any more. i was going to ask my doctor to check my levels on my next blood work...long story short. i forgot to pick up the androgel from the pharmacy and missed 1 days dose. let me tell you the next day i could not move. i was so fatigued and so much muscle pain. so i guess i can't stop androgel which bums me out. it took 2 days to get my energy back once i picked it up. anyways for as much as i hate putting the stuff on i don't really know where i'd be without it.

[Force1]

if you are on steroids please post your experiences

and numbers

thanks

I use rx steriods, very positive results.

numbers, a 100% increase in tcels in two years.

[pozniceguy]

I am not sure if this is the type of steroid you are asking about...I use Serostim..a natural steroid ( aka;  Human Growth Hormone)   I have been using it for several years ..one period of about 3 months it was not available  from manufacturer  and of course I  had to stop ....noticed increase in fatigue...but no noticeable change in CD4 or VL

[BKNYLivin]

I use rx steriods, very positive results.

numbers, a 100% increase in tcels in two years.

By rx steroids, I'm assuming you get these prescribed by your doctor. What exactly are you on, if you don't mind me asking? The whole fatigue thing has been driving me crazy recently and I have read that while Androgel works for some people, there are much more efficient alternatives. I'm wondering if my doctor would be open to me trying other stuff.

[bimazek]

i have never been on them do not have an rx

i just remember the guys in late 80s in la seemed to do well on them but then they stopped doing well after a while

i think it is a double edge sword

[boylikertampa]

I have been on Androgel for several years.   Do not feel immediate effects and can go a day or several without using and feel no effects.  But overall I think it helps my sex drive and energy.  Also have used Oxandrin for a 3-month trial...it reeally helped fill out my legs and arms and chest.  Insurance stopped it, but I just started it again.  I am on Trizivir (past 6 years).  If your dr. will prescribe and insurance will cover, I recommend steroids.

[Miss Philicia]

I used hormone replacement therapy ("steroid" has negative connotations) from '00 - '04 with absolutely no adverse effects in my lab numbers.  (Though to be honest I'm not even sure what the exact question about this topic is in the first and opening post in this thread after that overly long cut & paste).