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

Physicians in the field of reproductive health care have a special interest in reducing the incidence of human immunodeficiency virus (HIV) infection in women and their offspring. The majority of women with acquired immunodeficiency syndrome (AIDS) acquired infection through needle sharing. Sexual transmission of HIV appears to be less effective than transmission of other sexually transmitted diseases. The risk of male-to-female transmission from an infected partner has been estimated at 7-21%. The risk of perinatal transmission from the infected mother to her infant is far higher, however--at least 65%. There is also evidence that the immunosuppression of pregnancy may accelerate progression to AIDS in asymptomatic HIV carriers. In the absence of a vaccine or effective treatment, prevention of AIDS requires education about safe behaviors. A sizable decrease in the rate of transmission of HIV could occur if persons considered whether their partner might be infected before initiating sexual contact. Prevention of pediatric AIDS depends on the prevention of infection in women and the prevention of transmission from infected women. Women infected with HIV should be advised to avoid pregnancy and given highest priority for family planning services. Since many infected women are asymptomatic, HIV antibody testing is the only reliable way to determine whether a woman is actually infected. Such testing, however, should be limited to women believed at risk of HIV infection. Prenatal testing, if done early, can allow more options in the management of pregnancy, yet studies have found that women with positive HIV antibody tests do not elect to terminate their pregnancies at a higher rate than women whose test results are negative.
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PMID:The challenge of human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) in women and children. 328 Mar 48

Since its first report in 1981, acquired immunodeficiency syndrome (AIDS) has attracted great interest among clinicians. Pediatric cases of AIDS were reported only two years later. Recently a review of the literature revealed about 300 pediatric patients with AIDS who are now tabulated separately by the Centers for Disease Control of Atlanta. The classification of the pediatric AIDS is based on epidemiologic, immunologic and virologic data. Subjects at risk include infants born to intravenous drug-addicted mothers and infants who have received blood transfusions or blood products. The diagnosis of pediatric AIDS may be established in a patient who has a polyclonal hypergammaglobulinemia and T-cell immunodeficiency associated with antibody to human immunodeficiency virus (HIV) or isolation of retrovirus.
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PMID:[AIDS in childhood]. 332 Sep 90

Pathologic features of the arteries of different organs (heart, lungs, kidneys, spleen, intestine, brain) seen at autopsy in 6 children with acquired immune deficiency syndrome (AIDS) are described. Small and medium-sized arteries, which were the most commonly involved, showed intimal fibrosis with fragmentation of elastic tissue, fibrosis and calcification of media with variable luminal narrowing, and a vasculitis or perivasculitis that was seen only in the brain in association with AIDS encephalopathy. In 1 case aneurysms of the right coronary artery with thrombosis and myocardial infarction were seen. Vascular inflammation, seen only in the brain, may be related to the agent associated with AIDS encephalopathy. The fibrocalcific arterial lesions most closely resemble idiopathic arterial calcification of infancy, but because of differences in age incidence, clinicopathologic and immunologic features, and the size and distribution of the involved arteries, the arterial lesions of pediatric AIDS appear to constitute a distinctive arteriopathy. Infection, secondary to immunodeficiency and resulting in increased exposure to endogenous and exogenous elastases, may be the pathogenesis. Luminal narrowing caused by arterial lesions may play a contributory role in the pathogenesis of the atrophy, cell depletion, scarring, and necrosis or infarction found in organs of children with AIDS. Pediatricians should be alerted to the possibility of arterial involvement in pediatrics AIDS.
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PMID:Arteriopathy in children with acquired immune deficiency syndrome. 368 8

