Rv2617c and P36 are virulence factors of pathogenic mycobacteria involved in resistance to oxidative stress.

Virulence

Institute of Biotechnology, National Institute of Agricultural Technology (INTA, Instituto de Biotecnología, Instituto Nacional de Tecnología Agropecuaria) and IABIMO-National Scientific and Technical Research Council (CONICET, Consejo Nacional de Investigaciones Científicas y Tecnológicas), Hurlingham, Buenos Aires, Argentine.

Published: December 2019

In this study, we characterized the role of Rv2617c in the virulence of . Rv2617c is a protein of unknown function unique to complex (MTC) and , this protein interacts with the virulence factor P36 (also named Erp) and KdpF, a protein linked to nitrosative stress. Here, we showed that knockout of the gene in CDC1551 reduced the replication of the pathogen in a mouse model of infection and favored the trafficking of mycobacteria to phagolysosomes. We also demonstrated that Rv2617c and P36 are required for resistance to hydrogen peroxide treatment in and , respectively. These findings indicate Rv2617c and P36 act in concert to prevent bacterial damage upon oxidative stress.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930017PMC
http://dx.doi.org/10.1080/21505594.2019.1693714DOI Listing

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Rv2617c and P36 are virulence factors of pathogenic mycobacteria involved in resistance to oxidative stress.

Virulence

December 2019

Institute of Biotechnology, National Institute of Agricultural Technology (INTA, Instituto de Biotecnología, Instituto Nacional de Tecnología Agropecuaria) and IABIMO-National Scientific and Technical Research Council (CONICET, Consejo Nacional de Investigaciones Científicas y Tecnológicas), Hurlingham, Buenos Aires, Argentine.

In this study, we characterized the role of Rv2617c in the virulence of . Rv2617c is a protein of unknown function unique to complex (MTC) and , this protein interacts with the virulence factor P36 (also named Erp) and KdpF, a protein linked to nitrosative stress. Here, we showed that knockout of the gene in CDC1551 reduced the replication of the pathogen in a mouse model of infection and favored the trafficking of mycobacteria to phagolysosomes.

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