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Middle East respiratory syndrome coronavirus (MERS-CoV) causes severe acute respiratory disease in humans. MERS-CoV strains from early epidemic clade A and contemporary epidemic clade B have not been phenotypically characterized to compare their ability to infect cells and mice. We isolated the clade B MERS-CoV ChinaGD01 strain from a patient infected during the South Korean MERS outbreak in 2015 and compared the phylogenetics and pathogenicity of MERS-CoV EMC/2012 (clade A) and ChinaGD01 (clade B) in vitro and in vivo. Genome alignment analysis showed that most of clade-specific mutations occurred in the orf1ab gene, included mutations that were predicted to be potential glycosylation sites. Minor differences in viral growth but no significant differences in plaque-size and sensitivity to IFN-were detected between these two viruses in vitro. ChinaGD01 virus infection induced more weight loss and inflammatory cytokine production in human DPP4 transduced mice. Viral titers were higher in the lungs of ChinaGD01 infected mice as compared to EMC/2012 infection. Decreased virusspecific CD4+ and CD8+ T cells numbers were detected in the lungs of ChinaGD01 infected mice. Together, MERS-CoV evolution induced changes to reshape its pathogenicity and virulence in vitro and in vivo and to evade adaptive immune response to hinder viral clearance. [ABSTRACT FROM AUTHOR]