ciclesonide and Pneumonia--Viral

We treated two patients with severe respiratory failure due to coronavirus disease 2019 (COVID-19). Case 1 was a 73-year-old woman, and Case 2 was a 65-year-old-man. Neither of them had a history of autoimmune disease. Chest computed tomography scans before the antiviral therapy showed bilateral multiple patchy ground-glass opacities (GGO) consistent with COVID-19 pneumonia. The GGO regressed over the course of the antiviral treatment; however, new non-segmental patchy consolidations emerged, which resembled those of interstitial lung disease (ILD), specifically collagen vascular disease-associated ILD. We tested the patients' sera for autoantibodies and discovered that both patients had high anti-SSA/Ro antibody titers. In Case 1, the patient recovered with antiviral therapy alone. However, in Case 2, the patient did not improve with antiviral therapy alone but responded well to corticosteroid therapy (methylprednisolone) and made a full recovery. The relationship between some immunological responses and COVID-19 pneumonia exacerbation has been discussed previously; our discovery of the elevation of anti-SSA/Ro antibodies suggests a contribution from autoimmunity functions of the immune system. Although it is unclear whether the elevation of anti-SSA/Ro antibodies was a cause or an outcome of aggravated COVID-19 pneumonia, we hypothesize that both patients developed aggravated the COVID-19 pneumonia due to an autoimmune response. In COVID-19 lung injury, there may be a presence of autoimmunity factors in addition to the known effects of cytokine storms. In patients with COVID-19, a high level of anti-SSA/Ro52 antibodies may be a surrogate marker of pneumonia severity and poor prognosis.

Topics: Aged; Amides; Antibodies, Antinuclear; Antiviral Agents; Benzamidines; Betacoronavirus; Coronavirus Infections; COVID-19; Female; Glucocorticoids; Guanidines; Humans; Hydroxychloroquine; Lung Diseases, Interstitial; Male; Methylprednisolone; Pandemics; Pneumonia, Viral; Pregnenediones; Pyrazines; Recovery of Function; Respiratory Distress Syndrome; Respiratory Insufficiency; SARS-CoV-2; Severity of Illness Index; Tomography, X-Ray Computed

Drug repositioning is the only feasible option to immediately address the COVID-19 global challenge. We screened a panel of 48 FDA-approved drugs against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which were preselected by an assay of SARS-CoV. We identified 24 potential antiviral drug candidates against SARS-CoV-2 infection. Some drug candidates showed very low 50% inhibitory concentrations (IC

Topics: Animals; Anti-Inflammatory Agents; Antiviral Agents; Betacoronavirus; Cell Line; Chlorocebus aethiops; Coronavirus Infections; COVID-19; Drug Evaluation, Preclinical; Drug Repositioning; Humans; Niclosamide; Pandemics; Pneumonia, Viral; Pregnenediones; SARS-CoV-2; Vero Cells

No specific and effective anti-viral treatment has been approved for COVID-19 so far. Systemic corticosteroid has been sometimes administered to severe infectious diseases combined with the specific treatment. However, as lack of the specific anti-SARS-CoV-2 drug, systemic steroid treatment has not been recommended for COVID-19. We report here three cases of the COVID-19 pneumonia successfully treated with ciclesonide inhalation. Rationale of the treatment is to mitigate the local inflammation with inhaled steroid that stays in the lung and to inhibit proliferation of the virus by antiviral activity. Larger and further studies are warranted to confirm the result of these cases.

Topics: Administration, Inhalation; Aged; Betacoronavirus; Coronavirus Infections; COVID-19; COVID-19 Drug Treatment; Female; Glucocorticoids; Humans; Lung; Male; Pandemics; Pneumonia, Viral; Pregnenediones; Radiography, Thoracic; SARS-CoV-2; Ships; Tomography, X-Ray Computed

Topics: Administration, Inhalation; Anti-Inflammatory Agents; Betacoronavirus; Coronavirus Infections; COVID-19; Humans; Male; Middle Aged; Pandemics; Pneumonia, Viral; Pregnenediones; SARS-CoV-2

