Viral and host factors related to the clinical outcome of COVID-19
Xiaonan Zhang, Yun Tan, Yun Ling, Gang Lu, Feng Liu, Zhigang Yi, Xiaofang Jia, Min Wu, Bisheng Shi, Shuibao Xu, Jun Chen, Wei Wang, Bing Chen, Lu Jiang, Shuting Yu, Jing Lu, Jinzeng Wang, Mingzhu Xu, Zhenghong Yuan, Qin Zhang, Xinxin Zhang, Guoping Zhao, Shengyue Wang, Saijuan Chen & Hongzhou Lu
Nature (2020)
Abstract
In December 2019, the Coronavirus disease 2019 (COVID-19), caused by a novel coronavirus SARS-CoV-2, emerged in Wuhan, Hubei province, China1 and soon spread across the world. In this ongoing pandemic, public health concerns and the urgent need for effective therapeutic measures require a deep understanding of its epidemiology, transmissibility and pathogenesis. Here we analyzed the clinical, molecular and immunological data from 326 confirmed cases of COVID-19 in Shanghai. Genomic sequences of SARS-CoV-2 assembled from 112 quality samples together with sequences in the Global Initiative on Sharing All Influenza Data (GISAID) showed a stable evolution and suggested two major lineages with differential exposure history during the early phase of the outbreak in Wuhan. Nevertheless, they exhibited similar virulence and clinical outcomes. Lymphocytopenia, especially the reduced CD4+ and CD8+ T cell counts upon admission, was predictive of disease progression. High levels of IL-6 and IL-8 during treatment were observed in patients with severe or critical disease and correlated with decreased lymphocyte count. The determinants of disease severity seemed to stem mostly from host factors such as age, lymphocytopenia, and its associated cytokine storm, whereas viral genetic variation did not significantly affect the outcomes.
