It is known that cadaverine negatively interferes with the invasive process and it is likely that it has been lost during the initial steps of the pathoadaptation process. In turn, the lack of cadaverine may have induced an increased putrescine level, as we have observed in our EIEC collection and reproduced in an E. coli K-12 background. Since putrescine is a relevant intermediate in the synthesis of spermidine and, consequently, of N-acetyspermidine, an increase in putrescine may well have caused higher levels of both, spermidine and Nacetylspermidine. The inactivation of the speG gene would represent the last step, favouring the accumulation of spermidine and enhancing the survival in oxidative environments. In this view, the loss of speGfunction has already occurred in Shigella spp. and, banking on our data, could be regarded as an ongoing process in EIEC. In both microorganisms, the lack of speG increases the resistance to oxidative stress and confers higher survival within macrophages. Altogether, our observations agree well with the hypothesis that EIEC are an intermediate step during the transition of E. coli towards a full-blown Shigella phenotype, and further clarify mechanisms and strategies adopted by these bacterial pathogens during the infectious processes. The liver diseases caused by hepatitis B virus and hepatitis C virus infection are among the most important human health problems. The immunopathogenesis of virus infection and the development of antiviral drugs are hampered by the lack of suitable mouse models for both pathogens, because the mouse cannot be infected by HBV or HCV. Although chimpanzees are susceptible to both infections, their usage is limited by cost, availability, and ethical considerations. Other surrogate hepatotrophic viruses that infect ducks, woodchucks, and ground squirrels have been widely used to study virus VE-822 biology, however, they suffer from two important limitations: on the microbial side, surrogate viruses are genetically divergent from highly restricted human counterparts; and on the host side, the immunological studies in genetically outbred and immunologically uncharacterized hosts are difficult. HBV-transgenic mice have provided invaluable information on immunopathogenesis of HBV, whereas transgenic mice are immunologically tolerant to transgene products. Hydrodynamic transfection of the mouse liver by the HBV genome has also been reported to study HBV immunobiology, but it does not support bona fide viral infection. Therefore, a robust and reproducible mouse model of HBV or HCV infection is desperately needed, and studies based on chimeric mice appear to be the most promising. Establishing a chimeric mouse with a reconstituted liver and immune system derived from a single donor is critical to study MHC-restricted immune responses against pathogen-infected, transformed or autoimmune hepatocytes in a physiologic setting.