Abstract
Despite highly effective anti-retroviral therapy, HIV is thought to persist in patients within long-lived cellular reservoirs in the form of a transcriptionally inactive (latent) integrated provirus. Lentiviral latency has therefore come to the forefront of the discussion on the possibility of a cure for HIV infection in humans. Animal models of lentiviral latency provide an essential tool to study mechanisms of latency and therapeutic manipulation. Of the three animal models that have been described, the feline immunodeficiency virus (FIV)-infected cat is the most recent and least characterized. However, several aspects of this model make it attractive for latency research, and it may be complementary to other model systems. This article reviews what is known about FIV latency and chronic FIV infection and how it compares with that of other lentiviruses. It thereby offers a framework for the usefulness of this model in future research aimed at lentiviral eradication.
Highlights
It was estimated that 34 million people worldwide were living with HIV/Acquired immunodeficiency syndrome (AIDS) as of 2011, more than 1 million of whom were living in the United States [1]
While advancements made in highly active antiretroviral therapy (HAART) have dramatically increased survival time and quality of life for those infected with HIV, long term treatment is problematic for several reasons [2]
This study suggests that protein kinase C (PKC) is important for feline immunodeficiency virus (FIV) replication, and PKC-activators such as Prostratin may be useful in purging latent reservoirs
Summary
It was estimated that 34 million people worldwide were living with HIV/AIDS as of 2011, more than 1 million of whom were living in the United States [1]. CD4 + CD25+ and CD4 + CD25- T cells appear to possess different activation requirements, modulated by viral titer and cytokine stimuli, to reach threshold activation levels required to harbor a productive FIV infection [85] This holds implications for the differential ability of the two subsets to serve as potential latent reservoirs, though our research group has found both subsets to be equal in terms of latency status in the periphery during chronic FIV-C infection [10]. The molecular mechanism of FIV latency in human cell lines has not been reported; this form of latency may be due to differences in species-specific viral restriction factors and corresponding viral evasion mechanisms Another group demonstrated that a cellular clone of a feline T-cell line (FeT-J) chronically infected (>50 days) with FIV-A led to a latent phenotype, which was inducible by treatment with mitogens [88].
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