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Leishmania  species are sand fly-transmitted protozoan parasites that cause leishmaniasis, neglected tropical diseases that affect millions of people.  Leishmania  amastigotes must overcome a variety of host defenses, including reactive oxygen species (ROS) produced by the NADPH oxidase.  Leishmania  species encode three superoxide dismutases (SODs): the mitochondrial SODA and two glycosomal SODs (SODB1 and SODB2). SODs are metalloenzymes that function in antioxidant defense by converting superoxide to oxygen and hydrogen peroxide. Here, we investigated a role for SODB1 in  Leishmania  infection of macrophages and virulence in mice. We found that a single allele deletion of  SODB1  ( SODB1 /Δ sodb1 ) had minimal effects on the replication of axenically-grown  L .  major  promastigotes or differentiation to infective metacyclic promastigotes. Disruption of a single  SODB1  allele also did not affect  L .  donovani  differentiation to amastigotes induced axenically, or the replication of axenically-grown  L .  donovani  promastigotes and amastigotes. In contrast, the persistence of  SODB1 /Δ sodb1 L .  major  in WT macrophages was impaired, and the development of cutaneous lesions in  SODB1 /Δ sodb1 L .  major -infected C57BL/6 and BALB/c mice was strongly reduced. The reduced disease severity in mice was associated with reduced burdens of  SODB1 /Δ sodb1 L .  major  parasites in the foot at late, but not early times post-inoculation, as well as an impaired capacity to disseminate from the site of inoculation. Collectively, these data suggest that  SODB1  is critical for  L .  major  persistence in macrophages and virulence in mice.

SODB1 is essential for Leishmania major infection of macrophages and pathogenesis in mice