Could SARS-CoV-2 Have Bacteriophage Behavior or Induce the Activity of Other Bacteriophages?

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 (15N) 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.

Gut microbiota in COVID-19: key microbial changes, potential mechanisms and clinical applications

“…(2) SARS-CoV-2 infection was found to downregulate the expression of angiotensin-converting enzyme 2 (ACE2) and B0AT1 (a molecular ACE2 chaperone) on the luminal surfaces of intestinal epithelial cells, which may facilitate the growth of the pathogens 25 , 113 , 114 . (3) An in vitro study found that SARS-CoV-2 might directly infect bacteria 115 . In the second part, we propose that specific intrinsic ‘microbiome signatures’ at the point of SARS-CoV-2 infection could influence the severity of infection and host immune response by several putative mechanisms: (i) increased opportunistic pathogens might be further recognized by innate lymphocytes and intensify gut pro-inflammatory responses 185 .…”

The potential role of ischaemia–reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications

“…[ 19 , 682 ]). To this end, the suggestion of Brogna et al [ 683 ] that SARS-CoV-2 could act like a bacteriophage and use bacteria as replication hosts is of especial interest. The gut microbiome does of course contain many trillions of organisms [ 684 , 685 ], contributes massively to immunity and inflammation [ 686 ], provides a clear pathway between diet and health [ 687 ], and would be the most logical place for such a reservoir to persist.…”

GRP78, a Novel Host Factor for SARS-CoV-2: The Emerging Roles in COVID-19 Related to Metabolic Risk Factors

“…The bacterial GRP78 is essentially required for proper bacterial growth and mRNA/protein [ 84 ], and is a therapeutic target for both bacterial and viral infection [ 85 ]. Of note, SARS-CoV-2 is detected alive in feces specimens from COVID-19 patients [ 3 , 4 ]; SARS-CoV-2 has bacteriophage-like behavior, replicating in bacteria [ 86 ]; SARS-CoV-2 infection impairs gastrointestinal (GI) microbiota, which is associated with COVID-19 severity [ 87 ]. These data suggest that the interaction of GRP78 with SARS-CoV-2 could contribute to replication/transmission by GI/fecal bacteria, impair the microbiota, and affect the severity of COVID-19.…”