Why does HIV infection not lead to disseminated strongyloidiasis?

Mark E Viney, Michael Brown, Nicholas E Omoding, J Wendi Bailey, Michael P Gardner, Emily Roberts, Dilys Morgan, Alison M Elliott, James A G Whitworth

Research output: Contribution to journalArticlepeer-review

81 Citations (Scopus)


We investigated the hypothesis that host immunosuppression due to advancing human immunodeficiency virus (HIV) disease favors the direct development of infective larvae of Strongyloides stercoralis, which may facilitate hyperinfection and, hence, disseminated strongyloidiasis. To do this, we sought correlations between the immune status of the subjects and the development of S. stercoralis infections. Among 35 adults, there were significant negative rank correlations between CD4+ cell counts and the proportions of free-living male and female worms. Thus, in individuals with preserved immune function, direct development of S. stercoralis is favored, whereas, in individuals with lesser immune function, indirect development is relatively more common. These results may explain the notable absence of disseminated strongyloidiasis in advanced HIV disease. Because disseminated infection requires the direct development of infective larvae in the gut, the observed favoring of indirect development in individuals immunosuppressed by advancing HIV disease is not consistent with the promotion of disseminated infection.

Original languageEnglish
Pages (from-to)2175-80
Number of pages6
JournalThe Journal of Infectious Diseases
Issue number12
Publication statusPublished - 15 Dec 2004


  • AIDS-Related Opportunistic Infections/immunology
  • Adult
  • Animals
  • Antibodies, Helminth/blood
  • CD4-CD8 Ratio
  • CD4-Positive T-Lymphocytes/immunology
  • CD8-Positive T-Lymphocytes/immunology
  • Cohort Studies
  • Female
  • HIV Infections/complications
  • Humans
  • Larva/growth & development
  • Male
  • Strongyloides stercoralis/growth & development
  • Strongyloidiasis/immunology


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