Acquired immunodeficiency syndrome (AIDS) was first described in 1981, and it is currently one of the worst global health pandemics in recorded history. Worldwide, it was estimated in 2012 that there were 35.3 million infected persons with HIV/AIDS; 2.3 million new cases of HIV infection; and 1.6 million HIV-related deaths (UNAIDS, 2013). In the United States through 2011, the Centers for Disease Control and Prevention (2013a) estimated that there were more than 1.1 million infected individuals and more than 636,000 deaths (Centers for Disease Control and Prevention, 2013a). In 2010, women accounted for 20 percent of all HIV/AIDS cases among adults and adolescents, most of which resulted from heterosexual contact. Comparing 2008 with 2011, HIV incidence decreased in women, primarily black/African American women and women acquiring HIV through heterosexual contact.
The estimated number of perinatally acquired AIDS cases has decreased dramatically during the past two decades (Fig. 65-8). This is predominantly due to the implementation of prenatal HIV testing and antiviral therapy given to the pregnant woman and then to her neonate (De Cock, 2012). In addition, highly active antiretroviral therapy (HAART) has led to an increasing number of people living with chronic HIV infection and thus the associated comorbidities also affecting pregnancy (Fenton, 2007).
Causative agents of AIDS are RNA retroviruses termed human immunodeficiency viruses, HIV-1 and HIV-2. Most cases worldwide are caused by HIV-1 infection. Transmission is similar to hepatitis B virus, and sexual intercourse is the major mode. The virus also is transmitted by blood or blood-contaminated products, and infected mothers may infect their fetuses perinatally or by their breast milk. The primary determinant of HIV-1 transmission is the plasma HIV-1 viral load.
The common denominator of clinical illness with AIDS is profound immunodeficiency that gives rise to various opportunistic infections and neoplasms. Sexual transmission occurs when mucosal dendritic cells bind to the HIV envelope glycoprotein gp120. These dendritic cells then present the viral particle to thymus-derived lymphocytes, that is, T lymphocytes. These lymphocytes are defined phenotypically by the cluster of differentiation 4 (CD4) glycoprotein surface antigens. The CD4 site serves as a receptor for the virus. Coreceptors are necessary for viral entry into the cell, and two chemokine receptors—CCR5 and CXCR4—are the most frequently identified (Fauci, 2012; Sheffield, 2007). The CCR5 coreceptor is found on the cell surface of CD4 positive (CD4+) cells in high progesterone states such as pregnancy, possibly aiding viral entry (Sheffield, 2009).
After initial infection, the level of viremia usually decreases to a set point, and patients with the highest viral burden at this time progress more rapidly to AIDS and death (Fauci, 2007, 2012). And as shown in Figure 65-9, viral burden and neonatal infection incidence are directly related. Over time, the number of T cells drops insidiously and progressively, resulting eventually in profound immunosuppression. Although it is thought that pregnancy has minimal effects on CD4+ T-cell counts and HIV RNA levels, the latter are often higher 6 months postpartum than during pregnancy. Higher levels of inflammatory cytokines and a decrease in regulatory T cells in late pregnancy may contribute to maternal and fetal morbidity (Richardson, 2011).
Incidence of perinatal human immunodeficiency virus (HIV) infection plotted against plasma HIV-1 RNA levels in 1542 neonates born to mothers in the Women and Infants Transmission Study. (Data from Cooper, 2002.)
The incubation period from exposure to clinical disease is days to weeks, and the average is 3 to 6 weeks. Acute HIV infection is similar to many other viral syndromes and usually lasts less than 10 days. Common symptoms include fever and night sweats, fatigue, rash, headache, lymphadenopathy, pharyngitis, myalgias, arthralgias, nausea, vomiting, and diarrhea. After symptoms abate, the set point of chronic viremia is established. The progression from asymptomatic viremia to AIDS has a median time of approximately 10 years (Fauci, 2008). Route of infection, the pathogenicity of the infecting viral strain, the initial viral inoculum, and the immunological status of the host all affect the rapidity of progression.
