The Role of Infant and Early Childhood Gut Virome in Immunity and the Triggering of Autoimmunity-A Narrative Review

Abstract

Background: The bacterial gut microbiome has been the subject of many studies that have provided valuable scientific conclusions. However, many different populations of microorganisms that interact with each other to maintain homeostasis coexist inside the gut. The gut virome, especially, appears to play a key role in this interactive microenvironment. Intestinal viral communities, including bacteriophages, appear to influence health and disease, although their role has not yet been fully elucidated. In addition, bacteriophages or viruses that infect bacteria regulate bacterial growth, thus shaping the composition of the gut microbiome and affecting the immune system. Infant Gut Virome: The shaping of the gut microbiome during the first years of life has a significant role in the maturation of the infant's immune system. In contrast, early dysbiosis has been associated with chronic, including metabolic and autoimmune, disorders later in life. Purpose: Although viruses have been shown to be potential triggers of autoimmune diseases, there is a gap in the literature regarding the infant gut virome in autoimmunity development. Despite the lack of evidence, this review attempts to summarize and clarify what is known so far about this timely and important topic in the hope that its findings will contribute to future research.

Keywords: autoimmunity; bacteriophages; gut microbiome; gut virome; immune system; infant; neonates.

Figure 1

Changes in gut virome composition at different stages of human life.

Figure 2

Gut bacteriophages and immune system. TLR: Toll-like receptor, RIG-I: retinoic acid inducible gene I, cGAMP: cyclic-GMP-AMP synthase, NF-κB: nuclear factor-κB, IRF: interferon regulatory factor, IFN-I: type I interferon, IL: interleukin, and CXCL-10: C-X-C chemokine motif ligand 10.

Figure 3

Eukaryotic viruses and immune system. TLRs: Toll-like receptors, RIG-I: retinoic acid inducible gene I, MDA5: melanoma differentiation-associated protein 5, NLRs: Nod-like receptors, IFN: interferon, and VRE: vancomycin-resistant enterococcus.

Figure 4

Molecular mechanisms possibly involved in the development of T1DΜ. TNF: tumor necrosis factor, IFN: interferon, and IL: interleukin.

Figure 5

Early childhood gut virome as trigger of autoimmune diseases. T1DM: Type 1 diabetes mellitus and CD: celiac disease.

Figure 6

Molecular mechanisms possibly involved in the development of autoimmune diseases.