Human Immunodeficiency Virus Essay Research Paper Human

Human Immunodeficiency Virus Essay, Research Paper

Human Immunodeficiency Virus

The content of this paper is whether or not mutations undergone by the Human

Immunodeficiency Virus and 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. The

question dealing with how HIV survives in the immune system is important, not only in

the search for a cure for the virus and its inescapable 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 can survive

through mutations then we might be able to come up with a type of drug to confuse these

mutations allowing the immune system time to erase it before the onset of AIDS. In order

to be able to fully comprehend and analyze this question we must first prove 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 special enzyme that can construct a DNA molecule using an RNA template.

This enzyme, called RNA-directed DNA polymerase, is also known 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 then

distributed to all daughter cells during later 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

catch their antigens and display them on their own surfaces. Among millions of helper T

cells circulating in the bloodstream, a selected few are programmed to .read. that antigen

Binding the macrophage, the T cell then 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 tell 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 offset the viruses by

binding directly to their surfaces, preventing them from attacking other cells. Also, 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 first stage of the 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 burst 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 stage 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 constantly, 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

defective, but because the virus and cytotoxic cells are destroying them. This idea that

HIV is not just evading the immune system but attacking and disabling it is what

distinguishes HIV from other retroviruses. The hypothesis in question is whether or not

the mutations undergone by HIV allow it to survive in the immune system. This idea was

conceived by Martin A. Nowak, an immunologist at

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