Several clinical and laboratory manifestations will herald disease progression. Generalized lymphadenopathy, oral hairy leukoplakia, aphthous ulcers, and thrombocytopenia are common. A number of opportunistic infections associated with AIDS include esophageal or pulmonary candidiasis; persistent herpes simplex or zoster lesions; condyloma acuminata; pulmonary tuberculosis; cytomegaloviral pneumonia, retinitis, or gastrointestinal disease; molluscum contagiosum; Pneumocystis jiroveci pneumonia; toxoplasmosis; and others. Neurological disease is common, and approximately half of patients have central nervous system symptoms. A CD4+ count < 200/mm3 is also considered definitive for the diagnosis of AIDS.
There are unique gynecological issues for women with HIV, such as menstrual abnormalities, contraceptive needs, and genital neoplasia, that are discussed in Williams Gynecology, 2nd edition (Werner, 2012). Some of these as well as other STIs may persist into pregnancy (Cejtin, 2003; Stuart, 2005). Repeated pregnancy has no significant effect on the clinical or immunological course of viral infection (Minkoff, 2003).
The Centers for Disease Control and Prevention (2006, 2010a), The American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2011), and the United States Preventive Services Task Force (2012) recommend prenatal HIV screening using an opt-out approach. This means that the woman is notified that HIV testing is included in a comprehensive set of antenatal tests, but that testing may be declined. Women are given information regarding HIV but are not required to sign a specific consent. Through the use of such opt-out strategies, HIV testing rates have increased. Each provider should be aware of specific state laws concerning screening.
In areas in which the incidence of HIV or AIDS is 1 per 1000 person-years or greater, or in women at high risk for acquiring HIV during pregnancy, repeat testing in the third trimester is recommended (American College of Obstetricians and Gynecologists, 2011). High-risk factors include injection drug use, prostitution, a suspected or known HIV-infected sexual partner, multiple sexual partners, or a diagnosis of another sexually transmitted disease. Several states also recommend or require HIV testing at delivery.
Screening is performed using an enzyme-linked immunoassay with a sensitivity > 99.5 percent. A positive test is confirmed with either a Western blot or immunofluorescence assay (IFA), both of which have high specificity. According to the Centers for Disease Control and Prevention (2001), antibody can be detected in most patients within 1 month of infection, and thus, antibody serotesting may not exclude early infection. For acute primary HIV infection, identification of viral p24 core antigen or viral RNA or DNA is possible. False-positive confirmatory results are rare (Centers for Disease Control and Prevention, 2010b).
Women with limited prenatal care or with undocumented HIV status at delivery should have a “rapid” HIV test performed. These tests can detect HIV antibody in 60 minutes or less and have sensitivities and specificities comparable with those of conventional ELISAs (Chetty, 2012). A negative rapid test result does not need to be confirmed. However, in a woman exposed to HIV within the last 3 months, repeat testing is recommended. A positive rapid test result should be confirmed with a Western blot or IFA test. As shown in Table 65-6, peripartum and neonatal interventions to reduce perinatal transmission are based on the initial rapid testing results, and this can be discontinued if the confirmatory test is negative (American College of Obstetricians and Gynecologists, 2011; Centers for Disease Control and Prevention, 2010b). A detailed list of the rapid HIV tests currently available in the United States can be found at http://www.cdc.gov/hiv/policies/index.html (Centers for Disease Control and Prevention, 2007). The Mother-Infant Rapid Intervention at Delivery (MIRIAD) multicenter study indicated that rapid HIV testing can be used to identify infected women so that peripartum antiretroviral prophylaxis can be administered to mother and infant (Bulterys, 2004).
