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The Effects of Hiv Mutations on the Immune System

Essay by   •  August 28, 2010  •  Research Paper  •  2,065 Words (9 Pages)  •  2,611 Views

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INTRODUCTION 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. BACKGROUND 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.

Definition 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. The Body Fights

Back 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. HIV's Life Cycle 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

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