Ju st o u t T may 2 , 1 9 9 7 ▼ 1 3
REASONS FOR HOPE
here is much confusion about what
happens inside the bodies of people
with HIV before they develop AIDS.
In the early 1980s when AIDS was
It was once believed that HIV was a “latent stage” that led to
first encountered, it was seen as a
collection of diseases that were occurring in people
the disease called AIDS—we now know that isn ’t true
whose immune system was seriously damaged. It
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was several years before it was discovered that a
virus, now known as HIV (human immunodefi
by The Boston AIDS Writers Group
ciency virus), caused this damage. Had research
ers known in the beginning what they know now,
infected a cell, CD4 cells get other cells to fight
and the virus take place in the lymph system,
there would be no “syndrome” known as AIDS,
the germs with antibodies, and marshal another
where most T cells are housed. As HIV gains the
instead it would be referred to as the late stages of
kind of cell, called a CD8 cell, to kill the infected
upper hand, the architecture of the system is
HIV disease. As tests showed that people with
slowly destroyed. We know that cancer patients
cells. Therefore, losing CD4 cells impairs the
HIV appeared healthy for years before the dis
who receive radiation therapy have similar dam
body’s ability to fight illness. One reason HIV
eases now known as opportunistic infections be
may be so difficult to fight is that it infects these
age, and it makes them more likely to get other
gan, it was believed that HIV stayed in the body
CD4 cells, and the immune system then needs to
infections. Other casualties to the virus are the
for years, doing little, in what was called the
spleen— which in part helps filter out infections—
wipe out many of its own officers.
“latent stage.” There seemed to be no reason to
and the thymus.
There are two basic kinds of CD4 cells: those,
treat a virus that clinicians believed was dormant.
Finally, with so much going on, many re
called “memory cells,” that are programmed to
In recent years researchers have discovered
searchers believe that HIV begins to disrupt the
recognize specific invaders, and those, called
that there is no latent stage, and that the virus
communication between the immune cells. The
“naive cells,” that are ready to fight new illnesses
begins damaging the immune system earlier than
immune system communicates through chemical
the body hasn’t seen before. Losing too many
was first thought. When HIV first enters the body
messengers, which can be disrupted by HIV. The
memory cells leaves the body defenseless against
it reproduces at an astounding rate. The immune
result is that cells respond ineffectively.
diseases it has recognized and fought before.
system recognizes the threat and fights back; that
At the same time that the immune system
Losing too many naive cells leaves the system
first fight sometimes causes flu-like symptoms.
The immune system’s response is amazingly suc
cessful at reducing the amount of virus in the
body. Actually, this response against the virus is
more powerful than any of the strong antiviral
combinations now available, but for reasons not
completely understood, the immune system doesn’t
finish the job by eliminating all of the virus.
What follows is nothing like the image of HI V
quietly lying dormant, to emerge years later as
AIDS. Instead, what goes on inside the body is
like a war of major proportions. The immune
system itself becomes the main battlefield in this
fight for survival. On the one side, HIV hijacks T
cells and converts them into virus-producing fac
tories that turn out billions of new copies of the
virus every day. On the other side, the immune
system eliminates huge numbers of copies of the
virus, killing its own infected cells in the process.
It is a war that the immune system cannot win
on its own. So far there is only one known way for
a person with HIV to keep this infection manage
without a way to fight new diseases. Interestingly,
weakens, the virus itself multiplies faster and
able: through help from powerful antiviral thera
it is the naive cells that fight things like the
infects new types of cells. Eventually the virus is
pies. There is, however, debate over when is the
common cold, since each cold virus is different.
able to enter cells with ease, by using entrances
best time to start that antiviral treatment. The
Unfortunately, while reducing viral load usu
(receptors) not available to it earlier. In addition,
reason many researchers now believe it is best to
ally increases the number of CD4 cells, it now
because the virus is not always exact when it
start early, is their understanding of the hidden
appears that if all the memory cells which recog
makes copies of itself, many variations of the
damage being done before the immune system
nize a specific invader have been killed, taking
virus develop. The cells which are set to look for
becomes so weak that it can’t stop opportunistic
antivirals will not bring back those particular
and kill HIV may not recognize all of these
infections.
cells. And if all the naive cells are lost, then the
variations as the virus they are supposed to hunt
body may never be able to cope with an infection
down. Therefore the immune system is open to
it has not seen before, or relearn to fight illnesses
attack even as more “naive” cells are needed to
T he D amage D one
it “forgot.”