TABLE 65-6Strategy for Rapid Human Immunodeficiency Virus (HIV) Testing of Pregnant Women in Labor ||Download (.pdf) TABLE 65-6 Strategy for Rapid Human Immunodeficiency Virus (HIV) Testing of Pregnant Women in Labor
|If the rapid HIV test result in labor and delivery is positive, the obstetrical provider should take the following steps: |
Tell the woman she may have HIV infection and that her neonate also may be exposed
Explain that the rapid test result is preliminary and that false-positive results are possible
Assure the woman that a second test is being performed to confirm the positive rapid test result
To reduce the risk of transmission to the infant, immediate initiation of antiretroviral prophylaxis should be recommended without waiting for the results of the confirmatory test
Once the woman gives birth, discontinue maternal antiretroviral therapy pending receipt of confirmatory test results
Tell the women that she should postpone breast feeding until the confirmatory result is available because she should not breast feed if she is infected with HIV
Inform pediatric care providers (depending on state requirements) of positive maternal test results so that they may institute the appropriate neonatal prophylaxis
Maternal and Perinatal Transmission
Transplacental HIV transmission can occur early, and the virus has even been identified in specimens from elective abortion (Lewis, 1990). In most cases, however, mother-to-child transmission at the time of delivery is the most common cause of pediatric HIV infections. Between 15 and 40 percent of neonates born to non–breast-feeding, untreated, HIV-infected mothers are infected. Kourtis and colleagues (2001) have proposed a model for estimation of the temporal distribution of vertical transmission. They estimate that 20 percent of transmission occurs before 36 weeks’ gestation, 50 percent in the days before delivery, and 30 percent intrapartum. Transmission rates for breast feeding may be as high as 30 to 40 percent and are associated with systemic HIV viral burden (Kourtis, 2006, 2007a; Slyker, 2012). Vertical transmission is more common with preterm births, especially with prolonged membrane rupture. Analyzing data from the Perinatal AIDS Collaborative Transmission Study, Kuhn and coworkers (1999) reported a nearly fourfold increased risk with preterm delivery. Although an increased risk of perinatal transmission has been associated with membrane rupture in the past, recent analyses in the setting of combination antiviral therapy have not found this to be a risk factor with an HIV viral load < 1000 copies/mL (Cotter, 2012).
In nonpregnant individuals, there is an association between concomitant STIs and horizontal HIV transmission. There is also evidence that vertical perinatal transmission may be increased with STIs (Schulte, 2001; Watts, 2012). Women with maternal HSV-2 antibody have a significant 50-percent increased risk of intrapartum HIV-1 maternal-to-child transmission (Cowan, 2008). They attributed up to 25 percent of vertical transmission to maternal HSV-2 co-infection. Elevated cytokine and chemokine levels in the placenta, reflecting inflammation, are associated with in utero transmission (Kumar, 2012). A recent Cochrane analysis, however, has failed to show that sexually transmitted infection control is an effective HIV prevention strategy (Ng, 2011).
Perinatal HIV transmission is most accurately correlated with maternal plasma HIV RNA burden (Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal Transmission, 2012; Watts, 2002). As shown in Figure 65-9, cohort neonatal infection was 1 percent with < 400 copies/mL, and it was > 30 percent when maternal viral RNA levels were > 100,000 copies/mL. Transmission of HIV infection, however, has been observed at all HIV RNA levels, including those that were nondetectable by current assays. This may be attributed to discordance between the viral load in plasma and that in the genital secretions. Because of these findings, the viral load should not be used to determine whether to initiate antiretroviral therapy in pregnancy.
Effective contraception should be discussed if pregnancy is undesired. Certain antiviral medications decrease hormonal contraception efficacy and are discussed in Chapter 38 (Method-Specific Effects). Recommendations are also available at http://AIDSinfo.nih.gov and are updated frequently as new data become available. Counseling also includes education for decreasing high-risk sexual behaviors to prevent transmission and to decrease the acquisition of other sexually transmitted diseases. Currently used antiretroviral medications are reviewed to avoid those with high teratogenic potential should the woman become pregnant. A specific example is efavirenz, which has significant teratogenic effects on primate fetuses (Panel on Antiretroviral Guidelines for Adults and Adolescents, 2013). Preference should also include those that decrease HIV RNA viral load effectively before pregnancy.
Management During Pregnancy
These women need special attention and are seen in consultation by physicians with special interest in this field. At Parkland Hospital, the initial assessment of an HIV-infected pregnant woman includes:
Standard prenatal laboratory surveys that include serum creatinine, hemogram, and bacteriuria screening (Chap. 9, Typical Components of Routine Prenatal Care)
Plasma HIV RNA quantification—“viral load,” CD4+ T-lymphocyte count, and antiretroviral resistance testing
Serum hepatic aminotransferase levels
HSV-1 and -2, cytomegalovirus, toxoplasmosis, and hepatitis C serology screening
Baseline chest radiograph
Tuberculosis skin testing—purified protein derivative (PPD) or interferon-gamma release assay
Evaluation of need for pneumococcal, hepatitis B, hepatitis A, Tdap, and influenza vaccines
Sonographic evaluation to establish gestational age.
