Journal article
Establishment of HIV-1 latency in resting CD4 T cells depends on chemokine-induced changes in the actin cytoskeleton
PU Cameron, S Saleh, G Sallmann, A Solomon, F Wightman, VA Evans, G Boucher, EK Haddad, RP Sekaly, AN Harman, JL Anderson, KL Jones, J Mak, AL Cunningham, A Jaworowski, SR Lewin
Proceedings of the National Academy of Sciences of the United States of America | NATL ACAD SCIENCES | Published : 2010
Abstract
Eradication of HIV-1 with highly active antiretroviral therapy (HAART) is not possible due to the persistence of long-lived, latently infected resting memory CD4+ T cells. We now show that HIV-1 latency can be established in resting CD4+ T cells infected with HIV-1 after exposure to ligands for CCR7 (CCL19), CXCR3 (CXCL9 and CXCL10), and CCR6 (CCL20) but not in unactivated CD4+ T cells. The mechanism did not involve cell activation or significant changes in gene expression, but was associated with rapid dephosphorylation of cofilin and changes in filamentous actin. Incubation with chemokine before infection led to efficient HIV-1 nuclear localization and integration and this was inhibited by..
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Awarded by National Health and Medical Research Council of Australia
Funding Acknowledgements
This work was supported by National Health and Medical Research Council of Australia Program Grant 358399 and Project Grant 491154. S.R.L. was supported by National Health and Medical Research Council of Australia Practitioner Fellowship 478100.