Background: Over the past decade, the number of children infected with the human immunodeficiency virus (HIV) has increased dramatically because of an increase in the number of women of childbearing age who are infected with HIV. Only within the last 5 years have obstetricians in the United States been required to offer prenatal HIV testing; however, this testing is still not mandatory in all states.

Before prenatal testing was common, diagnosing HIV infections in a woman after diagnosing it in her child was not unusual. A proportion of the increased incidence of pediatric HIV is because of earlier identification, and the diagnosis of acquired immunodeficiency syndrome (AIDS) in a previously healthy child is not rare.

Prior to 1985, one way that children were infected was by blood-product transfusions, but improved screening tests have eliminated such transmission. A common way adolescents become infected is by being involved in high-risk behaviors such as unprotected intercourse, male homosexual intercourse, and intravenous (IV) drug abuse. The disease course in these cases progresses as it does in adult HIV infections. Vertically transmitted HIV can cause rapidly progressive disease, chronic progressive disease, or an adultlike course consisting of a significant clinical latency period before symptoms appear.

Pathophysiology: After HIV enters a host, the trimeric gp120 glycoproteins that protrude from its lipoprotein bilayer envelope bind to CD4 cell surface receptors and CCR5 or CXCR4 chemokine coreceptors. CD4 receptors are located on CD4 T lymphocytes, monocytes, and macrophages, but juxtapositioned coreceptors are also needed for viral infection. The V3 region of the gp120 glycoprotein determines cellular tropism, and tropism is involved in syncytial formation. M-tropic (nonsyncytial) strains prefer the CCR5 coreceptor and are the primary causes of infection. CCR5 chemokine coreceptor deficiency is present in as many as 10% of Europeans and 20% of Ashkenazi Jews, and it appears to confer some protection against infection. Once gp120 binds to the receptors, the associated gp41 transmembrane glycoprotein is inserted into the cell membrane and initiates cell-membrane fusion.

On entering the cell, the protease enzyme produces the reverse transcriptase and ribonuclease (RNAse) H enzymes that are responsible for synthesizing single-stranded DNA (ssDNA) molecules and primers necessary to produce the complementary DNA strand. Because reverse transcriptase lacks proofreading machinery, significant base-to-base variability results. The high mutation rate, combined with the high reproductive rate, results in substantial evolution and subsequent resistance to treatment.

Acute infection rapidly increases the viral load and causes a mild-to-moderate viremia. Although viral loads tend to diminish rapidly after acute infection in adults, viral loads decrease more slowly in vertically infected children and may not reach a baseline level until they are aged 4 or 5 years. Although infants possess a high number of antigen-presenting and effector cells compared with the number in adults, their cytokine production, proliferation, and cytotoxicity are reduced.