Treatment is recommended for all HIV-infected pregnant women. This may be a departure for those not receiving treatment when nonpregnant because they did not meet certain criteria. Treatment reduces the risk of perinatal transmission regardless of CD4+ T-cell count or HIV RNA level. Antiretroviral therapy is complicated, and pregnancy only adds to the complexity. In general, HAART is begun if the woman is not already receiving one of the regimens. Antiretroviral agents are grouped into several classes and used to design antiretroviral regimens (Table 65-7). The 2012 Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal Transmission classify each agent into five use categories: preferred, alternative, use in special circumstances, not recommended, and insufficient data to recommend use. The woman is counseled regarding risks and benefits of antiretroviral agents to make an informed decision as to her treatment regimen. Regardless of what regimen is begun, adherence is important because the risk of viral drug resistance is lessened.
TABLE 65-7Classes of Antiretroviral Drugs
The Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal Transmission (2012) has issued guidelines that detail management of different scenarios during pregnancy (Table 65-8). Women already taking HAART at pregnancy onset are encouraged to continue the regimen if there is adequate viral suppression. The neural-tube defect risk associated with efavirenz is restricted to the first 6 weeks of pregnancy. Thus, efavirenz can be continued if the woman presents after this time and if adequate virological suppression is documented. Until recently, addition of zidovudine to all regimens was recommended. Currently, however, in women with adequate viremia suppression with a regimen not containing zidovudine, continuation of the current regimen is appropriate. Zidovudine is given intravenously during labor and delivery to women with an HIV RNA viral load > 400 copies/mL or who have an unknown viral load near delivery (Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal Transmission, 2012). A 2 mg/kg load is infused over 1 hour followed by zidovudine 1 mg/kg/hr until delivery.
TABLE 65-8Recommendations for Antiviral Drug Use During Pregnancy ||Download (.pdf) TABLE 65-8 Recommendations for Antiviral Drug Use During Pregnancy
|Clinical Scenario ||Recommendations |
|HIV-infected woman taking antiretroviral therapy who becomes pregnant ||Continue current medication if viral suppression adequate and patient tolerating |
If virus detectable, order HIV antiretroviral drug-resistance testing
If first trimester, continue medications; if stopped, stop all medications and then reinitiate in the second trimester
Start IV ZDV in labor if HIV RNA level > 400 copies/mL or unknown near delivery
|HIV-infected woman who is antiretroviral naïve ||Order HIV antiretroviral drug-resistance testing |
– Avoid efavirenz in the early first trimester
– Use one or more NRTIs—ZDV, lamivudine, emtricitabine, tenofovir, or abacavir—if feasible
– Avoid nevirapine in women with a CD4+ count > 250 cells/mm3
HAART should be initiated as early as possible for maternal indications; if high CD4 T-lymphocyte count and low HIV RNA level, can consider delaying initiation of HAART until the second trimester
Start IV ZDV in labor if HIV RNA level > 400 copies/mL or unknown near delivery
|HIV-infected woman previously taking antiretroviral medications but not on medications currently ||Order HIV antiretroviral drug-resistance testing |
Initiate HAART with regimen based on prior therapy history and resistance testing
Avoid efavirenz in the early first trimester
Use one or more NRTIs—ZDV, lamivudine, emtricitabine, tenofovir, or abacavir—if feasible
Avoid nevirapine in women with a CD4+ count > 250 cells/mm3
Start IV ZDV in labor if HIV RNA level > 400 copies/mL or unknown near delivery
|HIV-infected woman on no antiretroviral medication who presents in labor ||Order initial HIV laboratory assessment (Management During Pregnancy) |
Start IV ZDV during labor—2 mg/kg IV load over 1 hour, then 1 mg/kg/hr until delivery
Women who have never received antiretroviral therapy—antiretroviral naïve—fall into two categories. First, women who meet the criteria for antiretroviral therapy initiation in nonpregnant adults are given HAART regardless of trimester. Because of an increased risk of hepatotoxicity, nevirapine is reserved for women with a CD4+ cell count < 250 cells/mm3. In general, the starting HAART regimen is two nucleoside reverse transcriptase inhibitors (NRTIs) plus a non-nucleoside reverse transcriptase inhibitor (NNRTI) or protease inhibitor(s). At Parkland Hospital as of 2014, our standard regimen in treatment-naïve women is lopinavir/ritonavir—formulated as Kaletra—plus zidovudine/lamivudine—formulated as Combivir. The lopinavir/ritonavir regimen should be increased in the late second and third trimester. Atazanavir, another protease inhibitor, is also now listed as a preferred agent and can be used in place of lopinavir/ritonavir. If used, it is combined with low-dose ritonavir boosting.