learn to recognize the new variations. These newly
Some of the damage has consequences that are
Meanwhile, theCD8 cells, which like soldiers
trained cells won’t be looking for the original
now understood, and some of it has consequences
do much of the killing of enemy infected cells, do
variations, making the immune system’s response
no one has been able to clearly define. Probably
not work as well as the HIV infection progresses.
very inefficient.
the best known damage caused by HIV is re
It may be the lack of CD4 cells—the officers that
flected in the slow but consistent reduction in the
give them the orders to kill. In addition, there is
S topping the D amage
number of a kind of white blood cell called the T-
evidence that HIV directly infects and kills CD8
helper cells, or CD4 cells, that for many years was
cells. Another possibility is that the CD8 cells are
One way to slow the damage, or at least
the best way to know one’s status. Everyone knew
reproducing so often that they prematurely age
prevent it from speeding up too much, is to stay
that when CD4 cells fell below 200, people began
and weaken, coming to resemble the cells of a
healthy. By staying healthy one can prevent in
getting opportunistic infections, but until recently
much older person. Whatever the cause of the
fections from invading the body, or at least stop
it was not clear what was going on before that
problem, it is clear that without effective CD8
them from gaining a foothold. Adding more in
time.
cells, or effective antivirals to keep the virus at
fections may further tax an already overworked
HIV reduces the number of CD4 cells—the
bay, continued deterioration of the immune sys
immune system. In addition, when the immune
officers of the immune system’s disease-fighting
tem is assured.
system fights infection, it also increases the amount
army. When they have determined that a germ has
The great battles between these immune cells
of virus being produced. Staying healthy involves
D am age control
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any number of things from watching what you eat,
exercising and getting plenty of rest to making
sure that contact is limited with friends who have
colds or other infections. It also includes practic
ing safer sex, since many infections other than
HIV, from herpes to Kaposi’s sarcoma, are sexu
ally transmitted and tax the immune system.
If, however, you want to stop the damage and
not just slow it down, you will need to use antiviral
medications. Antivirals may stop the continuing
damage if they are used together in combinations
that reduce the amount of virus to very low levels
using the most sensitive viral load tests (meaning
they measure as low as 400 or 500 copies of the
virus). It is hoped that once such drugs get the
amount of virus down to an undetectable level, it
is unlikely to go back up. However, this means
taking medicine on time, all the time and in the
right amounts.
Already there is some evidence from people
who started antivirals very early in the illness,
when their immune systems were fairly intact,
that the body can repair the damage caused by
HIV. There is a series of tests that determines how
well the immune system works. Early results from
these tests show that people who start antiviral
therapy early can recover the small amounts of
immune function they may have lost. But people
whose systems are more damaged before they
begin therapy usually do not recover all the way.
This does not mean that people with very low
levels of CD4 cells should give up, however,
because the majority of people with counts lower
than 50 have been dramatically helped by power
ful antiviral combinations. But if people start very
early when little damage is done, it may be pos
sible to avoid the damage altogether. There is
even a chance that if antiviral combinations are
used early enough the virus may be cleared by the
body, although tests to determine this will not be
completed for a few years.
P ros
and
C ons
That said, it would be logical to ask why
people don’t just take an antiviral combination
right away, as soon as they know that they are
infected with HIV. One of the reasons to wait is
the side effects of the drugs— some of which can
be severe. There are those who are early in the
disease and want to wait for better drugs, afraid
that using the ones we have now might preclude
them from using better ones later. And there are
people who are simply not ready to take medicines
every day, on time, for the rest of their lives. The
best argument for waiting is that it is not yet
known whether taking these powerful drugs for
long periods will have serious implications. But
even taking this into account, many researchers
now believe that the earlier one starts, the better.
The message is simple: There is no latent stage.
From the beginning HIV is running rampant and—
if it remains untreated— will cause damage which
can’t be felt or seen. There are now ways to control
that damage.
The Boston AIDS Writers Group consists o f
Robert Folan-Johnson and Lou Pesce o f ACT
UP Boston; David Scondras, Robert Krebs,
Derek Libby and Larry Bresslour o f Search for
a Cure; and Jeff Terry. For more information,
write Search fo r a Cure, 58 Burbank St.,
Boston, MA 02115; phone (617) 536-2474; or
e-mail lbresslour@sfac.org.
STEPHEN D. YEW,
D .M .D .
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