• The risk of mother-to-child transmission of HIV ranges from about 15 to 35 percent. 
• The lowest rates are reported in Europe. the highest in Africa. 
• Transmission is influenced by multiple factors. An important determinant may be viral load. 
• The presence of p24 antigenemia has consistently been associated with increased transmission. 
• Other factors associated with increased transmission include low maternal CD4 cell counts. advanced HIV disease and increased levels of beta., microglobulin. 
• Biologic and genetic variation of HIV mav also influence the risk of transmission. e.g., it has been suggested by some that syncytium-inducing virus, which is associated with advance clinical disease, may be more efficiently transmitted than non-syncytium-inducing virus.
•  High levels of maternal neutralizing- antibody have been shown to be associated with reduced transmission in some studies. 
• Other risk factors for mother-to-child transmission include chorioamnionitis and sexually transmitted diseases. 
• Mode of delivery, duration of labor, interval from time of membrane rupture to delivery and events during labor and delivery that can expose the infant to the mother's blood (e.g., episiotomy, severe lacerations) may also be important.

2. How is the virus transmitted from mother to infant?

• There is evidence from examinations of placental and fetal tissues that HIV infection can occur in utero. 
• Indirect evidence suggests that a substantial proportion of infants acquire the infection during the peripartum period. 
• HIV is present in breast milk and infants may also acquire infection through breast feeding.

3. What is known about the pathogenesis of the infection in the fetus infant?

• The HIV infects the CD4+ subset of T lymphocvtes in addition to other cell types. 
• Infection of helper T cells causes abnormalities of lymphocyte function. syncytium formation and cell death. 
• Because the CD4+ lymphocyte plays a key role in many arms of the immune svstem. including B cell function and suppressor T cell function. the resultant helper T cell lymphopenia and lymphocyte dysfunction produce the many immunologic defects that form the basis for the clinical manifestations of AIDS.
• The infection of a cell begins with the attachment of the HIV envelope glycoprotein to the cell’s CD4 molecule, which serves as the HIV receptor.
•  Co-receptors include the chemokine receptors and mediate attachment of monocytotropic (CCR5) and T-lymphocytotropic (CCXCR4) types of HIV. 
• The virus then fuses with the cell membrane, enters the cell, and becomes uncoated within the cytoplasm.
•  After transcription of the viral RNA into DNA by the reverse transcriptase enzyme of the virus, the DNA is circulated, and some of it is integrated into the host cell DNA in latent proviral form.
•  On activation, the proviral DNA is transcribed to RNA; then this RNA is translated so that the HIV proteins are synthesized. 
• The infection is characterized bv high level replication in lymphoid cells and low level replication or even latency in other lymphoid cells or macrophages. 
• Rate of progression is determined by both viral and host factors.

4. what are the abnormalities of the immune system?

• Absolute lymphopenia is common in adults with AIDS but appears to be less common in children. 
• In HIV-infected children, defects in B cell function are usually apparent earlier than those of cell-mediated immunity, and recurrent or serious bacterial infections are the result. 
• Both B cell abnormalities and deficient helper T lymphocyte function contribute to defective humoral immunity. 
• Despite abnormal B cell function, elevated serum immunoglobulin levels are a hallmark of HIV infection in children. 
• Other abnormalities seen in children with HIV infection include diminished interferon and interleukin-2 production as well as abnormal natural killer cell activity.

5. How is the viral infection detected in the infant?

• The diagnosis of HIV infection in infants born to HIV-infected mothers is made after the detection of the virus in culture, the HIV genome by the polymerase chain reaction, the viral antigen, or the persistence of HIV antibody beyond the age of 18 months. 
• The sensitivity of viral culture and PCR is only about 40% at birth. However, after one month, the sensitivity of viral culture is about 90%, and the sensitivity of PCR is probably even higher. 
• The presence of HIV antibody before 18 months of age may represent HIV infection in the infant or just passive transfer of maternal antibody.

6. Is prevention from mother to infant possible?

• In a randomized. placebo-controlled trial, investigators found that in pregnant women with CD4 counts greater than 200 per cubic millimeter and no previous antiretroviral drug treatment, a regimen of antepartum and intrapartum zidovudine for the mother and 6 weeks of zidovudine for the newborn reduced the risk of transmission by about two thirds from 25.5% to 8.3%. 
• Current trials employing combination antiretroviral therapy in pregnant women and their infants are ongoing. 
• Other approaches to reducing the transmission HIV from mother to child include avoidance of breast feeding and reduction in peripartum exposure (eg, avoidance of intrapartum invasive procedures, vaginal disinfection, aggressive treatment of sexually transmitted diseases. ??cesarean section).

7. What are the long-term consequences of the infection in the infant?

• HIV-related symptoms and signs are rarely present at birth but develop over subsequent months or years. 
• In about a quarter of infected children, HIV infection progresses rapidly to AIDS or death in the first year. 
• In the remainder, it progresses more slowly, with some children surviving beyond childhood years. 
• The proportion of infected individuals who have rapid progression of disease is higher in children than adults. 
• This may be explained by the immaturity of the immune system at the time of HIV acquisition, the infecting dose of virus, and the route of infection.
• Pneumocystis carinii pneumonia has a peak incidence between 3 and 6 months of age and is associated with a high mortality rate. 
• Neurologic manifestations are common in children with rapidly progressive disease, typically with manifestations developing in the second six months of life. 
• Recurrent bacterial infections and lymphocytic intestitial pneumonitis are important manifestations in children. 
• Problems with growth and pubertal development are observed among children entering adolescence.