Exposure to 56°C for 30 minutes and lipid solvents such as ether, 75% ethanol, chlorine-containing disinfectant, peracetic acid, and chloroform can effectively inactivate the virus

Exposure to 56°C for 30 minutes and lipid solvents such as ether, 75% ethanol, chlorine-containing disinfectant, peracetic acid, and chloroform can effectively inactivate the virus. Chlorhexidine has not been effective in inactivating the virus.

There is the possibility of aerosol transmission in a relatively closed environment for a long-time exposure to high concentrations of aerosol. As the novel coronavirus can be isolated in feces and urine, attention should be paid to feces or urine contaminated environment that may lead to aerosol or contact transmission.

CD4+ and CD8+ immunohistochemistry highlights a decreased number of T cells in the spleen and lymph nodes. Myelopoiesis is decreased in bone marrow.Degenerated or necrosed myocardial cells are present, along with mild infiltration of monocytes, lymphocytes and/or neutrophils in the cardiac interstitium. Shedding of endothelial cells, endovasculitis and thrombi are seen in some blood vessels.

Degeneration and focal necrosis of hepatocytes are found, accompanied by infiltration of neutrophils. The sinusoids are congested. The portal areas are infiltrated by lymphocytes and histiocytes.The kidneys are remarkable for proteinaceous exudates in the Bowman’s capsule around glomeruli, degeneration and shedding of renal tubules epithelial cells, and hyaline casts. Microthrombi and fibrotic foci are found in the kidney interstitium.

Cerebral hyperemia and edema are present, with degeneration of some neurons. Necrotic foci are noted in the adrenal glands. Degeneration, necrosis and desquamation of epithelium mucosae of variable degree are present in the esophageal, stomach and bowel.

Based on the current epidemiological investigation, the incubation period is one to 14 days,mostly three to seven days.The main manifestations include fever, fatigue and dry cough. Nasal congestion, runny nose, sore throat, myalgia and diarrhea are found in a few cases.Severe patients develop dyspnea and/or hypoxemia after one week and may progress rapidly to acute respiratory distress syndrome, septic shock, refractory metabolic acidosis, coagulopathy, multiple organ failure etc.

The patients with mild symptoms usually do not develop pneumonia but have low fever and mild fatigue.

In the early stages of the disease, peripheral WBC count is normal or decreased and the lymphocyte count is decreased. Some patients have elevated liver enzymes, lactate dehydrogenase (LDH), muscle enzymes and myoglobin. Elevated troponin is seen in some critically ill patients. Most patients have elevated C-reactive protein and erythrocyte sedimentation rate and normal procalcitonin. In severe cases, D-dimer increases and peripheral blood lymphocytes progressively decrease. Severe and critically ill patients often have elevated inflammatory factors.

Novel coronavirus nucleic acid can be detected in nasopharyngeal swabs, sputum, lower respiratory tract secretions, blood, feces and other specimens usingRT-PCR and/or NGS methods.NCP virus specific IgM becomes detectable around 3-5 days after onset; IgG reaches a titration of at least 4-fold increase during convalescence compared with the acute phase.

In the early stage, imaging shows multiple small patchy shadows and interstitial changes, more apparent in the peripheral zone of lungs. As the disease progresses, imaging shows multiple ground glass opacities and infiltration in both lungs.

Letting patients rest in bed and strengthening support therapy; ensuring sufficient caloric intake for patients; monitoring their water and electrolyte balance to maintain internal environment stability; closely monitoring vital signs and oxygen saturation.According to patients’ conditions, monitoring blood routine result, urine routine result, c-reactive protein (CRP), biochemical indicators (liver enzyme, myocardial enzyme, renal function etc.), coagulation function, arterial blood gas analysis, chest imaging and cytokines detection if necessary.Timely providing effective oxygen therapy, including nasal catheter and maskoxygenation and nasal high-flow oxygen therapy.

Antiviral therapy: Alpha-interferon, lopinavir/ritonavir, Ribavirin, chloroquine phosphate, Arbidol

Invasive mechanical ventilation:Lung protective ventilation strategy, namely low tidal volume (6-8ml/kg of ideal body weight) and low level of airway platform pressure (<30cmH2O) should be used to perform mechanical ventilation to reduce ventilator-related lung injury.

Rescue therapy: Pulmonary re-tensioning is recommended for patients with severe ARDS. With sufficient human resources, prone position ventilation should be performed for more than 12 hours per day. If the outcome of prone position ventilation is poor, extracorporeal membrane oxygenation (ECMO) should be considered as soon as possible.

Immunotherapy: For patients with extensive lung lesions and severe cases who also show an increased level of IL-6 in laboratory testing, Tocilizumab can be used for treatment.For patients with progressive deterioration of oxygenation indicators, rapid progress in imaging and excessive activation of the body's inflammatory response, glucocorticoids can be used in a short period of time (three to five days).

Child severe and critical cases can be given intravenous infusion of gamma-globulin.