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A computational model of inhibition of HIV-1 by interferon-alpha

By Edward P Browne, Benjamin Letham, Cynthia Rudin

Posted 09 Nov 2015
bioRxiv DOI: 10.1101/031005 (published DOI: 10.1371/journal.pone.0152316)

Type 1 interferons such as interferon-alpha (IFNa) inhibit replication of Human immunodeficiency virus (HIV-1) by upregulating the expression of genes that interfere with specific steps in the viral life cycle. This pathway thus represents a potential target for immune-based therapies that can alter the dynamics of host- virus interactions to benefit the host. To obtain a deeper mechanistic understanding of how IFNa; impacts spreading HIV-1 infection, we modeled the interaction of HIV- 1 with CD4 T cells and IFNa; as a dynamical system. This model was then tested using experimental data from a cell culture model of spreading HIV-1 infection. We found that a model in which IFNa; induces reversible cellular states that block both early and late stages of HIV-1 infection, combined with a saturating rate of conversion to these states, was able to successfully fit the experimental dataset. Sensitivity analysis showed that the potency of inhibition by IFNa; was particularly dependent on specific network parameters and rate constants. This model will be useful for designing new therapies targeting the IFNa; network in HIV-1-infected individuals, as well as potentially serving as a template for understanding the interaction of IFNa; with other viruses.

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