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Suppression of human immunodeficiency virus replication during acute measles.

Abstract
To determine the effect of measles virus coinfection on plasma human immunodeficiency virus (HIV) RNA levels, a prospective study of hospitalized children with measles was conducted between January 1998 and October 2000 in Lusaka, Zambia. Plasma HIV RNA levels were measured during acute measles and 1 month after hospital discharge. The median plasma HIV RNA level in 33 children with measles who were followed longitudinally was 5339 copies/mL at study entry, 60,121 copies/mL at hospital discharge, and 387,148 copies/mL at 1-month follow-up. The median plasma HIV RNA level in children without acute illness was 228,454 copies/mL. Plasma levels of immune activation markers were elevated during the period of reduced plasma HIV RNA. Plasma levels of several potential HIV suppressive factors also were elevated during acute measles. HIV replication is transiently suppressed during acute measles at a time of intense immune activation.
AuthorsWilliam J Moss, Judith J Ryon, Mwaka Monze, Felicity Cutts, Thomas C Quinn, Diane E Griffin
JournalThe Journal of infectious diseases (J Infect Dis) Vol. 185 Issue 8 Pg. 1035-42 (Apr 15 2002) ISSN: 0022-1899 [Print] United States
PMID11930312 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Antigens, CD
  • Chemokine CCL4
  • Chemokine CCL5
  • Macrophage Inflammatory Proteins
  • RNA, Viral
  • Receptors, Interleukin-2
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type II
Topics
  • Acute Disease
  • Antigens, CD (blood)
  • CD4 Lymphocyte Count
  • Chemokine CCL4
  • Chemokine CCL5 (blood)
  • Child, Preschool
  • Female
  • HIV (physiology)
  • Humans
  • Infant
  • Macrophage Inflammatory Proteins (blood)
  • Male
  • Measles (immunology, virology)
  • RNA, Viral (blood)
  • Receptors, Interleukin-2 (analysis)
  • Receptors, Tumor Necrosis Factor (blood)
  • Receptors, Tumor Necrosis Factor, Type II
  • Virus Replication

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