Longitudinal regulation over time of gene expression in mock infected and HIV-1 infected CD4+ T-cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE163405 | GEO | 2021/06/14
REPOSITORIES: GEO
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Project description:Aguilera 2014 - HIV latency. Interaction
between HIV proteins and immune response
This model is described in the article:
Studying HIV latency by
modeling the interaction between HIV proteins and the innate
immune response.
Aguilera LU,
Rodríguez-González J.
J. Theor. Biol. 2014 Nov; 360:
67-77
Abstract:
HIV infection leads to two cell fates, the viral productive
state or viral latency (a reversible non-productive state). HIV
latency is relevant because infected active CD4+ T-lymphocytes
can reach a resting memory state in which the provirus remains
silent for long periods of time. Despite experimental and
theoretical efforts, the causal molecular mechanisms
responsible for HIV latency are only partially understood.
Studies have determined that HIV latency is influenced by the
innate immune response carried out by cell restriction factors
that inhibit the postintegration steps in the virus replication
cycle. In this study, we present a mathematical study that
combines deterministic and stochastic approaches to analyze the
interactions between HIV proteins and the innate immune
response. Using wide ranges of parameter values, we observed
the following: (1) a phenomenological description of the viral
productive and latent cell phenotypes is obtained by bistable
and bimodal dynamics, (2) biochemical noise reduces the
probability that an infected cell adopts the latent state, (3)
the effects of the innate immune response enhance the HIV
latency state, (4) the conditions of the cell before infection
affect the latent phenotype, i.e., the existing expression of
cell restriction factors propitiates HIV latency, and existing
expression of HIV proteins reduces HIV latency.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000573.
To cite BioModels Database, please use:
BioModels Database:
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quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
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Public Domain Dedication for more information.
2015-03-30 | BIOMD0000000573 | BioModels
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Project description:Latent HIV-1 infection represents a barrier to virus eradication as latent HIV-1 is impervious to the effects of antiretroviral drugs and can avoid detection by the host immune system. Strategies to clear latent HIV-1 infection in patients have so far failed in clinical trials to increase the decay rate of the latent reservoir underscoring the need for continued study of HIV-1 latency. In this study, a genome-wide RNAi screen was performed to probe cellular factors involved in maintaining HIV-1 latency in HeLa cells latently infected with an HIV-1 reporter virus.
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