I. Definition. HIV is an enveloped RNA virus that is a member of the lentivirus subfamily of retroviruses. Infection is most commonly secondary to HIV-1. HIV-2 is rare in the United States but more common in West Africa. HIV results in a broad spectrum of disease, with AIDS representing the most severe end of the clinical spectrum.
II. Incidence. The Joint United Nations Program on HIV/AIDS approximated that 33.2 million people worldwide were infected with HIV-1 at the end of 2007. More than 95% of the total cases reside in developing countries. Every day, > 6800 persons become infected with HIV and >5700 persons die from AIDS, mostly because of inadequate access to HIV prevention and treatment services. An estimated 1200 children become infected with HIV every day, mostly acquiring infection vertically from their mothers. The mother-to-child transmission (MTCT) of HIV-1 has been reduced significantly over the past 10–15 years in developed countries; however, transmission rate in developing countries is still high at ~26%.
III. Pathophysiology. HIV-1 is particularly tropic for CD4+ T cells and cells of monocyte or macrophage lineage. After infection of the cell, viral RNA is uncoated and a double-strand DNA transcript is made. This DNA is transported to the nucleus and integrated into the host genome DNA. There is eventual destruction of both the cellular and humoral arms of the immune system. As well, HIV-1 gene products or cytokines elaborated by infected cells may affect macrophage, B-lymphocyte, and T-lymphocyte function. Hypergammaglobulinemia caused by HIV-induced polyclonal B-cell activation is often detected in early infancy. Disruption of B-cell function results in poor secondary antibody synthesis and response to vaccination. As well, profound defects in cell-mediated immunity occur, allowing a predisposition to opportunistic infections such as fungus, Pneumocystis jiroveci pneumonia (PCP), and chronic diarrhea. The virus can also invade the central nervous system and produce psychosis and brain atrophy.
IV. Risk factors
A.High-risk mother. Any infant born to a high-risk mother is at risk. High-risk mothers include intravenous (IV) drug users, hemophiliacs, spouses of bisexual males, women from areas where the disease is more prevalent in heterosexuals, and spouses of hemophiliacs. Several mechanisms for viral transmission exist, including maternal disease state, fetal exposure to infected maternal body fluids, depressed maternal immune response, and breast-feeding. Maternal plasma HIV RNA level is the best single predictor of MTCT risk. Other risk factors include mode of delivery, duration of rupture of membranes, prematurity and low birthweight, cervicovaginal viral load, low CD4+ cell count, maternal symptomatic HIV disease/AIDS, viral subtype and host genetic factors. MTCT may occur in utero, intrapartum, or postpartum through breast-feeding. Transplacental infection has been proven by evidence of infection in aborted first-trimester fetal tissues as well as isolation of HIV-1 in blood samples obtained with 48 h of birth. Potential routes of infection include mixture of maternal and fetal blood and infection across the placenta when its integrity is compromised (eg, placentitis [syphilitic] and chorioamnionitis).
B. Blood transfusion. Screening of blood donors has reduced but ...
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