The disbalance of the renin-angiotensin system was suggested to play an important role in the pathogenesis of the COVID-19 disease. Previously it has been shown that ACE2 expression in downregulated in the murine model in response to SARS-CoV infection and may be also induced by the recombinant spike protein alone. In case of natural infection the circulation of a soluble form of S protein is unlikely, however upon the transition into the fusion conformation, the S1 particles carrying the receptor-binding domains get separated from the membrane-bound moiety S2. The fate of the S1 particles liberated due to spontaneous firing of the S protein trimers exposed on the virion and on the external surface of the infected cells was never investigated.  We hypothesize that the soluble SARS-CoV-2 spike protein S1 subunits shed from the infected cells and from the virions in vivo may bind to the ACE2 receptor and trigger ACE2 downregulation.  Decreased ACE2 activity on the background of the constant or increased ACE activity in the lungs may lead to the prevalence of angiotensin II effects over angiotensin(1-7) connected to increased thrombosis, inflammation and pulmonary damage. This mechanism also suggests the link between the lowered S1 particles shedding reported for the S protein with D614G  mutation and the lack of  the elevated severity of the COVID-19 caused by the corresponding lineage of SARS-CoV-2 virus, despite the fact that is features increased infectivity and develops higher viral loads in vivo.

Acquisition of new prophages that are able to increase the bacterial fitness by lysogenic conversion is believed to be important strategy of bacterial adaptation to changing environment. However, in contrast to the factors determining the range of bacteriophage lytic activity, little is known about the factors that define the lysogenization host range. Bacteriophage phi24B is the paradigmal model of stx-converting phages, encoding the toxins of the Shiga-toxigenic E. coli (STEC). This virus has been shown to lysogenize the wide range of E. coli strains that is much broader than the range of the strains supporting its lytic growth. Therefore, phages produced by the STEC population colonizing the small intestine are potentially able to lysogenize symbiotic E. coli in the hindgut, and these secondary lysogens may contribute to the overall patient toxic load and to lead to the emergence of new pathogenic STEC strains. We demonstrate, however, that O antigen effectively limit the lysogenization of the wild E. coli strains by phi24B phage. The lysogens are formed from the spontaneous rough mutants and therefore have increased sensitivity to other bacteriophages and to the bactericidal activity of the serum if compared to their respective parental strains.