March 2019
https://www.sciencedirect.com/science/article/pii/S2452231718300356
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In the last decades, studies have revealed multiple and strong correlations between the host and its commensal microbiota consisting of bacteria, protozoa, fungi and viruses. This associated microbiota can positively or negatively influence the course of a wide range of infections. Here, we review the interactions between the host and its viral microbiota and discuss new paradigms from an evolutionary perspective. The viral adaptation to a microbial environment in a co-evolutionary approach is highlighted, as well as viral cross transmission in the context of the barriers imposed by the indigenous microbiota. In addition to reviewing the host-microbiota-virus relationships, we focus the discussion on microbiota-virus interactions that could be applied to preventive and therapeutic treatments.
1. Introduction
Viruses are the most abundant biological entities on Earth and have evolved with prokaryotes and eukaryotes for thousands of years. The abundance of viruses varies according to the environment and sometimes is relative to bacterial activity and colonization [1]. The human gut harbors a dense and complex microbial ecosystem, with presents not only prokaryotic and eukaryotic organisms but also viruses (virobiota, and their genes – virome). This indigenous microbiota can be associated with the host cells (eukaryotic virobiota) or with some of the approximately 2776 prokaryotic species that inhabit it (prokaryotic virobiota) and this interation may be beneficial or detrimental to the host [2]. An example of a positive effect is the adherence of phages to mucus forming an antimicrobial barrier in various host mucosal surfaces [3]. This co-evolutionary mechanism is called “non-host-derived immunity” and acts primarily controlling the abundance and equilibrium of bacterial populations [3], [4]. The evolutionary battle between viruses and prokaryotes was reported in the last years by studies on the “Kill the Winner” hypothesis, horizontal genetic exchange, CRISPR-encoding bacteria and viral anti-CRISPR proteins [5], [6], [7]. Investigation of these relationships has provided important biotechnological tools that can be used for genetic engineering such as CRISPR-Cas9 genome editing human cells [6].
Recent studies have shown that the host’s normal microbiota is able to influence the infections caused by various families of animal viruses [8], [9], [10]. Microbiota-virus interactions have been studied in germ-free mice or antibiotic-treated mice models highlighting the opposing modulating effects of commensal bacteria on the course of viral infections [9], [10]. Commensal bacteria can potentially influence viral infections either hindering or promoting the viral infection and sometimes aggravate the disease [8], [9]. Bacteria commonly isolates from human nasopharynx as Staphylococcus aureus, Pseudomonas species, Streptococcus pneumonia, Haemophilus influenzae and Streptococcus pyogenes has been associated with increased risk of death in adults and children infected with influenza [11].
This review highlights the important role of microbiota-virus interactions through an evolutionary perspective, emphasizing the viral adaptations to the microbial environment and the use of available resources by viruses. The cooperation or the competition with other components of the indigenous microbiota, as well as the co-evolution with host and viral cross-species transmission in the context of the barriers imposed by the endogenous microbiota are also addressed.
2. Viruses versus microbial ecosystem
Viral particles face numerous host-related challenges to reach the permissive cells, such as tissue specificities, body temperature and epithelial secretions including IgA, defensins and a mucus barrier, as well as environmental modifications due to microbiota metabolism and cellular composition such as pH, redox potential, lipopolysaccharide (LPS) and glycans. The gastrointestinal microbiota is the most complex and diverse ecosystem in mammals, quite different when compared to those present in other body sites, and there is a considerable variation in the constituents of the gut microbiota among apparently healthy individuals [12].
The presence of the microbiota or its products is associated with increases in the viral fitness for all enteric viruses studied so far, including Enterovirus C (poliovirus) [13], [14], Mammalian reovirus [13], Rotavirus A [15], Norwalk virus (norovirus) [16], [17], [18], [19] and Mouse mammary tumor virus (MMTV) [20], [21] (an enteric retrovirus). In this context, some findings suggest different mechanisms by which the enteric viruses could use bacteria and their products to withstand environmental adversities and cross the host cell barriers.
A study of poliovirus was the first to show that viral exposure to bacteria enhanced host cell binding and infection by the virus [13]. The enhancement of viral infectivity did not require live bacteria, and the presence of bacterial surface polysaccharides, including LPS and peptidoglycan (PGN), was sufficient [13]. LPS is the major cell wall component of Gram-negative bacteria with highest concentrations in the gut lumen [22]. Poliovirus can use LPS to promote attachment to the surface of permissive cells through direct facilitation of viral binding to its poliovirus receptor (Fig. 1A). In addition, LPS can enhance virion environmental stability by increasing its thermostability and resistance to chlorine bleach [13], [14]. A specific residue in the capsid protein of poliovirus VP1 was shown to be crucial for stabilization, and this ability is important to prevent premature conformational changes before uncoating [14] (Fig. 1B). A mechanism similar to the LPS-mediated stimulation of poliovirus was observed for human norovirus when it was discovered that it could infect human B cells [16]. Some specific commensal bacteria express a glycan called histo-blood group antigen (HBGA) that correlated with the ability of norovirus to attach and infect B cells [18]. The isolated HBGA was sufficient to stimulate viral attachment to the surface of B cells [19] (Fig. 1C) by using a mechanism apparently very similar to that of poliovirus-LPS attachment to its host receptor. However, the receptor used by human norovirus remains unknown precluding an understanding of the mechanism by which bacterial HBGA stimulates viral attachment [19].
This long article continues at: https://www.sciencedirect.com/science/article/pii/S2452231718300356
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