Similarity in viral and host promoters couples viral reactivation with host cell migration

Kathrin Bohn-Wippert, Erin N. Tevonian, Melina R. Megaridis and Roy D. Dar ()
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Kathrin Bohn-Wippert: University of Illinois at Urbana-Champaign
Erin N. Tevonian: University of Illinois at Urbana-Champaign
Melina R. Megaridis: University of Illinois at Urbana-Champaign
Roy D. Dar: University of Illinois at Urbana-Champaign

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Viral–host interactomes map the complex architecture of an evolved arms race during host cell invasion. mRNA and protein interactomes reveal elaborate targeting schemes, yet evidence is lacking for genetic coupling that results in the co-regulation of promoters. Here we compare viral and human promoter sequences and expression to test whether genetic coupling exists and investigate its phenotypic consequences. We show that viral–host co-evolution is imprinted within promoter gene sequences before transcript or protein interactions. Co-regulation of human immunodeficiency virus (HIV) and human C-X-C chemokine receptor-4 (CXCR4) facilitates migration of infected cells. Upon infection, HIV can actively replicate or remain dormant. Migrating infected cells reactivate from dormancy more than non-migrating cells and exhibit differential migration–reactivation responses to drugs. Cells producing virus pose a risk for reinitiating infection within niches inaccessible to drugs, and tuning viral control of migration and reactivation improves strategies to eliminate latent HIV. Viral–host genetic coupling establishes a mechanism for synchronizing transcription and guiding potential therapies.

Date: 2017
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DOI: 10.1038/ncomms15006

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