The second category contains treatment-naïve HIV-infected pregnant women who do not meet nonpregnant adult indications for antiretroviral therapy. These women are counseled regarding the benefits of initiating therapy to prevent perinatal viral transmission. Because of potential teratogenic effects, women may delay therapy until the second trimester. That said, however, earlier initiation may be more effective in reducing perinatal transmission (Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal Transmission, 2012; Read, 2012).
Women who have previously received antiretroviral therapy but are currently not taking medications should undergo HIV resistance testing because antiretroviral use increases their risk of drug resistance. Regimens may then be tailored based on prior medication use and response as well as current resistance patterns. The final group includes women who present in labor and who are taking no medications. These women are given intravenous zidovudine intrapartum (see Table 65-8). The National Perinatal HIV Hotline (1–888–448–8765) is a federally funded service that provides free consultation to providers.
CD4+ T-lymphocyte count, HIV RNA viral load measurement, complete blood count, and liver function tests are done 4 weeks after beginning or changing therapy to assess response and exclude toxicity. Thereafter, HIV RNA viral loads are measured monthly until RNA levels are undetectable. CD4 T-lymphocyte and HIV RNA levels can then be measured every trimester. If the HIV RNA viral load increases or does not decrease appropriately, then medication compliance and antiretroviral drug resistance are assessed. Poor adherence to therapy is a significant problem in pregnancy.
Although there was an association of early studies with glucose intolerance and protease inhibitor use, this has not been corroborated (Hitti, 2007; Tang, 2006). Standard serum glucose screening should be performed at 24 to 28 weeks unless indicated earlier. In addition, careful surveillance is important for interactions between antiretroviral drugs as well as therapies for opportunistic infection, hepatitis B and C, and tuberculosis (Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal Transmission, 2012; Piscitelli, 2001).
Complications of HIV Infection
Management of some HIV complications may be altered by pregnancy. If the CD4+ T-cell count is < 200/mm3, primary prophylaxis for Pneumocystis jiroveci (formerly P carinii) pneumonia is recommended with sulfamethoxazole-trimethoprim or dapsone. Pneumonitis is treated with oral or IV sulfamethoxazole-trimethoprim or dapsone-trimethoprim. Other symptomatic opportunistic infections that may develop are from latent or newly acquired toxoplasmosis, herpes virus, mycobacteria, and candida. The National Institutes of Health, Centers for Disease Control and Prevention, and Infectious Diseases Society of America (2013) have published guidelines for prevention and treatment of opportunistic infections. Maternal HIV infection has also been associated with fetal-growth restriction, preeclampsia, and preterm membrane rupture (Ndirangu, 2012; Rollins, 2007; Suy, 2006).
Even with treatment, the incidence of perinatal complications in HIV-infected women is increased, although the newer drug regimens may diminish these rates. Multiple studies reviewed in the 2012 Perinatal Treatment Guidelines address the association of antiretroviral medications with preterm delivery. Most of those have shown a small but significantly increased risk. Kourtis and colleagues (2007b) performed a metaanalysis of 14 European and U.S. studies and found no overall greater risk for preterm delivery. They did find, however, that women taking regimens that included a protease inhibitor had a small increased risk—1.3-fold—that was nevertheless significant. Antiretroviral medication use in the second half of pregnancy was shown by Lopez and associates (2012) to increase iatrogenic preterm birth but did not affect spontaneous preterm birth rates. This slightly increased frequency of preterm birth clearly is outweighed by the benefits of decreasing perinatal HIV transmission.
At least two follow-up studies of children from the Pediatric AIDS Clinical Trial Group (PACTG) 076 Study found no adverse effects at 18 months and up to a mean of 5.6 years after zidovudine exposure (Culnane, 1999; Sperling, 1998). Prenatal exposure to HAART may increase the risk for neonatal neutropenia and anemia, although no long-term hematological or hepatic toxicities have been documented (Bae, 2008; Dryden-Peterson, 2011). Preliminary data also show a possible effect on infant mitochondrial DNA proliferation and/or expression with maternal antiretroviral drug treatment (Cote, 2008; Hernandez, 2012; Jitratkosol, 2012). For these reasons, long-term follow-up is recommended for all infants exposed in utero to antiviral medications.
