Altered gut microbiome composition in HIV infection

Bandera, Alessandra; Benedetto, Ilaria De; Bozzi, Giorgio; Gori, Andrea

doi:10.1097/coh.0000000000000429

Cited by 90 publications

(48 citation statements)

References 48 publications

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“…For example, during HIV-1 infection, CD4+ T cells are rapidly depleted, especially in gut associated lymphoid tissue (GALT). As a likely consequence, the gut microbiome of HIV-1 infected individuals are distinct in composition from healthy individuals (Bandera et al, 2018; Zilberman-Schapira et al, 2016). Furthermore, dysbiosis and T cell depletion in HIV-1 infected patients may lead to the breakdown of the intestinal barrier, leading to the systemic distribution of bacterial products, as evidenced by increased circulating lipopolysaccharide (LPS) levels (Brenchley et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression

Kueck

Cassella

Holler

et al. 2018

eLife

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The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activation induces the expression of numerous genes, with many effects on cells. However, AhR activation is not known to affect the replication of viruses. We show that AhR activation in macrophages causes a block to HIV-1 and HSV-1 replication. We find that AhR activation transcriptionally represses cyclin-dependent kinase (CDK)1/2 and their associated cyclins, thereby reducing SAMHD1 phosphorylation, cellular dNTP levels and both HIV-1 and HSV-1 replication. Remarkably, a different antiviral stimulus, interferon gamma (IFN-γ), that induces a largely non-overlapping set of genes, also transcriptionally represses CDK1, CDK2 and their associated cyclins, resulting in similar dNTP depletion and antiviral effects. Concordantly, the SIV Vpx protein provides complete and partial resistance to the antiviral effects of AhR and IFN-γ, respectively. Thus, distinct antiviral signaling pathways converge on CDK/cyclin repression, causing inhibition of viral DNA synthesis and replication.

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Section: Discussionmentioning

confidence: 99%

The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression

Kueck

Cassella

Holler

et al. 2018

eLife

View full text Add to dashboard Cite

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“…For example, during HIV-1 infection, CD4+ T cells are rapidly depleted, especially in gut associated lymphoid tissue (GALT). As a likely consequence, the gut microbiome of HIV-1 infected individuals are distinct in composition from healthy individuals 50,51 . Furthermore, dysbiosis and T cell depletion in HIV-1 infected patients may lead to the breakdown of the intestinal barrier, leading to the systemic distribution of bacterial products, as evidenced by increased circulating lipopolysaccharide (LPS) levels 52 .…”

Section: Discussionmentioning

confidence: 99%

The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression

Bieniasz

Kueck

Cassella

et al. 2018

Preprint

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The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activation induces the expression of numerous genes, with many effects on cells.However, AhR activation is not known to affect the replication of viruses. We show that AhR activation in macrophages causes a block to HIV-1 and HSV-1 replication. We find that AhR activation transcriptionally represses cyclin-dependent kinase (CDK)1/2 and their associated cyclins, thereby reducing SAMHD1 phosphorylation, cellular dNTP levels and both HIV-1 and HSV-1 replication. Remarkably, a different antiviral stimulus, interferon gamma (IFN-g), that induces a largely non-overlapping set of genes, also transcriptionally represses CDK1, CDK2 and their associated cyclins, resulting in similar dNTP depletion and antiviral effects. Concordantly, the SIV Vpx protein provides complete and partial resistance to the antiviral effects of AhR and IFN-g, respectively.Thus, distinct antiviral signaling pathways converge on CDK/cyclin repression, causing inhibition of viral DNA synthesis and replication. KEYWORDSAryl hydrocarbon receptor, interferon gamma, human immunodeficiency virus, herpes simplex virus, cyclin-dependent kinase, SAMHD1

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“…Bacteroides are associated with modulating intestinal inflammation and Proteobacteria with pro-inflammatory responses. Intestinal dysbiosis has been associated with increased microbial translocation and monocyte activation markers, and inferior disease outcome [ 54 ]. The increased microbial translocation suggests a breach in the intestinal permeability.…”

Section: Main Textmentioning

confidence: 99%

Invasive non-typhoidal Salmonella in sickle cell disease in Africa: is increased gut permeability the missing link?

et al. 2018

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Non-typhoidal Salmonella usually induces self-limiting gastroenteritis. However, in many parts of Africa, especially in individuals who are malnourished, infected with malaria, or have sickle cell disease, the organism causes serious and potentially fatal systemic infections. Since the portal of entry of non-typhoidal Salmonella into the systemic circulation is by way of the intestine, we argue that an increased gut permeability plays a vital role in the initiation of invasive non-typhoidal Salmonella in these patients. Here, we will appraise the evidence supporting a breach in the intestinal barrier and propose the mechanisms for the increased risks for invasive non-typhoidal Salmonella infections in these individuals.

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Altered gut microbiome composition in HIV infection

Cited by 90 publications

References 48 publications

The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression

The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression

The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression

Invasive non-typhoidal Salmonella in sickle cell disease in Africa: is increased gut permeability the missing link?

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