Mononuclear phagocytes (monocytes, macrophages, and dendritic cells) play major roles in human immunodeficiency virus (HIV) persistence and disease pathogenesis. Macrophage antigen presentation and effector cell functions are impaired by HIV-1 infection. Abnormalities of macrophage effector cell function in bone marrow, lung, and brain likely result as a direct consequence of cellular activation and HIV replication. To further elucidate the extent of macrophage dysfunction in HIV-1 disease, a critical activation-specific regulatory molecule, nitric oxide (NO.), which may contribute to diverse pathology, was studied. Little, if any, NO. is produced by uninfected human monocytes. In contrast, infection with HIV-1 increases NO. production to modest, but significant levels (2-5 microM). Monocyte activation (with lipopolysaccharide, tumor necrosis factor alpha, or through interactions with astroglial cells) further enhances NO. production in HIV-infected cells, whereas its levels are diminished by interleukin 4. These results suggest a possible role for NO. in HIV-associated pathology where virus-infected macrophages are found. In support of this hypothesis, RNA encoding the inducible NO synthase (iNOS) was detected in postmortem brain tissue from one pediatric AIDS patient with advanced HIV encephalitis. Corresponding iNOS mRNA was not detected in brain tissue from five AIDS patients who died with less significant brain disease. These results demonstrate that HIV-1 can influence the expression of NOS in both cultured human monocytes and brain tissue. This newly described feature of HIV-macrophage interactions suggests previously unappreciated mechanisms of tissue pathology that result from productive viral replication.
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PMID:Regulation of nitric oxide synthase activity in human immunodeficiency virus type 1 (HIV-1)-infected monocytes: implications for HIV-associated neurological disease. 753 Jul 62

Simian immunodeficiency virus (SIV) infection of newborn rhesus macaques is a practical animal model of pediatric AIDS. Intravenous inoculation of rhesus newborns with uncloned SIVmac resulted in a high virus load, no antiviral immune responses, severe immunodeficiency, and a high mortality rate within 3 months. In contrast, immediate oral zidovudine (AZT) treatment of SIV-inoculated rhesus newborns either prevented infection or resulted in reduced virus load, enhanced antiviral immune responses, a low frequency of AZT-resistant virus isolates, and delayed disease progression with negligible toxicity. These results suggest that early chronic AZT treatment of human immunodeficiency virus-exposed newborns may have benefits that outweigh its potential side effects.
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PMID:Immediate zidovudine treatment protects simian immunodeficiency virus-infected newborn macaques against rapid onset of AIDS. 769 93

To evaluate how viral variants may affect disease progression in human pediatric AIDS, we studied the potential of three simian immunodeficiency virus (SIV) isolates to induce simian AIDS in newborn rhesus macaques. The three virus isolates were previously shown to range from pathogenic (SIVmac251 and SIVmac239) to nonpathogenic (SIVmac1A11) when inoculated intravenously into juvenile and adult rhesus macaques. Six newborn macaques inoculated with pathogenic, uncloned SIVmac251 developed persistent, high levels of cell-associated and cell-free viremia, had no detectable antiviral antibodies, and had poor weight gain; these animals all exhibited severe clinical disease and pathologic lesions diagnostic for simian AIDS and were euthanatized 10 to 26 weeks after inoculation. Two newborns inoculated with pathogenic, molecularly cloned SIVmac239 developed persistent high virus load in peripheral blood, but both animals had normal weight gain and developed antiviral antibodies. One of the SIVmac239-infected neonates exhibited pathologic lesions diagnostic for SAIDS and was euthanatized at 34 weeks after inoculation; the other SIVmac239-infected neonate remained alive and exhibited no significant clinical disease for more than 1 year after inoculation. In contrast, three newborn rhesus macaques inoculated with the nonpathogenic molecular clone, SIVmac1A11, had transient, low-level viremia, seroconverted by 10 weeks after inoculation, had normal weight gain, and remained healthy for over 1 year. These results indicate that (i) newborn rhesus macaques infected with an uncloned, virulent SIVmac isolate have a more rapid, fulminant disease course than do adults inoculated with the same virus, (ii) the most rapid disease progression is associated with lack of a detectable humoral immune response in SIV-infected infant macaques, (iii) a molecularly cloned, attenuated SIV isolate is nonpathogenic in neonatal macaques, and (iv) SIV-infected neonatal macaques exhibit patterns of infection, virus load, and disease progression similar to those observed in human immunodeficiency virus-infected children. This SIV/neonatal rhesus model of pediatric AIDS provides a rapid, sensitive model with which to compare the virulence of SIV isolates and to study the mechanisms underlying the differences in disease progression in human immunodeficiency virus-infected infants.
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PMID:Viral factors determine progression to AIDS in simian immunodeficiency virus-infected newborn rhesus macaques. 776 79

