The Commensal Microbiota and Viral Infection: A Comprehensive Review

Abstract

The human body is inhabited by a diverse microbial community that is collectively coined as commensal microbiota. Recent research has greatly advanced our understanding of how the commensal microbiota affects host health. Among the various kinds of pathogenic infections of the host, viral infections constitute one of the most serious public health problems worldwide. During the infection process, viruses may have substantial and intimate interactions with the commensal microbiota. A plethora of evidence suggests that the commensal microbiota regulates and is in turn regulated by invading viruses through diverse mechanisms, thereby having stimulatory or suppressive roles in viral infections. Furthermore, the integrity of the commensal microbiota can be disturbed by invading viruses, causing dysbiosis in the host and further influencing virus infectivity. In the present article, we discuss current insights into the regulation of viral infection by the commensal microbiota. We also draw attention to the disruption of microbiota homeostasis by several viruses.

Keywords: antibiotics; antiviral immunity; commensal microbiota; germ-free; virus; virus infectivity.

Figure 1

Mechanisms underlying the suppression of influenza virus infection by the commensal microbiota. During the influenza virus infection, organisms of the commensal microbiota, as well as their components (i.e., various TLR ligands) or metabolites (i.e., desaminotyrosine) activate the inflammasome, resulting in IL-1β and IL-18 production. The production of these two cytokines induces the migration of dendritic cells from the lung to the draining lymph nodes, where they act as antigen-presenting cells to prime virus-specific B cells, CD4⁺ T cells, CD8⁺ T cells, and macrophages. In addition, dendritic cells also secrete type I and type II interferons to stimulate the activation of T cells or macrophages. As a result, these effector cells secrete virus-specific antibodies or inflammatory cytokines or exert direct virus-killing effects to suppress the infection process of the influenza virus.

Figure 2

Mechanisms underlying the suppression of vaccinia virus infection by the commensal microbiota. During the vaccinia virus infection, the commensal microbiota primes virus-specific CD8+ T cells to secrete large amounts of IFN-γ, which critically mediates the corresponding antiviral immunity. In addition, during vaccinia virus infections, the activation of TLR2 by bacterial products is essential for recruiting mast cells to sites of viral infection. These mast cells also contribute to suppressing the viral infection by secreting an antiviral cathelicidin.