On day 11 (17 March), the patient’s clinical symptoms had resolved except for occasional cough and blood in sputum. The patient’s body temperature had decreased to within the normal range. SpO2 rose to 98%. Chest-CT scanning showed that inflammation was absorbed compared to the findings from 10 March, but irregular opacities remained in the mid-lower lobe of the right lung (Fig. 1c). On 18 March, the patient was discharged from the hospital. On 24 April, the patient came back for follow-up.

CT scanning clearly showed that inflammation was further absorbed compared to earlier findings (Fig. 1d). Blood cell counts and liver function tests were within the normal ranges (Table 1). We tested AMPK inhibitor the patient’s pulmonary function during his hospitalization (11 March) and found restricted pulmonary ventilation disorder (FEV1%:45%, FEV1/FEVC%:102%, FVC%:48) and diffuse dysfunction (DLCO%:49%). Approximately 5 weeks after the

patient was discharged from the hospital (24 April), pulmonary function tests became normal (FEV1%: 94%, FEV1/FVC%:114%, FVC%:86%. DLCO%:85). To the best of our knowledge, this is the first report of a patient who recovered from pneumonia caused by a lethal case of human avian-origin influenza virus H7N9. H7N9 virus was not found in the throat swab specimens obtained from this patient on 8 March; however, specific viral antibody IgG was detected in recovery serum (IgG:1:40) at the Chinese Centre for Disease Control and Prevention on 13 April. Therefore, this patient was confirmed to be infected with H7N9. The patient complained ZD1839 purchase of fever, cough, and blood in sputum and presented with decreased WBC count after virus infection. Blood test showed increased enzyme levels (LDH, CK, CK-MB, ALT, and AST), with especially high levels of LDH and CK. Chest-CT revealed ground glass changes, and hypoxaemia was noticed after admission, suggesting high H7N9 viral virulence. Antibacterial therapy did not yield positive results in the rapid progression

of the disease. We considered the possibility of influenza virus infection. Oseltamivir and amantadine were administered as antiviral therapy Cobimetinib cost on day 4 after admission. Although we did not use oseltamivir and amantadine in the first 48 h, clinical symptoms had significantly remitted. However, a 27-year-old male patient who was also positive for H7N9 died after active treatment for 6 days. Therefore, the prognosis of human H7N9 infection may be related to the viral load of H7N9, autoimmunity, and intervention time. The 27-year old patient was a pork trader in the live-poultry market and was admitted to the hospital almost a week after illness onset, during which time he was also actively positive for hepatitis B. The pathogenesis of human avian-origin influenza A (H7N9) virus infection is unknown.