Topics: Adult; Anti-Bacterial Agents; Anticoagulants; Anticonvulsants; Azithromycin; Betacoronavirus; Brain Edema; Brain Infarction; Clinical Laboratory Techniques; Coronavirus Infections; COVID-19; COVID-19 Drug Treatment; COVID-19 Testing; Decompression, Surgical; Enzyme Inhibitors; Epilepsy; Glucocorticoids; Humans; Hydroxychloroquine; Intracranial Hemorrhages; Lung; Magnetic Resonance Imaging; Male; Nephrosis; Olfaction Disorders; Pandemics; Pneumonia, Viral; Prednisone; Pregnenediones; SARS-CoV-2; Seizures; Severity of Illness Index; Sinus Thrombosis, Intracranial; Tomography, X-Ray Computed

Pulmonary surfactant is considered to be one of the soaps. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the other enveloped viruses become very weak against surfactant. The SARS virus binds to angiotensin-converting enzyme (ACE2) receptor and causes pneumonia. In the lung, the ACE2 receptor sits on the top of lung cells known as alveolar epithelial type II (AE2) cells. These cells play an important role in producing surfactant. Pulmonary surfactant is believed to regulate the alveolar surface tension in mammalian lungs. To our knowledge, AE2 cells are believed to act as immunoregulatory cells; however, pulmonary surfactant itself has not been believed to act as a defender against the enveloped viruses. This study hypothesises that pulmonary surfactant may be a strong defender of enveloped viruses. Therefore, old coronaviruses merely cause pneumonia. On the contrary, new SARS-CoV-2 can suppress the production of surfactant that binds to the ACE2 of AE2 cells. The coronavirus can survive in the lung tissue because of the exhaustion of pulmonary surfactant.

Topics: Ambroxol; Angiotensin-Converting Enzyme 2; Bromhexine; Clinical Trials as Topic; COVID-19; COVID-19 Drug Treatment; Crystallography, X-Ray; Humans; Models, Theoretical; Phagocytosis; Pneumonia, Viral; Pregnenediones; Pulmonary Alveoli; Pulmonary Surfactants; SARS-CoV-2; Surface Tension; Surface-Active Agents

Topics: Antiviral Agents; Betacoronavirus; Binding Sites; Coronavirus Infections; COVID-19; Endoribonucleases; Gene Expression; Glucocorticoids; Humans; Molecular Dynamics Simulation; Pandemics; Pneumonia, Viral; Pregnenediones; Protein Binding; Protein Interaction Domains and Motifs; Protein Structure, Secondary; RNA-Dependent RNA Polymerase; SARS-CoV-2; Structural Homology, Protein; Thermodynamics; Viral Nonstructural Proteins; Virus Replication

Since December 2019, coronavirus disease 2019 (COVID-19) has been an international public health emergency. The possibility of COVID-19 should be considered primarily in patients with new-onset fever or respiratory tract symptoms. However, these symptoms can occur with other viral respiratory illnesses. We reported a case of severe acute respiratory syndrome coronavirus 2 and influenza A virus coinfection. During the epidemic, the possibility of COVID-19 should be considered regardless of positive findings for other pathogens.

Topics: Amides; Anti-Bacterial Agents; Antiviral Agents; Betacoronavirus; Coinfection; Coronavirus Infections; COVID-19; Diagnosis, Differential; Glucocorticoids; Humans; Influenza A virus; Influenza, Human; Lung; Male; Middle Aged; Pandemics; Pneumonia, Viral; Pregnenediones; Pyrazines; Radiography; Real-Time Polymerase Chain Reaction; SARS-CoV-2

We report a coronavirus disease 2019 (COVID-19) case with rheumatoid arthritis taking iguratimod. The patient who continued iguratimod therapy without dose reduction was treated with ciclesonide had an uneventful clinical course, but prolonged detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was observed after resolution of symptoms. The effects of disease-modifying antirheumatic drugs (DMARDs) and ciclesonide on clinical course and viral shedding remain unknown and warrant further investigation.

Topics: Adult; Antirheumatic Agents; Arthritis, Rheumatoid; Betacoronavirus; Chromones; Coronavirus Infections; COVID-19; Female; Humans; Pandemics; Pneumonia, Viral; Pregnenediones; Real-Time Polymerase Chain Reaction; RNA, Viral; SARS-CoV-2; Sulfonamides; Thorax; Virus Shedding