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We propose that these phenotypic manifestations are more consistent with the attenuated virulence reported for the double ahpD-spr0371 mutant in the D39 strain [29]
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doi: 10.1152/ajpgi.00173.2003
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However, emerging clinical research is shedding light on the profound cellular dysfunctionsspecifically oxidative stress and mitochondrial failurethat drive these conditions
