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Changes of methylation at enhancers appear to be essential for HIV infection progression

ABSTRACT: We studied the influence of the European HIV-1 subtype B (most common in the Western and central Europe) and subtype A6 (prevalent in Eastern Europe including Ukraine and Russia) on host methylome during infection progression and in virus subtype specific manner. Our results show that regardless of virus subtype in the beginning of the infection HIV related methylation changes more frequently affect parts of the genome with low expression activity including heterochromatin and quiescent regions. However, the analysis of the methylomes of blood cells of PLWH at stage four of the infection showed that with the infection progression genomic regulatory elements that harbour infection related methylation changes are enhancers. We further showed that the effect of each of the virus subtype on host methylome is to a large extent similar and in general involve hypomethylation of loci associated with key pathways involved in viral infection. But our results also indicate that each of the virus subtype appears to at least to some extent affect host methylome in virus subtype specific manner. Most importantly we showed that progression related methylation changes that we identified are reversed with ART therapy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE272115 | GEO | 2025/06/25

REPOSITORIES: GEO

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Project description:Wodarz2007 - HIV/CD4 T-cell interaction A deterministic model illustrating how CD4 T-cells can influence HIV infection. This model is described in the article: Infection dynamics in HIV-specific CD4 T cells: does a CD4 T cell boost benefit the host or the virus? Wodarz D, Hamer DH. Math Biosci 2007 Sep; 209(1): 14-29 Abstract: Recent experimental data have shown that HIV-specific CD4 T cells provide a very important target for HIV replication. We use mathematical models to explore the effect of specific CD4 T cell infection on the dynamics of virus spread and immune responses. Infected CD4 T cells can provide antigen for their own stimulation. We show that such autocatalytic cell division can significantly enhance virus spread, and can also provide an additional reservoir for virus persistence during anti-viral drug therapy. In addition, the initial number of HIV-specific CD4 T cells is an important determinant of acute infection dynamics. A high initial number of HIV-specific CD4 T cells can lead to a sudden and fast drop of the population of HIV-specific CD4 T cells which results quickly in their extinction. On the other hand, a low initial number of HIV-specific CD4 T cells can lead to a prolonged persistence of HIV-specific CD4 T cell help at higher levels. The model suggests that boosting the population of HIV-specific CD4 T cells can increase the amount of virus-induced immune impairment, lead to less efficient anti-viral effector responses, and thus speed up disease progression, especially if effector responses such as CTL have not been sufficiently boosted at the same time. This model is hosted on BioModels Database and identified by: BIOMD0000000663. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. 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 CC0 Public Domain Dedication for more information.

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Changes of methylation at enhancers appear to be essential for HIV infection progression

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