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Simian immunodeficiency virus infection in neonatal macaques

  1. Author:
    Veazey, R. S.
    Lifson, J. D.
    Pandrea, I.
    Purcell, J.
    Piatak, M.
    Lackner, A. A.
  2. Author Address

    Tulane Univ, Hlth Sci Ctr, Div Comparat Pathol, Tulane Natl Primate Res Ctr, 18703 3 Rivers Rd, Covington, LA 70433 USA Tulane Univ, Hlth Sci Ctr, Div Comparat Pathol, Tulane Natl Primate Res Ctr, Covington, LA 70433 USA NCI, Frederick Canc Res & Dev Ctr, SAIC, Frederick, MD 21702 USA Veazey RS Tulane Univ, Hlth Sci Ctr, Div Comparat Pathol, Tulane Natl Primate Res Ctr, 18703 3 Rivers Rd, Covington, LA 70433 USA
    1. Year: 2003
  1. Journal: Journal of Virology
    1. 77
    2. 16
    3. Pages: 8783-8792
  2. Type of Article: Article
  1. Abstract:

    Children with human immunodeficiency virus infection often have higher viral loads and progress to AIDS more rapidly than adults. Since the intestinal tract is a major site of early viral replication and CD4(+) T-cell depletion in adults, we examined the effects of simian immunodeficiency virus (SIV) on both peripheral and intestinal lymphocytes from 13 neonatal macaques infected with SlVmac239. Normal neonates had more CD4(+) T cells and fewer CD8(+) T cells in all tissues than adults. Surprisingly, neonates had substantial percentages of CD4(+) T cells with an activated, memory phenotype (effector CD4(+) T cells) in the lamina propria of the intestine compared to peripheral lymphoid tissues, even when examined on the day of birth. Moreover, profound and selective depletion of jejunum lamina propria CD4(+) T cells occurred in neonatal macaques within 21 days of infection, which was preceded by large numbers of SIV-infected cells in this compartment. Furthermore, neonates with less CD4(+) T-cell depletion in tissues tended to have higher viral loads. The persistence of intestinal lamina propria CD4(+) T cells in some neonates with high viral loads suggests that increased turnover and/or resistance to CD4(+) T- cell loss may contribute to the higher viral loads and increased severity of disease in neonatal hosts.

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