Dilated cardiomyopathy in children with acquired immunodeficiency syndrome:

Joshi, Vijay V.; Gadol, C.; Connor, Edward; Oleske, James M.; Mendelson, Jenny; Marı́n-Garcı́a, José

doi:10.1016/s0046-8177(88)80318-6

Cited by 56 publications

(11 citation statements)

References 16 publications

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“…According to these data, the only stromal cells that may be a target for HIV-1 remain thymic DC. Recent studies of HIV-1-seropositive children and of simian immunodeficiency virus-infected monkeys in vivo indicate an atrophy of the thymus with alterations of thymic stroma cells (7,25,35,36). DC from various origins were described as a potential reservoir for HIV-1 in blood and lymph nodes (28,32,39,40).…”

Section: Ugh Either Infectedmentioning

confidence: 99%

Two subpopulations of human triple-negative thymic cells are susceptible to infection by human immunodeficiency virus type 1 in vitro

Valentin

Nugeyre

Vuillier

et al. 1994

J Virol

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Some infants infected with human immunodeficiency virus type 1 (HIV-1) rapidly develop a fatal disease characterized by a severe lymphopenia. To explain the immune dysfunction, we proposed a mechanism by which a nongeneration of CD4+ T cells is caused by HIV-1 infection of thymic cells. To examine this hypothesis, we infected primary triple-negative (TN; phenotypically CD3- CD4- CD8-), CD1a- TN, or CD1a+ TN thymic cell subsets. Our data indicate that by flow cytometry, TN, CD1a- TN, and CD1a+ TN cells remain CD4 negative throughout the culture period. We demonstrated that TN and CD1a+ TN thymic cell subsets are susceptible to HIV-1 as is the entire thymic cell population, whereas CD1a- TN cells are not. A limited number of infected TN cells are expressing HIV-1 but the level of transcription is very high in permissive cells, as detected by in situ hybridization. We then performed blocking experiments on TN cells to examine the mechanism of HIV-1 entry into these cells. CD4 (OKT4a) monoclonal antibody blocks their infection. Finally, infection experiments on two subpopulations of TN cells (CD2+ CD7+ and CD2- CD7-) indicate that infected TN cells may correspond to both immature thymocytes and thymic dendritic cells. These data are of particular interest since infection of thymic stromal cells might result in an impairment of T-cell differentiation, which may explain a nongeneration of functional CD4+ T-cell population in the thymus. This phenomenon may play a role in AIDS pathogenesis, in particular in infants born from seropositive mothers.

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Section: Ugh Either Infectedmentioning

confidence: 99%

Two subpopulations of human triple-negative thymic cells are susceptible to infection by human immunodeficiency virus type 1 in vitro

Valentin

Nugeyre

Vuillier

et al. 1994

J Virol

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“…Severe cardiomyopathy is not common, but when computer-assisted analysis of echocardiography is done, myocardial dysfunction is seen with regularity (153). The primary insult on the myocardium has been ascribed to a variety of causes including HIV infection, opportunistic infection, immune dysregulation, and antiretroviral drugs (125,156). A myocardial biopsy may be necessary to obtain a definitive etiologic diagnosis so that appropriate therapy can be initiated.…”

Section: Organ-specific Manifestations Of Pediatric Hiv Infectionmentioning

confidence: 99%

Pediatric human immunodeficiency virus infection

Domachowske

1996

Clin Microbiol Rev

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In the past decade, an increase in pediatric human immunodeficiency virus (HIV) infection has had a substantial impact on childhood morbidity and mortality worldwide. The vertical transmission of HIV from mother to infant accounts for the vast majority of these cases. Identification of HIV-infected pregnant women needs to be impoved so that appropriate therapy can be initiated for both mothers and infants. While recent data demonstrate a dramatic decrease in HIV transmission from a subset of women treated with zidovudine during pregnancy, further efforts at reducing transmission are desperately needed. This review focuses on vertically transmitted HIV infection in children, its epidemiology, diagnostic criteria, natural history, and clinical manifestations including infectious and noninfectious complications. An overview of the complex medical management of these children ensues, including the use of antiretroviral therapy. Opportunistic infection prophylaxis is reviewed, along with the important role of other supportive therapies.

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“…Childhood mortality due to cardiac complications ranges from 1% to 9%. 2,4,8,10,[12][13][14][15][16][17][18][19][20][21][22][23] The ever-increasing number of children born to HIVpositive mothers, coupled with the complex etiopathogenesis of heart involvement and the need for further understanding of the natural history of clinical cardiac manifestations during childhood, led us to study children exposed perinatally to HIV-1. This is an eightyear clinical, electrocardiographic, and echocardiographic follow-up study.…”

mentioning

confidence: 99%