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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of human immunodeficiency virus (HIV) infection in women of the reproductive age group has been increasing and, with it, vertical transmission of the virus to their infants. It is currently believed that intrauterine transplacental infection of the fetus is the most important mechanism of vertical transmission; thus, a recent focus of investigation has been on the role of the placenta in maternofetal HIV infection. However, the mechanisms by which infectious agents cross the placenta to infect the fetus remain largely unknown. Some lessons of possible relevance to issues related to vertical HIV transmission may be gained by reviewing the experience with other agents that can affect the fetus and newborn. This communication examines current virologic and clinicopathologic features of perinatal HIV infection in light of concepts of placental and fetal infection with other viral agents in an attempt to find a model of vertical HIV transmission.
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PMID:Human immunodeficiency virus and the placenta. Current concepts of vertical transmission in relation to other viral agents. 185 65

2/3 of the reported cases of the acquired immune deficiency syndrome (AIDS) in children have no risk factor except a mother belonging to a group with an increased prevalence of infection with human immunodeficiency virus (HIV). There is evidence of transplacental passage of the virus during early and late gestation, but the incidence of fetal and neonatal infection in newborn babies of seropositive mothers has not yet been determined. This article presents the clinical and serological outcome of 24 babies aged 6 months born to mothers who were drug addicts and positive for HIV antibodies. At 6 months 12 babies were seropositive and 12 seronegative. 1 seropositive baby died of Pneumocystis carinii pneumonia at 4 months, and another was diagnosed as suffering from AIDS related complex at the age of 3 months. All the other babies thrived, the results of their follow up being entirely normal. These 2 cases indicate that early morbidity and mortality are a severe problem, but their incidence seems to be restricted to about 10% of the offspring. Unfortunately, nothing can yet be said about long term morbidity and mortality. Cesarean section does not seem to protect the fetus from infection. These data may be helpful in counselling seropositive women before or in early gestation, as they suggest that the risk of fetal infection and severe postnatal morbidity is high. Unfavorable perinatal outcome, usually associated with drug addiction, was similar in seropositive and seronegative women: a detrimental effect of the virus in this regard was not evident.
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PMID:HIV infection and AIDS in newborn babies of mothers positive for HIV antibody. 310 24

To understand viral and host factors that contribute to transplacental transmission of human immunodeficiency virus, we developed an animal model using pregnant female macaques infected with simian immunodeficiency virus (SIV). Pregnant females were inoculated intravenously during midgestation with either a well-characterized primary isolate of SIV (SIV/DeltaB670) or a combination of SIV/DeltaB670 and the macrophage-tropic molecular clone SIV/17E-Fr. The viral genetic diversity in five infected female macaques and their in utero-infected infants was analyzed. All of the mothers harbored a genetically diverse virus population at parturition, whereas a single genotype from the maternal quasispecies was identified in the infants at birth. Only one of two variants was found in the infants: SIV/17E-Fr (two cases) or a genotype contained within the SIV/DeltaB670 quasispecies (three cases). The macrophage-tropic properties of both transmitted genotypes were suggested by productive replication in primary rhesus macrophage cultures in vitro and the clonal presence in central nervous system tissue of infected monkeys with encephalitis. These observations provide compelling evidence for both genotypic and phenotypic selection in transplacental transmission of SIV and suggest a critical role for macrophages in fetal infection in utero.
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PMID:Genotypic selection of simian immunodeficiency virus in macaque infants infected transplacentally. 749 11

A prospective study of transplacental transmission of human immunodeficiency virus (HIV) showed an increased rate of spontaneous fetal demise in HIV-seropositive mothers: 14 losses in 124 pregnancies. HIV was detected in placental and fetal tissues in 7 of 14 by in situ hybridization. The proportion of fetal infection far exceeded the transmission rate of 13% in liveborn babies. No association was seen between fetal transmission and a maternal history of drug abuse or coinfections; mothers with AIDS more often had fetal loss associated with HIV transmission than did asymptomatic mothers. In affected fetuses, HIV was detected in many tissues and was associated with thymic pathology. This suggests that maternal HIV infection increases the risk for pregnancy loss associated with HIV transmission. The possibility that HIV may be fetotoxic, that thymic dysfunction may interfere with pregnancy progression, or that the intrauterine milieu in HIV-seropositive pregnancies may be unfavorable (or a combination of factors) should be considered.
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PMID:Excess intrauterine fetal demise associated with maternal human immunodeficiency virus infection. 759 2

Counseling for infections during pregnancy has traditionally focused on the clinical and laboratory findings of infection in the mother and the estimated risk of fetal damage associated with possible transmission of infection to the child. Now, with the use of techniques for fetal sampling, it is possible to diagnose infections of the fetus in utero and to correlate that information with the occurrence of fetal damage. The techniques that are available for sampling include amniocentesis, cordocentesis and chorionic villus sampling. The laboratory tests include: a) isolation of the organism in appropriate laboratory systems; b) detection of the DNA or RNA of the organism directly or with amplification with techniques such as PCR; c) detection of the organism by fluorescence or in situ hybridization; and d) identification of IgM or IgA fetal antibody to the organism by ELISA or similar methods. In utero infections can be documented for agents such as rubella, cytomegalovirus, parvovirus, Toxoplasma gondii and human immunodeficiency virus type 1. Further information is needed concerning the sensitivities and specificities of these methods for identifying fetal infection and predicting fetal damage.
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PMID:In utero diagnosis of congenital infections by direct fetal sampling. 803 96

