# Transcription of _Listeria monocytogenes_ Key Virulence Genes on Tomato, Cucumber and Carrot
## 1 Introduction  
_Listeria monocytogenes_ is the etiological agent of foodborne listeros, the latest reports on which mention in the United States of America a total of 32 illnesses, 31 hospitalizations and 3 deaths (2017 annual report available at [[https://www.cdc.gov/fdoss/annual-reports/index.html](https://www.cdc.gov/fdoss/annual-reports/index.html)]([https://www.cdc.gov/fdoss/annual-reports/index.html](https://www.cdc.gov/fdoss/annual-reports/index.html)) (accessed on 20 May 2021)) and in the EU a total of 2621 confirmed cases, 1339 hospitalizations and 300 deaths (2019 annual report available at [[https://www.efsa.europa.eu/en/efsajournal/pub/6406](https://www.efsa.europa.eu/en/efsajournal/pub/6406)]([https://www.efsa.europa.eu/en/efsajournal/pub/6406](https://www.efsa.europa.eu/en/efsajournal/pub/6406)) (accessed on 20 May 2021)). The virulence potential of this foodborne pathogen relies on the ability to cross the intestinal epithelial cells, escape from host defensive responses and disseminate through lymph and blood [1]. This infection requires the coordinated expression of a series of genes, including _hly_, _plcA_, _plcB_, _inI_A, _inB_, _inCl_ and _inI_]. _hly_ encodes for listeriolysin O (LLO) a cholesterol-dependent pore-forming toxin that, among several functions, it facilitates internalization into host cells and escape from host phagosomes through a pore-dependent mechanism [2]. _plcA_ and _plcB_ encode for phosphatidylinositol phospholipase C and phosphatidylcholine phospholipids C, respectively. The cooperation of both phospholipipases with LLO is required for escape of the pathogen from the phagocytic vacuole [3]. Internalins InIA, InIb, InIC and InI] are necessary for effective invasion. InIA and InIB bind to E-cadherin and the hepatocyte growth factor receptor, respectively, which are receptors of the eukaryotic cell membrane. In both cases, bacterial endocytosis is induced [1]. InIC enables cell-to-cell spread of the pathogen by facilitating the formation of protrusions in the cell membrane of apical junctions [4]. InI] is also important, as suggested by the significantly attenuated virulence capacity of the deletion mutant [5]; however, the mode of action is yet to be identified. The transcriptional control of these genes has been assigned to the alternative sigma factor B (\(\sigma^{\text{B}}\)) and the positive regulatory factor A (Prfa). The alternative sigma factor B is encoded by _sigB_ and has a key role in \(L\)_monocytogenes_ survival in nature and inthe gastrointestinal tract. It controls the transcription of more than 200 genes, affecting substantially _L. monocytogenes_ responses to environmental stimuli and virulence [6]. The latter is achieved through the transcriptional control of several virulence-associated genes, including _prfA_. The latter encodes PrfA that directly regulates transcription of twelve key virulence genes and indirectly a total of 145 genes. Thus, it possesses a key role in directing cellular homeostasis and fine-tuning the virulence machinery of _L. monocytogenes_[7]. The effect that several factors associated with food processing may have on the transcription of genes related to _L. monocytogenes_ virulence has been studied to some extent. However, only a few studies address the combined effect that the food matrix, storage time and temperature as well as strain diversity may have. More accurately, [PERSON] et al. [8], [PERSON] et al. [9], [PERSON] et al. [10, 11] and [PERSON] et al. [12] studied the transcription of key virulence genes of the pathogen on meat products, [PERSON] et al. [13] and [PERSON] et al. [14] on fish products, [PERSON] et al. [11] and [PERSON] et al. [15] on dairy products and [PERSON] et al. [16] and [PERSON] et al. [17] on fruits and vegetables.