## 3 Bacteriophages  
Bacteriophages are viruses that exclusively infect bacteria. Although there were arguments regarding the discovery of phages, it has been acknowledged that the first scientists to discover the phages were [PERSON] and [PERSON] [82; 83]. [PERSON], an English medical bacteriologist, postulated that viruses were the causative agents of this phenomenon after observing a similar process in Micrococcus [84; 85; 86]. According \begin{table}
\begin{tabular}{p{113.8 pt} p{113.8 pt} p{113.8 pt}} \hline \hline
**Virulence Factor** & **Gene** & **Role in Pathogenesis** & **References** \\ \hline Shiga toxin & _stx1_ (a, c, and d) and strx2 (a to g) & Stx toxin is composed of 2 subunits, A and B. The A subunit is an RNA-glycosate that interacts with the 60S rRNA, inhibiting protein synthesis, causing cell death. & [76] \\ \hline Locus of Entrocyte Effacement (LEE) pathogenicity island (PAI) & _lor_ & \begin{tabular}{l} LEE-PAI encodes several genes like _ehu_A, _ehu_B, and _ehu_J, which are involved in the adhesion mechanism called the attaching-and-effacing (A/E) lesion, such as type III secretion system (TTSS), an outer membrane adhesion (intimin), its translocated intimin receptor (TIR), and secreted proteins with signal transduction. \\ \end{tabular} & [77] \\ \hline Intimin & _enc_ & \begin{tabular}{l} The eae gene is carried by the LEE-PAI and encodes an outer membrane adhesion protein called Intimin. This protein interaction with the bacterial translocated intimin receptor (Tir) leads to the attachment of the STEC cell to the host intestinal mucosa, resulting in the A/E lesions \\ \end{tabular} & [76; 78] \\ \hline EHEC hemolysin (EHEC-_hly_) & _elix_A or EHEC-_hly_A & \begin{tabular}{l} EHEC-_hly_A is part of an operon composed of four genes (EHEC-_hly_C, EHEC-_hly_A, EHEC-_hly_B, and EHEC-_hly_C) encoded on the OP157 \\ plasmid. EHEC-_hly_A codes the structural protein of EHEC-Hly. The proteins coded by EHEC-_hly_B and EHEC-_hly_D are responsible for the transport of EHEC-Hly out of the bacterial cell, and in its turn, \\ EHEC-_hly_C product is responsible for EHEC-Hly post-translational activation. EHEC-Hly is responsible for forming pores into the cell membrane and is found as free or in association with outer membrane vesicles (OMy). Both forms target the human intestinal epithelial and microvascular endothelial cells, but in different manners. When in the free form, EHEC-Hly is responsible for lysing the cells, but when in association with OMV, induces cell apoptosis. \\ \end{tabular} & \begin{tabular}{l} Immunoglobulin-binding (Eib) G is encoded by the gene _eib_G, and it can bind to human IgG and IgA. It can also participate in bacterial adhesion to host epithelial cells. Toxin Efa-1 is like LiAfA and ToveB, and they are thought to be associated with cell adherence, lymphostatin activity, or induction of secretion of type III effectors in the STEC strain. \\ \end{tabular} & [78] \\ \hline Serine protease autotransporters & _esp_P & \
\begin{tabular}{l} Encoded on the OP157 plasmid, it is important for biofilm formation and for adherence to T84 intestinal epithelial cells. \\ \end{tabular} & [78] \\ \hline Long Polar Fimbirae and _E. coli_ YcbQ laminin-binding fimbrie (ELF) & lfp and elf &
\begin{tabular}{l} Able to attach the extracellular matrix protein laminin, which contributes to colonization of the GI tract \\ \end{tabular} & [76] \\ \hline \hline \end{tabular}
\end{table} 
Table 1: Key virulence factors associated with _E. coli_ O157:H7 and their function in pathogenesis. to [PERSON] findings, the presence of an imperceptible microorganism was detected in stool samples obtained from dysentery patients, which were devoid of bacteria due to filtration [87]. The occurrence of clear zones observed in bacterial lawns can be attributed to the presence of \"invisible germs\". [PERSON] provided the initial elucidation regarding the mechanism by which these viruses proliferate by exploiting bacteria, resulting in the death and subsequent disintegration of the bacteria.