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Cysteine S-nitrosylation (SNO) is a reversible post-translational modification that controls complex cell behaviors by regulating protein interactions and signal transduction events. Here, we identified a cluster of\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      secreted effector proteins that are SNO-modified in a host inducible nitric oxide synthase (iNOS)-dependent manner. Among these were the rhoptry protein 5 (ROP5) paralogs, major virulence determinants in\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      and an immunodominant antigen in B6 mice. ROP5 was necessary for Type I and Type II parasites to evade IFN-\u03b3-mediated immune clearance in iNOS-deficient macrophages. RNS led to the loss of ROP5 association with the parasitophorous vacuole membrane (PVM), which is necessary for the known functions of ROP5. Infection with ROP5 knockout parasites rescued the susceptibility of iNOS-deficient mice to infection with Type II\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      . Together, these data indicate that RNS can promote cell-autonomous parasite clearance by inhibiting the function of ROP5 alleles at the PVM.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      RNS are necessary for cell-autonomous immunity to\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      infection; however, the molecular mechanisms by which RNS regulate parasite control remain poorly understood. Our findings support a model in which post-translational modification of ROP5 by RNS is a conserved mechanism of inhibiting the functions of divergent ROP5 paralogs. These data provide a specific example of how host RNS are used to counter\n                      <jats:italic toggle=\"yes\">T. gondii<\/jats:italic>\n                      immune evasion effectors that can be applied to understand how nitrosylation regulates the function of other parasite effectors and the role of RNS in the control of other intracellular pathogens.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/msphere.00309-26","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T13:16:56Z","timestamp":1782825416000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Cysteine-S-nitrosylation inhibits ROP5-mediated immune evasion in\n                    <i>Toxoplasma gondii<\/i>"],"prefix":"10.1128","volume":"11","author":[{"given":"S. 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