Wang W.-K.SHEY-YING CHENLiu I.-J.CHUAN-LIANG KAOChen H.-L.BOR-LUEN CHIANGJANN-TAY WANGWANG-HUEI SHENGPO-REN HSUEHYang C.-F.PAN-CHYR YANGSHAN-CHWEN CHANG2020-03-242020-03-2420041058-4838https://scholars.lib.ntu.edu.tw/handle/123456789/478755Although viral replication and overwhelming immune responses are believed to contribute to the progression of severe acute respiratory syndrome (SARS), little is known about the temporal relationship between viral load, ribavirin, proinflammatory cytokines, and clinical progression. We report that ribavirin was not effective in reducing the SARS coronavirus load in 3 of 8 probable cases studied and that elevated levels of interleukin (IL)-6 and IL-8 subsequent to the peak viral load were found in 8 and 6 cases, respectively. The nadir lymphocyte count during lymphopenia, the peak level of lactate dehydrogenase, and the peak density of pulmonary infiltrates lag further behind the peak viral load by a median of 4, 5, and 3.5 days, respectively. These findings provide important information for therapeutic strategies to treat SARS.[SDGs]SDG3interleukin 6; interleukin 8; lactate dehydrogenase; ribavirin; adult; article; clinical article; disease course; drug efficacy; female; human; lung infiltrate; lymphocyte count; lymphocytopenia; male; priority journal; severe acute respiratory syndrome; virus load; virus replication; Adult; Antiviral Agents; Female; Humans; Interleukin-6; Interleukin-8; Male; Middle Aged; Ribavirin; SARS Virus; Severe Acute Respiratory Syndrome; Time Factors; Viral Loadjournal article10.1086/423808154728642-s2.0-4744370932