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HIV-1 Infection of Trophoblasts Is Independent of gp120/CD4 Interactions but Relies on Heparan Sulfate Proteoglycans
Gaël Vidricaire, Sonia Gauthier and Michel J. Tremblay
The Journal of Infectious Diseases
Vol. 195, No. 10 (May 15, 2007), pp. 1461-1471
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30088306
Page Count: 11
You can always find the topics here!Topics: HIV 1, Viruses, T lymphocytes, Infections, Trophoblasts, Cell lines, Internalization, Epithelial cells, Heparin, Journalism
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Mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1) is the leading cause of HIV infection in infants. Direct infection of trophoblasts-cells forming the placental barrier-may cause this transmission. Entry of HIV-1 into trophoblasts is unusual for this retrovirus, because it is associated with endocytosis. However, given that trophoblasts express no or few receptors/coreceptors required for virus internalization, the mechanism underlying this event remains ambiguous. In the present study, we show that HIV-1 entry and infection of polarized trophoblasts are independent not only of CD4 but also of envelope (Env) glycoproteins gpl20 and gp41. Virus internalization, cytoplasmic release, reverse transcription, integration, and HIV-1 gene expression occurred with both fusion-incompetent and Env-deficient viruses. Importantly, fusion-independent infection was observed when we used viruses produced in a natural cellular reservoir (i.e., primary human cells). Finally, HIV-1 requires heparan sulfate proteoglycans for uptake in trophoblasts. Together, our findings illustrate that HIV-1 utilizes an unusual pathway for entering human polarized trophoblasts.
The Journal of Infectious Diseases © 2007 Oxford University Press