Abstract
Viruses are obligate intracellular pathogens that require the protein synthesis machinery of the host cells to replicate. These microorganisms have evolved mechanisms to avoid detection from the host immune innate and adaptive response, which are known as viral evasion mechanisms. Viruses enter the host through skin and mucosal surfaces that happen to be colonized by communities of thousands of microorganisms collectively known as the commensal microbiota, where bacteria have a role in the modulation of the immune system and maintaining homeostasis. These bacteria are necessary for the development of the immune system and to prevent the adhesion and colonization of bacterial pathogens and parasites. However, the interactions between the commensal microbiota and viruses are not clear. The microbiota could confer protection against viral infection by priming the immune response to avoid infection, with some bacterial species being required to increase the antiviral response. On the other hand, it could also help to promote viral evasion of certain viruses by direct and indirect mechanisms, with the presence of the microbiota increasing infection and viruses using LPS and surface polysaccharides from bacteria to trigger immunosuppressive pathways. In this work, we reviewed the interaction between the microbiota and viruses to prevent their entry into host cells or to help them to evade the host antiviral immunity. This review is focused on the influence of the commensal microbiota in the viruses' success or failure of the host cells infection.
Highlights
The mucosal surfaces of the human body contain complex communities of microorganisms collectively referred to as microbiota; these bacteria are a key factor in health and disease due to their participation in the development of the immune system and their host-protection against pathogens (Human Microbiome Project Consortium, 2012a,b; Lloyd-Price et al, 2016).Viruses are a large and heterogeneous group of dependent biological agents that require the hostcell machinery to replicate
It was supposed that bacteria removal, by antibiotics or the lack of these microorganisms in germ-free models, would increase the predisposition to viral infections; on the other hand, it was found that microbiota ablation decreases the infectivity of pathogenic viruses
Most viruses access the human body through mucosal surfaces that are traditionally described as rich in a diversity of commensal pathogens
Summary
The mucosal surfaces of the human body contain complex communities of microorganisms collectively referred to as microbiota; these bacteria are a key factor in health and disease due to their participation in the development of the immune system and their host-protection against pathogens (Human Microbiome Project Consortium, 2012a,b; Lloyd-Price et al, 2016). Vancomycin treatment in healthy adults improves RV vaccine immunogenicity and RV shedding through the increase of Proteobacteria and a reduction in Bacteroidetes (Harris et al, 2018) These studies show that the complete commensal microbiota downregulates the antiviral response to RV infection and only particular taxa can enhance the immunity against viruses. It was reported that bacterial flagellin promotes viral infection in an in vitro model using lentiviral pseudoviruses encoding the glycoproteins of influenza, Measles, Ebola, Lassa, and Vesicular stomatitis virus in pulmonary epithelial cell culture through TLR5 and NF-κB activation (Benedikz et al, 2019) This finding is exciting since previously, it was reported that flagellin had a protective effect against RV infection in mice (Zhang et al, 2014). This represents a clear example of a virus-bacteria-virus interaction that ends in increased susceptibility to the disease, in this case, head and neck cancer
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