Human Immunodeficiency Virus

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

In order to be able to fully comprehend and analyze this question we mustfirst ascertain what HIV is, how the body attempts to counter the effects ofviruses 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 thecore of HIV is a double molecule of ribonucleic acid, RNA. When the virusinvades 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 particularenzyme that can construct a DNA molecule using an RNA template. This enzyme,called RNA-directed DNA polymerase, is also referred to as reversetranscriptase because it reverses the normal cellular process oftranscription. The DNA molecules produced by reverse transcription are theninserted into the genetic material of the host cell, where they areco-replicated with the host's chromosomes; they are thereby distributed toall daughter cells during subsequent cell divisions. Then in one or more ofthese daughter cells, the virus produces RNA copies of its genetic material.
These new HIV clones become covered with protein coats and leave the cell tofind 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. Amongmillions of helper T cells circulating in the bloodstream, a select few areprogrammed to ?read? that antigen. Binding the macrophage, the T cellbecomes activated. Once activated, helper T cells begin to multiply. Theythen stimulate the multiplication of those few killer T cells and B cellsthat are sensitive to the invading viruses. As the number of B cellsincreases, helper T cells signal them to start producing antibodies.
Meanwhile, some of the viruses have entered cells of the body - the onlyplace they are able to replicate. Killer T cells will sacrifice these cellsby chemically puncturing their membranes, letting the contents spill out,thus disrupting the viral replication cycle. Antibodies then neutralize theviruses by binding directly to their surfaces, preventing them from attackingother cells. Additionally, they precipitate chemical reactions that actuallydestroy the infected cells. As the infection is contained, suppresser Tcells halt the entire range of immune responses, preventing them fromspiraling out of control. Memory T and B cells are left in the blood andlymphatic system, ready to move quickly should the same virus once againinvade the body.

In the initial stage of HIV infection, the virus colonizes helper T cells,specifically CD4+ cells, and macrophages, while replicating itself relativelyunnoticed. As the amount of the virus soars, the number of helper cellsfalls; macrophages die as well. The infected T cells perish as thousands ofnew viral particles erupt from the cell membrane. Soon, though, cytotoxic Tand B lymphocytes kill many virus-infected cells and viral particles. Theseeffects limit viral growth and allow the body an opportunity to temporarilyrestore its supply of helper cells to almost normal concentrations. It is atthis time the virus enters its second stage.

Throughout this second phase the immune system functions well, and the netconcentration of measurable virus remains relatively low. But after a periodof time, the viral level rises gradually, in parallel with a decline in thehelper population. These helper T and B lymphocytes are not lost because thebody?s ability to produce new helper cells is impaired, but because the virusand cytotoxic cells are destroying them. This idea that HIV is not justevading the immune system but attacking and disabling it is whatdistinguishes HIV from other retroviruses.

The hypothesis