Prophage Gene Enhances Intracellular Survival of .

BACKGROUND

Induced by the pathogen , tuberculosis remains one of the most dangerous infectious diseases in the world. As a special virus, prophage is domesticated by its host and are major contributors to virulence factors for bacterial pathogenicity. The function of prophages and their genes in is still unknown.

METHODS

is a prophage gene in . We constructed recombinant () to observe bacteria morphology and analyze the resistance to various adverse environments. Recombinant and control strains were used to infect macrophages, respectively. Furthermore, we performed ELISA experiments of infected macrophages.

RESULTS

Rv2650c affected the spread of colonies of and enhanced the resistance of to macrophages and various stress agents such as acid, oxidative stress, and surfactant. ELISA experiments revealed that the Rv2650c can inhibit the expression of inflammatory factors TNF-α, IL-10, IL-1β, and IL-6.

CONCLUSION

This study demonstrates that the prophage gene can inhibit the spread of colonies and the expression of inflammatory factors and promote intracellular survival of . These results build the foundation for the discovery of virulence factors of , and provide novel insights into the function of the prophage in .