HIV and the immune system

Human immunodeficiency virus (HIV) is a retrovirus that gradually destroys the immune system's function. When the retrovirus becomes active, the patient develops acquired immunodeficiency syndrome (AIDS), which is characterized by profound immunological deficits, opportunistic infection, secondary infections, and malignant neoplasms.

HIV disables and kills CD4+ T cells, which lowers the immune system's capability to fight infection. The number of CD4+ T cells triggers other cells in the immune system to attack invading organisms. HIV lowers the CD4+ T cell count and thereby inhibits other immune system cells to go on the attack.

A healthy person who is not HIV positive, has between 800 and 1200 CD4+ T cells per cubic millimeter (mm3) of blood. HIV reduces this count to 200 mm3. This is equal to or less than 14%. Infected patients are particularly vulnerable to opportunistic infections and cancers.

In addition to the T-cell count, the viral load (VL) is a test used to evaluate the status of the patient's immune system. The higher the number, the higher the viral load.

HIV is transmitted in three ways: injection of infected blood or blood products, sexual contact, and maternal-fetal transmission. Occupational exposure to HIV accounts for a small number of transmissions usually from a needle-stick.

HIV uses three enzymes to genetically encode, replicate, and assemble a new HI virus within a host cell. HIV can replicate only inside cells. These enzymes are reverse transcriptase, integrase, and protease.

The HI virus enters the cell through the CD4 molecule on the cell surface. Once inside the cell, the virus is uncoated with the help of the reverse transcrip-tase enzyme enabling the virus' single stranded RNA to be converted into DNA.

The viral DNA migrates to the nucleus of the cell where it is spliced into the host DNA with the help of the integrase enzyme. Once combined, the HIV DNA is called the provirus and is duplicated each time the cell divides. The protease enzyme assists in the assembly of a new form of the viral particles.

Patients with HIV undergo Highly Active Antiretroviral Therapy (HAART) that uses antiretroviral medications designed to slow or inhibit reverse transcriptase and protease enzymes. The Food and Drug Administration approved the first reverse transcriptase (RT) inhibitor in 1987. The first protease inhibitor was approved in 1995. No integrase inhibitors have been approved as yet.

HAART decreases the viral load to undetectable levels, thereby preserving and increasing the number of CD4+ T cells. HAART also prevents resistance to disease and keeps the patient in good clinical condition and prevents secondary infections and cancer.

The patient must adhere to HAART therapy as the virus becomes resistant and the antiretroviral agents lose their therapeutic effect. In addition, patients must avoid opportunistic infections and aggressive prophylaxis and treatment of opportunistic infections that do occur is recommended. Nutritional therapy, complementary therapy, and supportive care are also necessary.

Antiretroviral therapy is offered to patients who have less than 500 CD4+ T cells mm3 or whose plasma HIV RNA levels are greater than 10,000 copies/mL (B-DNA assay) or 20,000 copies/mL (R-PCR assay). Therapy should be considered for all HIV-infected patients who have detectable HIV RNA in plasma. There are risks and benefits to early initiation of antiretroviral therapy in the asymptomatic HIV-infected patient.

Potential Benefits

• Control of viral replication and mutation

• Reduction of viral burden

• Prevention of progressive immunodeficiency

• Maintenance of the normal immune system

• Reconstruction of the normal immune system

• Delay in the progression to acquired immunodeficiency syndrome and prolongation of life

• Decreased risk of selection of resistant virus

• Decreased risk of drug toxicity

• Possible decreased risk of viral transmission

Potential Risks

• Reduction in quality of life from adverse drug effects

• Inconvenience of taking the regimen of medications

• Earlier development of drug resistance

• Transmission of drug-resistant virus

• Limitation in future choices of antiretroviral agents as a result of development of resistance

• Unknown longterm toxicity of antiretroviral drugs

• Unknown duration of effectiveness of current antiretroviral therapies

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