Journal Article Why does HIV infection not lead to disseminated strongyloidiasis? Get access M.E. Viney, M.E. Viney Search for other works by this author on: Oxford Academic PubMed Google Scholar M. Brown, M. Brown Search for other works by this author on: Oxford Academic PubMed Google Scholar N.E. Omoding, N.E. Omoding Search for other works by this author on: Oxford Academic PubMed Google Scholar J.W. Bailey, J.W. Bailey Search for other works by this author on: Oxford Academic PubMed Google Scholar M.P. Gardner, M.P. Gardner Search for other works by this author on: Oxford Academic PubMed Google Scholar E. Roberts, E. Roberts Search for other works by this author on: Oxford Academic PubMed Google Scholar D. Morgan, D. Morgan Search for other works by this author on: Oxford Academic PubMed Google Scholar A. Elliott, A. Elliott Search for other works by this author on: Oxford Academic PubMed Google Scholar J.A.G. Whitworth J.A.G. Whitworth Search for other works by this author on: Oxford Academic PubMed Google Scholar Transactions of The Royal Society of Tropical Medicine and Hygiene, Volume 97, Issue 6, November-December 2003, Page 632, https://doi.org/10.1016/S0035-9203(03)80091-3 Published: 01 November 2003

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.