ABSTRACT The oral cavity, as the entry point to the body, may play a critical role in the pathogenesis of SARS-CoV-2 infection that has caused a global outbreak of the coronavirus disease 2019 (COVID-19). Available data indicate that the oral cavity may be an active site of infection and an important reservoir of SARS-CoV-2. Considering that the oral surfaces are colonized by a diverse microbial community, it is likely that viruses have interactions with the host microbiota. Patients infected by SARS-CoV-2 may have alterations in the oral and gut microbiota, while oral species have been found in the lung of COVID-19 patients. Furthermore, interactions between the oral, lung, and gut microbiomes appear to occur dynamically whereby a dysbiotic oral microbial community could influence respiratory and gastrointestinal diseases. However, it is unclear whether SARS-CoV-2 infection can alter the local homeostasis of the resident microbiota, actively cause dysbiosis, or influence cross-body sites interactions. Here, we provide a conceptual framework on the potential impact of SARS-CoV-2 oral infection on the local and distant microbiomes across the respiratory and gastrointestinal tracts (‘ oral-tract axes ’), which remains largely unexplored. Studies in this area could further elucidate the pathogenic mechanism of SARS-CoV-2 and the course of infection as well as the clinical symptoms of COVID-19 across different sites in the human host.
【저자키워드】 severe acute respiratory syndrome coronavirus 2, Angiotensin-converting enzyme 2 (ACE2), microbiota, oral-gut axis, oral-lung axis, 【초록키워드】 COVID-19, coronavirus disease, SARS-CoV-2, Diseases, SARS-COV-2 infection, Infection, lung, Local, virus, outbreak, Microbiome, gut microbiota, Critical, microbial community, interactions, mechanism, gastrointestinal tract, homeostasis, COVID-19 patients, Interaction, Gut, clinical symptom, alteration, human host, pathogenic, pathogenesis of SARS-CoV-2, Host, Alter, Course, caused, occur, 【제목키워드】 SARS-CoV-2, Infection, Host, implication, Potential,