Although the mechanisms for maternal transmission are unknown, approximately half of the infants congenitally infected with the human immunodeficiency virus type 1 (HIV-1) seem to become infected late in gestation or during delivery. Previously, we have developed a rhesus monkey model for congenital infection by injecting cell-free simian immunodeficiency virus (SIV) directly into amniotic fluid. Our results suggested that fetal infection may have occurred via skin or mucous membrane exposure. Mucosal surfaces have also been implicated as a portal of virus entry by a study in which the presence of serosanguinous fluid in neonatal gastric aspirates correlated with an increased rate of HIV-1 transmission. To test whether cell-free virus could transverse intact neonatal mucosal surfaces, we administered SIVmac251 orally to four rhesus monkey neonates within 1 hr following cesarean section delivery. All four neonates developed viremia and were positive by cocultivation and PCR. Seroconversion occurred in three of the four neonates. The SIV dose given was within physiological range as shown by end-point dilution of virus stock and viremic plasma samples of juvenile rhesus monkeys. This primate model for mucosal transmission of cell-free virus features a high infection rate, thus making studies of mucosal immunity and the development of strategies to prevent intrapartum virus transmission possible.
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PMID:Mucosal infection of neonatal rhesus monkeys with cell-free SIV. 806 15

Intraamniotic infection is a common (2-4%) event in labor. The predictors of IAI include preterm labor or rupture of membranes, abnormal vaginal flora (e.g., GBS, sexually transmitted disease, bacterial vaginosis), obstetric manipulations (e.g., vaginal exams, internal fetal monitoring) in the presence of ruptured membranes, and diminished host response (due to smoking, drug abuse, obesity, immunodeficiency states, etc.). Group B Streptococcus and Enterobacteriaceae are the most important organisms associated with the polymicrobial infection. Anaerobes predict post-cesarean section complications. Neonatal pneumonia (2-5%) and early neonatal sepsis (1-4%) are the outcomes of the greatest concern and are caused by group B streptococcal or aerobic gram-negative rod infections. These outcomes are kept to a minimum if maternal antibiotic chemotherapy is started interpartum with agents that are safe, cross the placenta, and are active against GBS and Escherichia coli (e.g., ampicillin plus gentamicin). Anaerobic coverage should be added (clindamycin) if a cesarean section is performed. Antipyretics such as acetaminophen will reduce the hyperthermic stress on the fetus, and persistent fetal tachycardia after antipyretics may indicate fetal infection. Continuous electronic fetal monitoring is appropriate in cases of IAI, and providers should be prepared for neonatal resuscitation, early neonatal intravenous antibiotics, and respiratory support at delivery.
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PMID:Chorioamnionitis and intraamniotic infection. 829 82

The rising prevalence of infection with the human immunodeficiency virus type 1 (HIV-1) in young women will increase the number of infected children worldwide. Because HIV-1 seems to be transmitted mostly intrapartum, fetal infection probably occurs mainly via skin or mucous membrane exposure. A model for this route of fetal infection has been established in primates. After injecting the simian immunodeficiency virus (SIV) into amniotic fluid during late gestation, six of seven rhesus monkeys were born infected. All infected neonates were viable and showed signs of disease, such as low birth weights, lymphadenopathy, and rashes. Cytotoxic T-cell responses to SIV were absent in neonates, but present in mothers. The high fetal infection rate allows studies of lentiviral immunopathogenesis during ontogeny and the development of strategies to prevent maternal HIV-1 transmission.
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PMID:Simian immunodeficiency virus infection via amniotic fluid: a model to study fetal immunopathogenesis and prophylaxis. 843 76

The increase in the number of human immunodeficiency virus-1 (HIV-1)-infected children is a direct consequence of the heterosexual spread of the disease to women and the growing number of HIV-positive i.v. drug users. It is not known how the majority of infants born to HIV-1-infected women escape HIV-1 infection, and, for those infected, the timing of HIV-1 transmission has yet to be determined. In addition, the role of maternal antibodies in the prevention of HIV-1 transmission to the fetus is unclear. We have previously demonstrated a correlation between vertical transmission and the absence of high-affinity/avidity antibodies to a peptide, KRI-HIGPGRAFYT, which corresponds to a region of the primary neutralizing domain of the gp120 V3 loop of HIVMN (MN-PND). The present study examines the correlation between the presence of these high affinity antibodies in women completing a pregnancy or undergoing an elective abortion and the detection of HIV-1 infection in their aborted fetuses. In several instances, transmission occurred despite high-affinity antibodies to the MN-PND. We have, therefore, evaluated the reactivity of sera to different MN-PND variants. In one infant born to a mother with high-affinity/avidity antibodies to KRI-HIGPGRAFYT (classic MN-PND), the infected baby developed antibodies to an MN-PND variant peptide against which his mother did not mount a humoral immune response during pregnancy. This finding indicates that fetal infection with MN-PND escape mutants arising during pregnancy may occur during a period when the mother is serologically negative.
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PMID:Maternofetal transmission of human immunodeficiency virus-1: the role of antibodies to the V3 primary neutralizing domain. 843 79

Recent technological advances have led to the development of several types of invasive procedures in the fetus principally for the diagnosis and management of fetal disorders. The risk of infection to the fetus related to these procedures needs evaluation. Although there are few reports of fetal infection, proper infection control procedures must be observed because the most common consequence of infection is fetal loss. Fetal blood sampling in the presence of chorioamnionitis is a risk factor that warrants prophylactic antibiotics. Conversely, clinical specimens taken from the fetus in the absence of chorioamnionitis are more likely to become contaminated with maternal skin flora, and a positive fetal blood culture is not necessarily significant. There is probably a small but finite risk of transmission of maternal viral infections such as human immunodeficiency virus, hepatitis B and C, cytomegalovirus and herpes simplex during invasive procedures. Obstetric departments undertaking invasive fetal diagnosis and treatment must have an adequate policy for infection control procedures.
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PMID:Risk of fetal infection from invasive procedures. 909 15


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