Manifestations of pulmonary disease in pediatric AIDS patients differ from those in adults. To evaluate whether differences in the frequency of alveolar macrophage (AM) infection with human immunodeficiency virus type 1 (HIV-1) could account for these clinical distinctions, we undertook a comparative analysis of HIV-1 DNA in AMs from pediatric and adult AIDS patients by enzymatic amplification. A higher frequency of viral DNA detection in pediatric cases (100%) compared with adults (67%) was observed. The sensitivity of detection was 1 viral DNA copy per 4000 AMs; matched peripheral blood mononuclear cells from six of seven pediatric and eight of nine adult patients tested HIV-1 DNA positive. Adult but not pediatric patients exhibited a marked alveolar lymphocytosis, 32% mean lymphocyte count compared with 7.0%, respectively. These results suggest that the burden of HIV-1 in the lungs of pediatric AIDS patients is greater than that in adults.
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PMID:Uniform detection of HIV-1 in alveolar macrophages of pediatric but not adult AIDS patients. 831 56

Microglia are associated with central nervous system (CNS) pathology of both Alzheimer's disease (AD) and the acquired immunodeficiency syndrome (AIDS). In AD, microglia, especially those associated with amyloid deposits, have a phenotype that is consistent with a state of activation, including immunoreactivity with antibodies to class II major histocompatibility antigens and to inflammatory cytokines (interleukin-1-beta and tumor necrosis factor-alpha). Evidence from other studies in rodents indicate that microglia can be activated by neuronal degeneration. These results suggest that microglial activation in AD may be secondary to neurodegeneration and that, once activated, microglia may participate in a local inflammatory cascade that promotes tissue damage and contributes to amyloid formation. In AIDS, microglia are the primary target of retroviral infection. Both ramified and ameboid microglia, in addition to multinucleated giant cells, are infected by the human immunodeficiency virus (HIV-1). The mechanism of microglial infection is not known since microglia lack CD4, the HIV-1 receptor. Microglia display high affinity receptors for immunoglobulins, which makes antibody-mediated viral uptake a possible mechanism of infection. In AIDS, the extent of active viral infection and cytokine production may be critically dependent upon other factors, such as the presence of coinfecting agents. In the latter circumstance, very severe CNS pathology may emerge, including necrotizing lesions. In other circumstances, HIV infection of microglia probably leads to CNS pathology by indirect mechanisms, including release of viral proteins (gp120) and toxic cytokines. Such a mechanism is the best hypothesis for the pathogenesis of vacuolar myelopathy in adults and the diffuse gliosis that characterizes pediatric AIDS, in which very little viral antigen can be detected.
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PMID:Microglia and cytokines in neurological disease, with special reference to AIDS and Alzheimer's disease. 842 65

In order to investigate the relationship between human immunodeficiency virus (HIV-1) infection and protein-energy malnutrition (PEM), all 101 malnourished children who were admitted to the Department of Pediatrics of the National University Hospital between February and July of 1989 (median age = 2.5 years), and who were accompanied by their mother were screened for HIV-1 antibody. Mothers were also screened and interviewed. Mother-child pairs were followed-up 2 years later to determine mortality and clinical status. Fourteen per cent of malnourished children were HIV-1 seropositive. Only one seropositive child had a seronegative mother. This child had a history of multiple blood transfusions and injections. Among children above 15 months of age, HIV-1 seropositivity was more common among marasmic children than among malnourished children presenting with oedema at admission to the hospital. Also, HIV-1 infection was found more frequently among chronically malnourished children (low height for age and weight for age) than among acutely malnourished children (low weight for height). Mortality during the 2-year follow-up was 75 per cent among HIV-1 seropositive children and 23 per cent among HIV-1 seronegatives (mortality density ratio = 6.2; 95 per cent confidence interval = 2.2-17.4). Severe, chronic PEM should always alert health workers to the possible diagnosis of pediatric AIDS, and its implications for treatment and prognosis.
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PMID:HIV-1 infection among malnourished children in Butare, Rwanda. 849 71

Simian immunodeficiency virus (SIV) infection of newborn rhesus macaques is a rapid, sensitive animal model of human pediatric AIDS. Newborn macaques were readily infected by uncloned SIVmac following oral-conjunctival exposure and had persistently high viremia and rapid development of AIDS. In contrast, when 3 pregnant macaques were vaccinated against SIV, 2 of the newborns that had transplacentally acquired antiviral antibodies were protected against mucosal SIV infection at birth. These results suggest that intervention strategies such as active immunization of human immunodeficiency virus (HIV)-infected pregnant women and anti-HIV immunoglobulin administration may decrease the rate of perinatal HIV infection.
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PMID:Vaccination of pregnant macaques protects newborns against mucosal simian immunodeficiency virus infection. 864 4


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