Journal article

HIV integration and the establishment of latency in CCL19-treated resting CD4( ) T cells require activation of NF-kappa B

Suha Saleh, Hao K Lu, Vanessa Evans, David Harisson, Jingling Zhou, Anthony Jaworowski, Georgina Sallmann, Karey Y Cheong, Talia M Mota, Surekha Tennakoon, Thomas A Angelovich, Jenny Anderson, Andrew Harman, Anthony Cunningham, Lachlan Gray, Melissa Churchill, Johnson Mak, Heidi Drummer, Dimitrios N Vatakis, Sharon R Lewin Show all

RETROVIROLOGY | BMC | Published : 2016

Abstract

BACKGROUND: Eradication of HIV cannot be achieved with combination antiretroviral therapy (cART) because of the persistence of long-lived latently infected resting memory CD4(+) T cells. We previously reported that HIV latency could be established in resting CD4(+) T cells in the presence of the chemokine CCL19. To define how CCL19 facilitated the establishment of latent HIV infection, the role of chemokine receptor signalling was explored. RESULTS: In resting CD4(+) T cells, CCL19 induced phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt), nuclear factor kappa B (NF-κB), extracellular-signal-regulated kinase (ERK) and p38. Inhibition of the phosphoinositol-3-kinase (PI3K) an..

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Grants

Awarded by National Institutes of Health (NIH)


Awarded by NHMRC


Awarded by NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES


Awarded by NATIONAL INSTITUTE ON DRUG ABUSE


Funding Acknowledgements

SRL is an Australian National Health and Medical Research Council (NHMRC) Practitioner Fellow. This work was supported by grants from the National Institutes of Health (NIH) U19-AI096109 and 1R56AI095073-01A1 (SRL and PUC), R21DA031036 and R21AI106472 (DV), the American Foundation for AIDS Research (SS, PUC, SRL) and the NHMRC (491154 and 1002761).