STAT2 is a member of the signal transducer and activator of transcription (STAT) protein family members. In response to cytokines and growth factors (e.g., interferon [IFN]), STAT proteins are phosphorylated and then form complexes that translocate to the cell nucleus where they act as transcription activators. 
Although the Zika virus (ZIKV) NS5 protein evades the human IFN signaling response by binding to and degrading STAT2, it is unable to bind efficiently to mouse STAT2 and thus lacks the ability to antagonize the mouse IFN response.
C57BL/6 hSTAT2 KI mice have the human STAT2 knock-in allele on the C57BL/6 genetic background. The human STAT2 knock-in allele has the endogenous mouse Stat2 coding sequence (spanning from part of exon 2 through part of exon 24) replaced with the corresponding human STAT2 coding sequences. Western blot of splenocytes stimulated with poly(I:C) confirmed the loss of mouse STAT2 and the expression of human STAT2.
 Both heterozygous and homozygous mice are viable and fertile with no developmental, behavioral or reproductive abnormalities. 
 Because C57BL/6 hSTAT2 KI homozygotes express human STAT2 in place of mouse STAT2, they are an immunocompetent C57BL/6 mouse model useful for studying ZIKV pathogenesis - allowing researchers to overcome the inherent inability of ZIKV strains to bind and degrade mouse STAT2.

C57BL/6 hSTAT2 KI mice have the human STAT2 knock-in allele on the C57BL/6 genetic background. Humanized STAT2 knock-in mice are useful for studying immune system cytokine signaling. More specifically, because they overcome the inherent inability of Zika virus (ZIKV) to bind and degrade mouse STAT2, C57BL/6 hSTAT2 KI homozygotes are an immunocompetent C57BL/6 mouse model for studying ZIKV pathogenesis.

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