Immune System Essay, Research Paper


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C.J. Stimson


The subject of this paper is the human immunodeficiency virus, HIV, and

whether or non mutants undergone by the virus let it to last in the

immune system. The cost of handling all individuals with AIDS in 1993 in the

United States was $ 7.8 billion, and it is estimated that 20,000 new instances of

AIDS are reported every 3 months to the CDC. This inquiry covering with how

HIV survives in the immune system is of critical importance, non merely in the

hunt for a remedy for the virus and its inevitable syndrome, AIDS ( Acquired

Immunodeficiency Syndrome ) , but besides 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 mutants so we might be able to come up with a

type of drug to retard these mutants leting the immune system clip to

expunge it before the oncoming of AIDS.


In order to be able to to the full grok and analyse this inquiry we must

foremost determine what HIV is, how the organic structure attempts to counter the effects of

viruses in general, and how HIV infects the organic structure.


HIV is the virus that causes AIDS. HIV is classified as a RNA Retrovirus.

A retrovirus uses RNA templets to bring forth DNA. For illustration, within the

nucleus of HIV is a dual molecule of ribonucleic acid, RNA. When the virus

invades a cell, this familial stuff is replicated in the signifier of DNA.

But, in order to make so, HIV must foremost be able to bring forth a peculiar

enzyme that can build a Deoxyribonucleic acid molecule utilizing an RNA templet. This enzyme,

called RNA-directed DNA polymerase, is besides referred to as contrary

RNA polymerase because it reverses the normal cellular procedure of

written text. The Deoxyribonucleic acid molecules produced by contrary written text are so

inserted into the familial stuff of the host cell, where they are

co-replicated with the host & # 8217 ; s chromosomes ; they are thereby distributed to

all girl cells during subsequent cell divisions. Then in one or more of

these girl cells, the virus produces RNA transcripts of its familial stuff.

These new HIV clones become covered with protein coats and leave the cell to

happen other host cells where they can reiterate the life rhythm.

The Body Fights Back

As viruses begin to occupy the organic structure, a few are consumed by macrophages,

which seize their antigens and expose them on their ain surfaces. Among

1000000s of assistant T cells go arounding in the blood stream, a choice few are

programmed to? read? that antigen. Adhering the macrophage, the T cell

becomes activated. Once activated, helper T cells begin to multiply. They

so excite the generation of those few slayers T cells and B cells

that are sensitive to the invading viruses. As the figure of B cells

additions, helper T cells signal them to get down bring forthing antibodies.

Meanwhile, some of the viruses have entered cells of the organic structure & # 8211 ; the lone

topographic point they are able to retroflex. Killer T cells will give these cells

by chemically puncturing their membranes, allowing the contents slop out,

therefore interrupting the viral reproduction rhythm. Antibodies so neutralize the

viruses by adhering straight to their surfaces, forestalling them from assailing

other cells. Additionally, they precipitate chemical reactions that really

destruct the septic cells. As the infection is contained, suppresser Thymine

cells halt the full scope of immune responses, forestalling them from

gyrating out of control. Memory T and B cells are left in the blood and

lymphatic system, ready to travel rapidly should the same virus one time once more

occupy the organic structure.

HIV? s Life Cycle

In the initial phase of HIV infection, the virus colonizes helper T cells,

specifically CD4+ cells, and macrophages, while retroflexing itself comparatively

unnoticed. As the sum of the virus zooms, the figure of assistant cells

falls ; macrophages die every bit good. The septic T cells perish as 1000s of

new viral atoms erupt from the cell membrane. Soon, though, cytotoxic T

and B lymph cells kill many virus-infected cells and viral atoms. These

effects limit viral growing and let the organic structure an chance to temporarily

reconstruct its supply of assistant cells to about normal concentrations. It is at

this clip the virus enters its 2nd phase.

Throughout this 2nd stage the immune system maps good, and the net

concentration of mensurable virus remains comparatively low. But after a period

of clip, the viral degree rises bit by bit, in analogue with a diminution in the

helper population. These helper Thymine and B lymph cells are non lost because the

organic structure? s ability to bring forth new helper cells is impaired, but because the virus

and cytotoxic cells are destructing them. This thought that HIV is non merely

hedging the immune system but assailing and disenabling it is what

distinguishes HIV from other retroviruses.


The hypothesis in inquiry is whether or non the mutants undergone by HIV

let it to last in the immune system. This thought was conceived by Martin

A. Nowak, an immunologist at the University of Oxford, and his coworkers when

they considered how HIV is able to avoid being detected by the immune system

after it has infected CD4+ cells. The footing for this hypothesis was

excogitated from the evolutionary theory and Nowak? s ain theory on HIV


Evolutionary Theory

The evolutionary theory provinces that opportunity mutant in the familial stuff

of an single being sometimes yields a trait that gives the being a

survival advantage. That is, the affected person is better able than its

equals to get the better of obstructions to endurance and is besides better able to reproduce

prolifically. As clip goes by, offspring that portion the same trait become

most abundant in the population, outcompeting other members until another

single acquires a more adaptative trait or until environmental conditions

alteration in a manner that favours different features. The force per unit areas exerted

by the environment, so, determine which traits are selected for spread in a


Nowak? s Theory on HIV Survival

When Nowak considered HIV? s life rhythm it seemed apparent that the bug

was peculiarly good suited to germinate off from any force per unit areas it confronted

( this thought being derived from the evolutionary theory ) . For illustration, its

familial make-up alterations invariably ; a high mutant rate increases the

chance T

hat some familial alteration will give rise to an advantageous trait.

