Abstract:
SARS-CoV-2 has become one of the most studied viruses of the last century. It was assumed that the only possible host for these types of viruses was mammalian eukaryotic cells. Our recent studies show that microorganisms in the human gastrointestinal tract affect the severity of COVID-19 and for the first time provide indications that the virus might replicate in gut bacteria. In order to further support these findings, in the present work, cultures of bacteria from the human microbiome and SARS-CoV-2 were analyzed by electron and fluorescence microscopy. The images presented in this article, in association with the nitrogen (15 N) isotope-labeled culture medium experiment, suggest that SARS-CoV-2 could also infect bacteria in the gut microbiota, indicating that SARS-CoV-2 could act as a bacteriophage. Our results add new knowledge to the understanding of the mechanisms of SARS-CoV-2 infection and fill gaps in the study of the interactions between SARS-CoV-2 and non-mammalian cells. These findings could be useful in suggesting specific new pharmacological solutions to support the vaccination campaign.
Interesting findings.
Our previous work showed that people with COVID-19 had toxin-like peptides, which were almost identical to the toxic components of animal venoms, such as conotox, phospholipases A2, phosphodiesterases, zinc metal proteinases, and bradykinins, in both blood, feces, and urine [6]. In a later study, we observed spontaneous replication of SARS-CoV-2 in bacterial cultures from patient feces for up to 30 days and beyond [7,8]. For that matter, there have also been other researchers who have studied the relationship between the gut microbiota and COVID-19. Wang et al., 2021, for example, found significant alterations in the gut and respiratory microbiome in COVID-19 patients, finding that there was an increase in pathogenic bacteria and a decrease in beneficial ones [9].
[…]
Another very interesting finding emerged from a bioinformatics analysis that revealed that some members of commensal upper respiratory tract (URT) bacteria express proteins that bind the SARS-CoV-2 spike glycoprotein, for example the ACE2-like protein. Based on this analysis and available data showing a decline in the population of these bacteria in the elderly, it has also been proposed that some commensal bacteria of the upper respiratory tract prevent SARS-CoV-2 infectivity and that a decrease in these bacteria contributes to infection severity [11]. The same authors, in another study observed that N501Y mutations in the receptor-binding domain (RBD) of the SARS-CoV2 spike glycoprotein may allow increased binding to the ACE2 receptor when natural products (NPs) of upper respiratory tract bacteria are present [12].