Why Does HIV Infection Not Lead to Disseminated Strongyloidiasis?
Author(s) -
Mark Viney,
Michael Brown,
Nicholas Omoding,
J. Wendi Bailey,
Michael P. Gardner,
Emily Roberts,
Dilys Morgan,
Alison M. Elliott,
James Whitworth
Publication year - 2004
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/425935
Subject(s) - strongyloides stercoralis , strongyloidiasis , immunology , immune system , immunosuppression , biology , disease , immunopathology , strongyloides , virology , medicine , helminths
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.
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