This great familial variableness stems from a belongings of the viral enzyme

contrary RNA polymerase. As stated above, in a cell, HIV uses contrary

RNA polymerase to copy its RNA genome into double-strand DNA. The virus

mutates quickly during this procedure because contrary RNA polymerase is instead

mistake prone. It has been estimated that each clip the enzyme transcripts RNA into

Deoxyribonucleic acid, the new DNA on mean differs from that of the old coevals in

one site. This form makes HIV one of the most variable viruses known.

HIV? s high reproduction rate further increases the odds that a mutant

utile to the virus will originate. To to the full appreciate the extent of HIV

generation, expression at the Numberss published on it ; a billion new viral

atoms are produced in an septic patient each twenty-four hours, and in the absence of

immune activity, the viral population would on norm dual every two


With the cognition of HIV? s great evolutionary potency in head, Nowak and

his co-workers conceived a scenario they thought could explicate how the virus

resists complete obliteration and therefore causes AIDS, normally after a long clip

span. Their proposal assumed that changeless mutant in viral cistrons would

lead to uninterrupted production of viral discrepancies able to hedge the immune

defences runing at any given clip. Those discrepancies would emerge when

familial mutants led to alterations in the construction of viral peptides

recognized by the immune system. Frequently such alterations exert no consequence on

immune activities, but sometimes they can do a peptide to go unseeable

to the organic structure? s defences. The affected viral atoms, bearing fewer

recognizable peptides, would so go more hard for the immune system

to observe.

The Model

Using the theory that he had developed on the endurance of HIV, along with

the evolutionary theory, Nowak devised a theoretical account to imitate the kineticss and

growing of the virus. The equations that formed the bosom of the theoretical account

reflected characteristics that Nowak and his co-workers thought were of import in

the patterned advance of HIV infection: the virus impairs immune map chiefly

by doing the decease of CD4+ assistant T cells, and higher degrees of virus

consequence in more T cell decease. Besides, the virus continuously produces flight

mutations that avoid to some degree the current immunologic onslaught, and these

mutations spread in the viral population. After awhile, the immune system

finds the mutations expeditiously, doing their population to shrivel.

The simulation managed to reproduce the typically long hold between

infection by HIV and the eventual crisp rise in viral degrees in the organic structure. It

besides provided an account for why the rhythm of flight and repression does

non travel on indefinitely but culminates in uncontrolled viral reproduction, the

about complete loss of the assistant T cell population and the oncoming of AIDS.

After the immune system becomes more active, survival becomes more

complicated for HIV. It is no longer plenty to retroflex freely ; the virus

besides has to be able to guard off immune onslaughts. Now is when Nowak predicts

that choice force per unit area will bring forth increasing diverseness in peptides

recognized by immune forces. Once the defensive system has collapsed and is

no longer an obstruction to viral endurance, the force per unit area to diversify

evaporates. In patients with AIDS, we would once more expect choice for

the fastest-growing discrepancies and a lessening in viral diverseness.

Long-run surveies affecting a little figure of patients have confirmed some

of the mold anticipations. These probes, conducted by several

research workers & # 8211 ; including Andrew J. Leigh Brown of the University of Edinburgh,

et al. & # 8211 ; tracked the development of the alleged V3 section of a protein in the

outer envelop of HIV for several old ages. V3 is a major mark for antibodies

and is extremely variable. As the computing machine simulation predicted, viral samples

obtained within a few hebdomads after patients become septic were likewise in the

V3 part. But during subsequent old ages, the part diversified, therefore doing

a rapid addition in the sum of V3 discrepancies and a progressive lessening in

the CD4+ cell count.

The theoretical account presented by Nowak is highly hard to verify with clinical

trials entirely, mostly because the diversified interactions between the virus

and the immune system are impossible to supervise in item. Consequently,

Nowak turned to a computing machine simulation in which an ab initio homogenous viral

population evolved in response to immunologic force per unit area. He reasoned that if

the mathematical theoretical account produced the known forms of HIV patterned advance, he

could reason the evolutionary scenario had some virtue. To verify his

theoretical account, he turned to the experiments done on the V3 protein section in HIV.

These experiments demonstrated that the peptides were mutating and that

these mutants were taking to a diminution in assistant lymph cells.


Before we begin to reply the inquiry that this paper is look intoing, an

rating of our primary experiment beginning is necessary, this being a

publication of Nowak? s theoretical account. Upon rating of this beginning, a job is

exposed, this being that because there was no experiment performed to

substantiate this theoretical account, we have no thought if the mold anticipations are

true. Although there were old non-directly related experiments ( i.e. ,

V3 experiment ) that Nowak referred to to apologize his theoretical account there was

ne’er an experiment done entirely based on the theoretical account. Because the V3 findings

were in agreement with the findings of Nowak? s theoretical account, we can presume that the

theoretical account has some virtue.

This absence of an experiment is what leads to the boundaries that one

brushs when experimenting with HIV mutants. These boundaries being

that because HIV replicates and mutates non-linearly, it is impossible to

history all its viral kineticss conscientiously.

The deficiency of experimental informations based on Nowak? s theoretical account along with the

insufficiency of experiments covering with HIV mutants leads to the decision

that at present, there is no reply to this inquiry. Although, other

inquiries have been exposed, including: does the virus mutate at random or

is it systematic? And how does the virus know where to mutate in order to

continue lasting undetected?

These are all inquiries that must foremost be answered before we even begin to

attempt to find if viral mutants are what allows HIV to last in the

immune system.

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