Blockade of the C5a–C5aR axis alleviates lung damage in hDPP4-transgenic mice infected with MERS-CoV

Jiang, Yuting; Zhao, Guangyu; Song, Nianping; Li, Pei; Chen, Yuehong; Guo, Yan; Li, Junfeng; Du, Lanying; Jiang, Shibo; Guo, Renfeng; Sun, Shihui; Zhou, Yusen

Middle East respiratory syndrome coronavirus (MERS-CoV) first emerged in November 2012 in Saudi Arabia 1 . As of February 9, 2018, MERS has been reported in 27 countries with 2143 laboratory-confirmed cases, including 750 deaths (~35% mortality rate). MERS-CoV is similar to severe acute respiratory syndrome coronavirus (SARS-CoV), which is in the same β-coronavirus genus as MERS-CoV and caused an outbreak during 2002-2003 with a 9.6% fatality rate 2 . MERS-CoV leads to progressive severe pneumonia in infected patients, with diffuse alveolar damage occurring during the acute phase. More severe infections are accompanied by considerable extrapulmonary organ dysfunction in the later phase [3] [4] [5] [6] . SARS-CoV infections have been shown to lack type I interferon responses or cause lymphopenia with decreased numbers of CD4 + and CD8 + T cells during the acute phase 7 . However, the mechanism that contributes to severe clinical symptoms in MERS-CoV infections has still not been elucidated, owing to an absence of autopsy studies. The limited data from in vitro and ex vivo studies indicate that MERS-CoV induces a substantial cytopathic effect 8 and dysregulation of host immune responses, similar to SARS-CoV 9, 10 .