Important note: Information in this article was accurate in June 1999. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; Monday, June 14 & 21, 1999
Daniel J. DeNoon, Senior Editor
CW HENDERSON PUBLISHER -- New evidence directly links HIV to thrombocytopenia (TP).
TP is one of the major hematopoietic defects seen in patients with HIV infection. It often occurs in the context of bone-marrow invasion by neoplasms or opportunistic infections, but some HIV infected patients develop TP of unknown etiology.
Frosso Voulgaropoulou of Washington University, St. Louis, Missouri, and colleagues now show that HIV strains with the syncytium- inducing (SI) phenotype can be isolated from the bone marrow of HIV infected patients with TP. These strains differ significantly from those isolated from patients with TP of known etiology.
"Our data suggest that AIDS patients with hematopoietic dysfunction caused by the invasion of bone marrow by neoplasms or opportunistic pathogens sustain HIV-1 strains with an NSI [non- syncytium inducing] phenotype," Voulgaropoulou et al. reported. On the contrary, two of three patients with HIV associated hematopoietic dysfunction and TP have SI HIV-1 strains in the bone marrow Therefore, the presence of SI HIV-1 strains in the bone marrow may constitute another mechanism for the development of TP, either by infection of megakaryocytes or their precursors or by infection of cells of the bone marrow microenvironment."
Voulgaropoulou et al. published their findings in the Journal of Virology ("Distinct Human Immunodeficiency Virus Strains in the Bone Marrow Are Associated with the Development of Thrombocytopenia," J Virol 1999 Apr;73(4):3497-504.
The researchers isolated HIV from the blood and bone marrow of 12 patients. From these isolates they constructed infectious molecular clones and characterized their cellular tropism.
The viral quasispecies isolated from the bone marrow of the TP patients differed from those without TP.
"In the patients with TP, the amino acids arginine and serine preferentially occupied positions 11 and 13 of the HIV-1 V3 loop whereas the amino acids glycine and histidine were selected against in these positions," Voulgaropoulou et al. wrote.
Although the number of patients in the study was too small for definitive proof, the authors noted that their data shed light on the etiology of HIV associated TP.
"The presence of SI HIV-1 strains in the bone marrow may constitute another mechanism for the development of TP," they concluded.
This work was supported by grants from the Public Health Service.
The corresponding author for this study is Lee Ratner, Departments of Medicine, Pathology, and Molecular Microbiology, Box 8069, 660 S. Euclid Ave., St. Louis, Missouri 63110. Phone: (314) 362-8863. Fax: (314) 747-2797. Email: <lratner@imgate.wustl.edu>.
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