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Viruses are infectious agents that use a host cell to replicate. Human immunodeficiency virus (HIV) is a type of a virus known as a retrovirus, which is a class of viruses made up of RNA (ribonucleic acid) molecules. RNA is a variation of DNA, which comprises the molecular make-up of most cells' genetic material. Retroviruses use an enzyme called reverse transcriptase to make DNA copies of their RNA, which is then incorporated into the DNA of the host cell.

Human immunodeficiency virus (HIV) attacks the body's immune system, multiplying and spreading from cell to cell at incredible speed, damaging and destroying cells. At first, the immune system fights back by producing new cells, but eventually, HIV causes so much damage that the immune system can no longer keep up. When this happens, T-cells drop below 200 and AIDS develops.

Immune System
The immune system is the body's defense against disease and illness. It is a complex network of organs, cells, and proteins that

• defends the body against invasion by foreign disease-bearing organisms, such as HIV;
• identifies and destroys abnormal cells, such as cancer cells; and
• flushes dead and damaged cells out of the body.

The immune system readily recognizes and identifies disease-causing bacteria, viruses, fungi, and other abnormal cells. When an abnormality is detected, messages are sent from cell to cell to invoke an "attack" to destroy the abnormal cells. Afterwards, the immune system "remembers" the ordeal so that, if the same pathogen (disease-causing organism) invades the body again, it can quickly and readily come to the body's defense. This remarkable ability to remember a foreign substance and how to attack it is the basis of vaccination.

The immune system is made up of a variety of different types of cells (e.g., leukocytes, lymphocytes, phagocytes, B cells, CD8+ cells). HIV targets CD4+ cells, also called helper T-cells. Health care professionals often use the terms "CD4+ cell" and "T-cell" interchangeably. Helper T-cells are immune system managers. They "instruct" other cells when to start and stop carrying out their various duties.

HIV and the Immune System
HIV interferes with the immune response in the following ways:

• HIV replicates more quickly than the immune system cells and challenges the immune system's speed and efficacy.
• HIV targets CD4+ cells, the cellular managers of the immune system, destroying their ability to activate other immune system cells.
• HIV destroys CD4+ cells and puts demands on the body to replace them.

The immune system can replace as many as 10 billion CD4+ cells a day; but, after years of fending off the virus, it begins to wear down. The gap between the number of cells destroyed by the virus and the number that can be replaced grows wider over time and eventually leads to AIDS.

Healthy, uninfected people have between 800 and 1200 CD4+ cells per mm of blood. HIV causes the number of CD4+ cells to decline to dangerously low levels, making a patient who is infected with the virus very vulnerable to the opportunistic infections (e.g., cancers, neurological conditions, diarrhea, weight loss) that characterize AIDS. This also puts the patient at high risk for unusual infections. According to the Centers for Disease Control, a CD4+ cell count below 200/mm is a criterion for AIDS.

In many cases, there is a long time lag between initial infection with HIV and the development of symptoms. Based on several studies in the United States and other Western countries, the median time lag is 10 years, meaning that 50% of people who are infected with HIV develop symptoms before 10 years and 50% develop symptoms after 10 years.

According to these same studies, approximately 10% of people infected with HIV develop symptoms within 2 or 3 years and about 10% are asymptomatic (i.e., do not experience symptoms) after 12 years. A number of factors may account for this, including genetic differences among individual patients, genetic differences in HIV strains, and the presence of other infections that affect the speed and effectiveness of HIV.

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