Human Immunodeficiency Virus Infection
QUICK LOOK AT THE CHAPTER AHEAD
Acquired immunodeficiency syndrome (AIDS) is a chronic progressive disease affecting multiple organs. AIDS is caused by a viral infection with the human immunodeficiency virus (HIV) that affects the helper T lymphocytes, monocytes, and macrophages. As the virus proliferates the immune system begins to fail. HIV replicates by invading T cells and other immune system cells, thus weakening the system. Since it was first identified in 1981, HIV has reached pandemic proportions. This chapter explores the impact of HIV infection on childhood and adolescence.
Currently, over 3 million children worldwide are infected with HIV. In the United States African-American and Latino children have higher rates of infection and death from this disease than children from other ethnic groups. HIV infection is a leading cause of death in adolescents and young adults aged 13 to 24 years. Approximately half of all new HIV cases occur in adolescents and young adults mainly due to unsafe sexual practices and intravenous drug use, although adolescents and young adults do not generally identify these activities as high risk.
The signs of early HIV infection may be nonspecific in children, yet the disease often progresses more rapidly in infants and young children than it does in adults.
Children who are infected during perinatal development have an average life span of 7 to 15 years. HIV infection is suspected in high-risk children if they exhibit failure to thrive, developmental delays, and/or have frequent bacterial infections and chronic encephalopathy.
Approximately 91% of pediatric HIV transmissions occur from mother to child (vertical transmission). Virus transmission can occur through the placenta, through exposure to maternal blood and vaginal secretions during the birth process, or through breast milk. The risk of HIV infection passing from mother to infant is greatest if the mother’s viral load is above 1,000 copies/mL and CD4 count is low and if there was a long period of time from rupture of the membranes to delivery. When the mother receives zidovudine and other antiretroviral therapies during pregnancy and delivery and when newborns are placed on antiretroviral therapy during the first 6 weeks of life, the risk of HIV infection in the infant is reduced. From 1992 to 2001 maternal and newborn treatment with antiretrovirals reduced perinatal HIV transmission by 83%. Newborns of HIV-infected mothers who did not have antiviral therapy during pregnancy and childbirth had a 15-30% chance of becoming infected, whereas infants born to HIV-infected mothers who were on antiretroviral therapy had only a 1-8% chance of becoming infected.
At birth, 30% of HIV-positive newborns infected while in utero have detectable levels of HIV antibodies. If the infection was acquired during the birth process, the newborn will not test positive for the infection until they are 2 to 4 weeks of age. Uninfected infants have maternal
HIV serum antibodies present for up to 18 months before seroconverting to a negative antibody titer. Blood transfusions, sexual abuse, sharing contaminated needles, and unsafe sexual practices are modes of HIV transmission (termed horizontal transmission) for children, adolescents, and young adults. Counseling concerning HIV transmission paths and diagnostic testing is vital for adolescents and young adults who engage in high-risk behavior.
HIV serum antibodies present for up to 18 months before seroconverting to a negative antibody titer. Blood transfusions, sexual abuse, sharing contaminated needles, and unsafe sexual practices are modes of HIV transmission (termed horizontal transmission) for children, adolescents, and young adults. Counseling concerning HIV transmission paths and diagnostic testing is vital for adolescents and young adults who engage in high-risk behavior.
Although HIV infects all age groups, children and adults are affected somewhat differently. HIV progresses more rapidly in infants and young children than in adults. Infants who do not receive antiretroviral treatment rapidly progress from an HIV-positive status to AIDS within a year and most die by age 2. This rapid progression may occur because of the high viral load passed from mother to infant. Opportunistic infections occur early and frequently in the course of the disease in children. Bacterial infections, lymphoid interstitial pneumonitis, and Pneumocystis carinii pneumonia may begin when the infant is only 3 months old. Because of the danger of developing P. carinii pneumonia, all infants born to HIV-infected mothers should receive Bactrim as a prophylaxis measure beginning at 4 to 6 weeks of age.
PATHOPHYSIOLOGY
Two major types of the virus account for most HIV infections: HIV-1 is found in most areas of the world and HIV-2 is found primarily in West African nations.
As a retrovirus HIV carries its genetic code for reproduction in its ribonucleic acid (RNA). Once inside the CD4 cell the virus uses an enzyme called reverse transcriptase to convert its viral RNA to deoxyribonucleic acid (DNA). The viral DNA is then integrated into the CD4 cell’s DNA. The virus replicates inside the CD4 cell and buds from the cell surface destroy the CD4 cell membrane, releasing millions of viral copies into the bloodstream.
The plasma viral load, or number of viral particles per millimeter of blood, is an indicator of clinical progression of the disease. A viral load below 10,000 copies/mm signals control of the disease and a low
probability of disease progression. In contrast, a viral load above 100,000 copies/mm signals a poor prognosis and a high likelihood that the disease will progress rapidly. The aim of antiviral therapy is to reduce the viral load to a level at which the body’s immune system can keep the virus in check. Treatment failure is indicated by a rising viral load even in the absence of symptoms.
probability of disease progression. In contrast, a viral load above 100,000 copies/mm signals a poor prognosis and a high likelihood that the disease will progress rapidly. The aim of antiviral therapy is to reduce the viral load to a level at which the body’s immune system can keep the virus in check. Treatment failure is indicated by a rising viral load even in the absence of symptoms.
In the acute stage of the disease process the infected child may be asymptomatic, except for short-lived (2 weeks or less), mild, flu-like symptoms. During the asymptomatic phase of the infection, which may last a few weeks or years depending on the strength of the child’s immune system and the amount of virus transmitted during infection, the body’s T cells are numerous enough to keep the virus in control. The virus can be transmitted to others even if no symptoms are present. During the persistent generalized lymphadenopathy stage, the child presents with several enlarged lymph nodes. Eventually, the number of viral cells will greatly outnumber healthy T cells, resulting in a weakened immune system and the development of opportunistic infections, neurological disease, and neoplasms characteristic of AIDS. Table 34-1 gives the Centers for Disease Control and Prevention classification system for disease progression.