Abstract
Results We have observed that SIVmac 239 infects human lymphoid cells much less efficiently than HIV-1. However, ectopic expression of HIV-1 Tat rescued SIV infection. As host cell type can influence viral gene expression, we tested different cell lines for their ability to support lentiviral latency. In both T (Jurkat TAg and C8166) and T-B hybrid cell lines (CEMX174) SIV exhibited a greater ability to remain transcriptionally silent within the human genome than HIV-1 or HIV-2. The different behaviour in terms of latency was particularly evident in CEMX174 cells, where HIV Tat activation caused more than 20-fold increase in the number of GFP-positive cells infected with SIV, while it had little effect on cells challenged with HIV-1 or HIV-2. The lower level of productive infection displayed by SIVmac239 was not due to a reduced ability of SIV Tat to trigger viral expression in human cells because SIV Tat overexpression reactivated latent SIV as well as HIV Tat did. Moreover, HIV-1 chimeric viruses harboring the U3 region of SIV behaved like the parental HIV-1 viruses, suggesting that viral determinants of SIV latency reside in a part of the lentiviral genome different from the promoter region.
Highlights
Infected cells represent a major obstacle to the cure of infection with human immunodeficiency virus type 1 (HIV-1)
In human cell lines transduction with SIVmac239 largely establishes a latent infection which is reactivated by overexpressing HIV-1 or SIVmac239 Tat
We have observed that SIVmac 239 infects human lymphoid cells much less efficiently than HIV-1
Summary
Identifying features of the lentiviral genome crucial for the establishment of latency Serena Ziglio1*, Giada Mattiuzzo, Jeremy Luban, Massimo Pizzato. From Frontiers of Retrovirology: Complex retroviruses, retroelements and their hosts Cambridge, UK. From Frontiers of Retrovirology: Complex retroviruses, retroelements and their hosts Cambridge, UK. 16-18 September 2013
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