Prenatal HIV Transmission
Maternal HAART treatment along with intrapartum zidovudine prophylaxis has dramatically reduced the perinatal HIV transmission risk from approximately 25 percent to 2 percent or less. HAART during pregnancy was reported to be associated with a decreased incidence of placental villitis, which may partially account for the lower HIV transmission rate in treated women (Stewart, 2014a). Optimal management of labor is uncertain, but if labor is progressing with intact membranes, artificial rupture and invasive fetal monitoring are avoided. Labor augmentation is used when needed to shorten the interval to delivery to further decrease the transmission risk. Operative delivery with forceps or vacuum extractor is avoided if possible. Postpartum hemorrhage is managed with oxytocin and prostaglandin analogues. Methergine and other ergot alkaloids adversely interact with reverse transcriptase and protease inhibitors to cause severe vasoconstriction.
Cesarean delivery has been recommended to decrease HIV prenatal transmission. An earlier metaanalysis of 15 prospective cohort studies by the International Perinatal HIV Group (1999) included 8533 mother-neonate pairs. Vertical HIV transmission was shown to be reduced by about half when cesarean was compared with vaginal delivery. When antiretroviral therapy was given in the prenatal, intrapartum, and neonatal periods along with cesarean delivery, the likelihood of neonatal transmission was reduced by 87 percent compared with vaginal delivery and without antiretroviral therapy. The European Mode of Delivery Collaboration (1999) has reported similar findings.
Based on these observations, the American College of Obstetricians and Gynecologists (2010b) concluded that scheduled cesarean delivery should be discussed and recommended for HIV-infected women whose HIV-1 RNA load exceeds 1000 copies/mL. Scheduled delivery is recommended at 38 weeks’ gestation in these women. Although data are insufficient to estimate such benefits for women whose HIV RNA levels are < 1000 copies/mL, it is unlikely that scheduled cesarean delivery would confer additional risk reduction if the woman has been taking antiviral therapy (Jamieson, 2007; Read, 2005). If cesarean delivery is performed for obstetrical indications, it should be performed at 39 weeks with standard perioperative antimicrobials for prophylaxis. HIV-infected women undergoing a scheduled cesarean delivery should be given IV zidovudine as a loading dose followed by 2 more hours of continuous maintenance therapy—a total of 3 hours of infused zidovudine.
Vertical transmission is increased by breast feeding, and it generally is not recommended for HIV-positive women in the United States (Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal Transmission, 2012; Read, 2003). The probability of HIV transmission per liter of breast milk ingested is estimated to be similar in magnitude to heterosexual transmission with unsafe sex in adults (Richardson, 2003). As with other exposures, risk is related to the maternal HIV RNA level, HIV disease status, breast health, and duration of breast feeding (De Cock, 2000; John-Stewart, 2004). Most transmission occurs in the first 6 months, and as many as two thirds of infections in breast-fed infants are from breast milk. In the Petra Study Team (2002) from Africa, the prophylactic benefits of short-course perinatal antiviral regimens were diminished considerably by 18 months of age due to breast feeding. The World Health Organization (2010) has recommended exclusive breast feeding the first 6 months of life for infants of women living in developing countries in which infectious diseases and malnutrition are the primary causes of infant deaths. Breast feeding can be continued for 12 months until a nutritionally adequate diet is available.
Many otherwise healthy women with normal CD4+ T-cell counts and low HIV RNA levels may discontinue treatment after delivery and be closely monitored according to adult guidelines. The exception is the woman who plans another pregnancy in the near future. Stewart and colleagues (2014b) showed that interpregnancy viral load suppression is associated with less vertical transmission in a subsequent pregnancy. Psychosocial support is essential during this time, especially while awaiting diagnostic testing for pediatric infection. Contraceptive needs are complex and also may entail condoms in discordantly infected couples. As discussed in Chapter 38 (Method-Specific Effects), antiretroviral drugs may affect oral contraceptive hormone levels and possibly of injectable agents (Stuart, 2012). Intrauterine devices may be an acceptable choice in some women with normal immunocompetence and a low risk for STIs. The Centers for Disease Control and Prevention has recently revised the recommendations for the use of hormonal contraception among women at high risk for HIV infection or infected with HIV (Tepper, 2012). It reaffirmed prior recommendations that hormonal contraception use is safe for these women and that condom use should be encouraged regardless of contraceptive method.