## 2 Results and Discussion
### The Host Transcriptome Upon Infection
Many prokaryotic species generate hydrogen sulfide, but the biochemistry and physiological role of this gas in non-sulfur utilizing bacteria remain largely unknown. However, the inactivation of key enzymes in sulfur metabolism in _Staphylococcus aureus, Bacillus anthracis, Pseudomonas aeruginosa_, and _Escherichia coli_ suppresses H2S production makes certain pathogens highly sensitive to a multitude of antibiotics [62]. The mechanism of H2S-mediated antibiotic resistance relies on the modification of oxidative stress imposed by antibiotics [62]. Is activation of sulfur metabolism a universal mechanism of preparing the cell to cope with environmental threats? We have previously reported that the H2S metabolism is activated in the marine bacterium _Shewanella haltica_ upon cold stress [63]. We suggested there that the cold stress may activate some metabolic preparation pathways for upcoming anaerobic conditions. In addition, a study by [PERSON] et al. revealed a profound impact of the Stx phage presence in _E. coli_ on carbon source utilization and sulfur metabolism [53]. The Stx2a prophage appears to reprogram the carbon metabolism of its bacterial host by turning down aerobic metabolism in favor of mixed acid fermentation [53]. It was shown that many sulfur metabolism pathways were upregulated [53]. Here, we also observed such changes and thus hypothesize that the upregulation of sulfur metabolism may be a general, non-specific cellular response to various environmental threats. _Summary of this section._ After analysis of the hosts' transcriptomes upon P1_vir_ infection, we found that intensive cellular reprogramming is held mostly at 30 min of infection. However, we also observed some important events unique to the _dk_s_A mutant at 10 min of infection, such as the upregulated expression of genes directly involved in the sulfur metabolism. How exactly P1_vir_ development benefits from this upregulation remains unclear, however, we speculate that this may be linked to obtaining new energy sourcesor global reprogramming via H\({}_{2}\)S signaling functions. Moreover, we have discovered downregulation of cold-shock genes and upregulation of heat shock genes. Since cold shock and heat shock proteins usually play multiple roles in bacterial cells, by employing globally-acting factors, the phage can efficiently take over the host metabolism. The shifting expression of global-acting regulators may be an elegant element of the control-taking strategy. By analyzing Gene Ontology terms, we can see how the host cells are reprogramed by P1_vir_ and how this reprogramming is reflected in cellular metabolism. In general, there are many similarities between metabolic responses of both hosts to phage infection. Phage P1_vir_ is taking control of the protein, sugar, lipid, and nucleotide metabolism. We observed downregulation of nonessential and energy-consuming bacterial processes, e.g., some biosynthetic pathways, and transport or response to DNA damage stimulus, and upregulation of processes essential for phage development, e.g., several catabolic processes or nucleotide biosynthesis. Both hosts are reacting by activating the SOS response or upregulating the heat shock proteins. We can also find interesting differences between the hosts in metabolic response to phage infection, which may reflect slightly different ways in which the phage executes its strategy for obtaining energy and resources during development. Upon infection, the _dk_s_A host upregulates transport of different molecules and several catabolic processes, including hydrogen sulfide biosynthesis, as well as the DNA replication process. Moreover, downregulated proteolysis in the _dk_s_A host in the later stage of infection may also influence the regulation of phage development. All of these observations fit into the \"minor improvements\" scenario that results in the enhanced development of P1_vir_ in a DksA-deficient host when combined.