Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton

Cameron, Paul U., Saleh, Suha, Sallmann, Georgina, Solomon, Ajantha, Wightman, Fiona, Evans, Vanessa A., Boucher, Genevieve, Haddad, Elias K., Sekaly, Rafick-Pierre, Harman, Andrew N., Anderson, Jenny L., Jones, Kate L., Mak, Johnson, Cunningham, Anthony L., Jaworowski, Anthony and Lewin, Sharon R. 2010, Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton, National academy of science. Proceedings, vol. 107, no. 39, pp. 16934-16939, doi: 10.1073/pnas.1002894107.

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Title Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton
Author(s) Cameron, Paul U.
Saleh, Suha
Sallmann, Georgina
Solomon, Ajantha
Wightman, Fiona
Evans, Vanessa A.
Boucher, Genevieve
Haddad, Elias K.
Sekaly, Rafick-Pierre
Harman, Andrew N.
Anderson, Jenny L.
Jones, Kate L.
Mak, JohnsonORCID iD for Mak, Johnson
Cunningham, Anthony L.
Jaworowski, Anthony
Lewin, Sharon R.
Journal name National academy of science. Proceedings
Volume number 107
Issue number 39
Start page 16934
End page 16939
Total pages 6
Publisher National Academy of Sciences
Place of publication Washington, D. C.
Publication date 2010-09-28
ISSN 0027-8424
Keyword(s) actins
CD4-Positive T-Lymphocytes
cell nucleus
HIV infections
virus integration
virus internalization
virus latency
virus replication
Summary 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 the actin stabilizer jasplakinolide. We propose a unique pathway for establishment of latency by direct HIV-1 infection of resting CD4+ T cells during normal chemokine-directed recirculation of CD4+ T cells between blood and tissue.
Language eng
DOI 10.1073/pnas.1002894107
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2010, National Academy of Sciences
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Document type: Journal Article
Collection: School of Medicine
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