HIV, Cancer, and the Microbiota: Common Pathways Influencing Different Diseases

Herrera, Sabina; Martínez-Sanz, Javier; Serrano‐Villar, Sergio

doi:10.3389/fimmu.2019.01466

Cited by 17 publications

(10 citation statements)

References 129 publications

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“…Exposure of HSCs to HIV-1 results in the production of reactive oxygen species (ROS), and expression of collagen and tissue inhibitor of matrix metalloproteinases-1 (TIMP1) [ 35 ]. These events, together with abnormalities in the gut microbial communities, significantly contribute to the high rates of liver cancer in PLWH [ 36 ] ( Figure 1 ).…”

Section: Prevalence Of Non-aids Defining Cancers Increases Despitementioning

confidence: 99%

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Isaguliants

Bayurova

Avdoshina

et al. 2021

Cancers

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People living with human immunodeficiency virus (HIV-1) are at increased risk of developing cancer, such as Kaposi sarcoma (KS), non-Hodgkin lymphoma (NHL), cervical cancer, and other cancers associated with chronic viral infections. Traditionally, this is linked to HIV-1-induced immune suppression with depletion of CD4+ T-helper cells, exhaustion of lymphopoiesis and lymphocyte dysfunction. However, the long-term successful implementation of antiretroviral therapy (ART) with an early start did not preclude the oncological complications, implying that HIV-1 and its antigens are directly involved in carcinogenesis and may exert their effects on the background of restored immune system even when present at extremely low levels. Experimental data indicate that HIV-1 virions and single viral antigens can enter a wide variety of cells, including epithelial. This review is focused on the effects of five viral proteins: envelope protein gp120, accessory protein negative factor Nef, matrix protein p17, transactivator of transcription Tat and reverse transcriptase RT. Gp120, Nef, p17, Tat, and RT cause oxidative stress, can be released from HIV-1-infected cells and are oncogenic. All five are in a position to affect “innocent” bystander cells, specifically, to cause the propagation of (pre)existing malignant and malignant transformation of normal epithelial cells, giving grounds to the direct carcinogenic effects of HIV-1.

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Section: Prevalence Of Non-aids Defining Cancers Increases Despitementioning

confidence: 99%

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Isaguliants

Bayurova

Avdoshina

et al. 2021

Cancers

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show abstract

“…While some authors advocate a similar oral bacterial microbiome between human immunodeficiency virus (HIV) patients and healthy individuals [180,181], others have found considerably reduced microbial diversity amongst HIV-positive persons, with increased abundance of the pathogenic genera Megasphaera, Campylobacter, Veillonella and Prevotella, and decreased abundance of commensal forms such as Lactobacillus and Streptococcus species [46,177]. Indeed, the gut microbiome in HIV infection resembles many other proinflammatory conditions such as inflammatory bowel disease of the gut [182].…”

Section: The Prodigy Of Hiv and All Players Of The Microbiomementioning

confidence: 99%

The Role of the Microbiome in Oral Squamous Cell Carcinoma with Insight into the Microbiome–Treatment Axis

Sami

Elimairi

Stanton

et al. 2020

IJMS

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Oral squamous cell carcinoma (OSCC) is one of the leading presentations of head and neck cancer (HNC). The first part of this review will describe the highlights of the oral microbiome in health and normal development while demonstrating how both the oral and gut microbiome can map OSCC development, progression, treatment and the potential side effects associated with its management. We then scope the dynamics of the various microorganisms of the oral cavity, including bacteria, mycoplasma, fungi, archaea and viruses, and describe the characteristic roles they may play in OSCC development. We also highlight how the human immunodeficiency viruses (HIV) may impinge on the host microbiome and increase the burden of oral premalignant lesions and OSCC in patients with HIV. Finally, we summarise current insights into the microbiome–treatment axis pertaining to OSCC, and show how the microbiome is affected by radiotherapy, chemotherapy, immunotherapy and also how these therapies are affected by the state of the microbiome, potentially determining the success or failure of some of these treatments.

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“…The significance of gut microbiota in the maintenance of health has recently attracted considerable attention, as increasing evidence demonstrates that the gut microbiota regulates various physiological functions of the host (1)(2)(3)(4). In accordance with this, it has been shown that dysbiosis of the intestinal ecosystem is correlated with a wide variety of diseases, including inflammatory bowel disease, allergy, cancer, autism, and metabolic syndrome (3,(5)(6)(7)(8)(9). Although it is difficult to determine whether such differences in gut microbiota are the cause or the result of these diseases, studies have demonstrated that change in microbiota or specific bacteria is actually involved in the onset, pathogenesis, and prevention of the diseases (10)(11)(12).…”

Section: Introductionmentioning

confidence: 92%

Regulation of Gene Expression through Gut Microbiota-Dependent DNA Methylation in Colonic Epithelial Cells

et al. 2020

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A huge number of commensal bacteria inhabit the intestine, which is equipped with the largest immune system in the body. Recently, the regulation of various physiological functions of the host by these bacteria has attracted attention. In this study, the effects of commensal bacteria on gene expression in colonic epithelial cells (CoECs) were investigated with focus on regulation of DNA methylation. RNA sequencing analyses of CoECs from conventional, germ-free, and MyD88 2/2 mice indicated that, out of the genes affected by commensal bacteria, those downregulated in a MyD88-independent manner were most frequently observed. Furthermore, when the 59 regions of genes downregulated by commensal bacteria in CoECs were captured using a customized array and immunoprecipitated with the anti-methyl cytosine Ab, a certain population of these genes was found to be highly methylated. Comprehensive analysis of DNA methylation in the 59 regions of genes in CoECs from conventional and germ-free mice upon pulldown assay with methyl-CpG-binding domain protein 2 directly demonstrated that DNA methylation in these regions was influenced by commensal bacteria. Actually, commensal bacteria were shown to control expression of Aldh1a1, which encodes a retinoic acid-producing enzyme and plays an important role in the maintenance of intestinal homeostasis via DNA methylation in the overlapping 59 region of Tmem267 and 3110070M22Rik genes in CoECs. Collectively, it can be concluded that regulation of DNA methylation in the 59 regions of a specific population of genes in CoECs acts as a mechanism by which commensal bacteria have physiological effects on the host.

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HIV, Cancer, and the Microbiota: Common Pathways Influencing Different Diseases

Cited by 17 publications

References 129 publications

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind

The Role of the Microbiome in Oral Squamous Cell Carcinoma with Insight into the Microbiome–Treatment Axis

Regulation of Gene Expression through Gut Microbiota-Dependent DNA Methylation in Colonic Epithelial Cells

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