The topic of this paper is the human immunodeficiency virus, HIV, and
whether or not mutations undergone by the virus allow it to survive in the
immune system. The cost of treating all persons with AIDS in 1993 in the
United States was $7.8 billion, and it is estimated that 20,000 new cases of
AIDS are reported every 3 months to the CDC. This question dealing with how
HIV survives in the immune system is of critical importance, not only in the
search for a cure for the virus and its inevitable syndrome, AIDS (Acquired
Immunodeficiency Syndrome), but also so that over 500,000 Americans already
infected with the virus could be saved. This is possible because if we know
that HIV survives through mutations then we might be able to come up with a
type of drug to retard these mutations allowing the immune system time to
expunge it before the onset of AIDS.

In order to be able to fully comprehend and analyze this question we must
first ascertain what HIV is, how the body attempts to counter the effects of
viruses in general, and how HIV infects the body.

HIV is the virus that causes AIDS. HIV is classified as a RNA Retrovirus.
A retrovirus uses RNA templates to produce DNA. For example, within the
core of HIV is a double molecule of ribonucleic acid, RNA. When the virus
invades a cell, this genetic material is replicated in the form of DNA .
But, in order to do so, HIV must first be able to produce a particular
enzyme that can construct a DNA molecule using an RNA template. This enzyme,
called RNA-directed DNA polymerase, is also referred to as reverse
transcriptase because it reverses the normal cellular process of
transcription. The DNA molecules produced by reverse transcription are then
inserted into the genetic material of the host cell, where they are
co-replicated with the host's chromosomes; they are thereby distributed to
all daughter cells during subsequent cell divisions. Then in one or more of
these daughter cells, the virus produces RNA copies of its genetic material.
These new HIV clones become covered with protein coats and leave the cell to
find other host cells where they can repeat the life cycle.

As viruses begin to invade the body, a few are consumed by macrophages,
which seize their antigens and display them on their own surfaces. Among
millions of helper T cells circulating in the bloodstream, a select few are
programmed to “read” that antigen. Binding the macrophage, the T cell
becomes activated. Once activated, helper T cells begin to multiply. They
then stimulate the multiplication of those few killer T cells and B cells
that are sensitive to the invading viruses. As the number of B cells
increases, helper T cells signal them to start producing antibodies.
Meanwhile, some of the viruses have entered cells of the body - the only
place they are able to replicate. Killer T cells will sacrifice these cells
by chemically puncturing their membranes, letting the contents spill out,
thus disrupting the viral replication cycle. Antibodies then neutralize the
viruses by binding directly to their surfaces, preventing them from attacking
other cells. Additionally, they precipitate chemical reactions that actually
destroy the infected cells. As the infection is contained, suppresser T
cells halt the entire range of immune responses, preventing them from
spiraling out of control. Memory T and B cells are left in the blood and
lymphatic system, ready to move quickly should the same virus once again
invade the body.

In the initial stage of HIV infection, the virus colonizes helper T cells,
specifically CD4+ cells, and macrophages, while replicating itself relatively
unnoticed. As the amount of the virus soars, the number of helper cells
falls; macrophages die as well. The infected T cells perish as thousands of
new viral particles erupt from the cell membrane. Soon, though, cytotoxic T
and B lymphocytes kill many virus-infected cells and viral particles. These
effects limit viral growth and allow the body an opportunity to temporarily
restore its supply of helper cells to almost normal concentrations. It is at
this time the virus enters its second stage.

Throughout this second phase the immune system functions well, and the net
concentration of measurable virus remains relatively low. But after a period
of time, the viral level rises gradually, in parallel with a decline in the
helper population. These helper T and B lymphocytes are not lost because the
body’s ability to produce new helper cells is impaired, but because the virus
and cytotoxic cells are destroying them. This idea that HIV is