School of Medicine and Health Sciences Poster Presentations
Influence of Sex as an Intrinsic Biological Variable in a Primary Cell Model of HIV Latency
Poster Number
270
Document Type
Poster
Status
Postdoc
Abstract Category
HIV/AIDS
Keywords
HIV, HIV latency, primary cell, sex differences
Publication Date
Spring 2018
Abstract
Background
Several cohort studies have shown that there are sex differences in the pathogenesis of HIV-1. Recently, it has been shown that females are more likely to develop a lower reservoir size than male during long-term ART. The immunologic and virologic mechanisms underlying these clinically relevant observations are not currently understood. We wanted to address whether sex was an intrinsic difference in CD4 T cells that could explain some of the clinical observations.
Methods
We have used a primary cell model of HIV-1 latency that recapitulates the generation of latently infected cultured TCM and uses a replication competent virus and ART. Using this primary cell model, we have characterized whether sex influences the intrinsic ability of HIV to replicate and to establish latency in cultured TCM cells. Furthermore, we have characterized the ability of different Latency-Reversing Agents (LRAs) to reactivate latent HIV.
Results
We have found that cultured TCM from both sexes can replicate HIV at similar ratio and generate equal levels of latent infection. Analysis of the ability of several LRAs to reactivate latent HIV suggest that sex is not an intrinsic biological variable to the activity of these specific LRAs.
Conclusions
Our results show that sex is not an intrinsic biological variable in CD4 T cells in terms of the ability of HIV to replicate, to establish latency or to reactivate from latency with several LRAs. Other extrinsic factors may be accountable for the sex differences observed clinically.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Open Access
1
Influence of Sex as an Intrinsic Biological Variable in a Primary Cell Model of HIV Latency
Background
Several cohort studies have shown that there are sex differences in the pathogenesis of HIV-1. Recently, it has been shown that females are more likely to develop a lower reservoir size than male during long-term ART. The immunologic and virologic mechanisms underlying these clinically relevant observations are not currently understood. We wanted to address whether sex was an intrinsic difference in CD4 T cells that could explain some of the clinical observations.
Methods
We have used a primary cell model of HIV-1 latency that recapitulates the generation of latently infected cultured TCM and uses a replication competent virus and ART. Using this primary cell model, we have characterized whether sex influences the intrinsic ability of HIV to replicate and to establish latency in cultured TCM cells. Furthermore, we have characterized the ability of different Latency-Reversing Agents (LRAs) to reactivate latent HIV.
Results
We have found that cultured TCM from both sexes can replicate HIV at similar ratio and generate equal levels of latent infection. Analysis of the ability of several LRAs to reactivate latent HIV suggest that sex is not an intrinsic biological variable to the activity of these specific LRAs.
Conclusions
Our results show that sex is not an intrinsic biological variable in CD4 T cells in terms of the ability of HIV to replicate, to establish latency or to reactivate from latency with several LRAs. Other extrinsic factors may be accountable for the sex differences observed clinically.