ABSTRACT
INTRODUCTION: Coronavirus disease 2019 (COVID-19) is an extremely infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The outbreak of this virus has resulted in significant morbidity and mortality throughout the world. We have seen an unprecedented spread of this virus, leading to extreme pressure on health-care services. Mycoplasma pneumoniae causes atypical bacterial pneumonia and is known to co-infect patients with viral pneumonias. METHODS: In this retrospective study, patients' data of 580 inpatients with confirmed SARS-CoV-2 infection were reviewed retrospectively over a 3-month period which included the the first peak of COVID-19 infections in the UK. RESULTS: Eight patients with COVID-19 and M. pneumoniae coinfection were identified - four males and four females. All patients were Caucasian, with an age range of 44-89 years. 37.5% of patients were hypertensive, whereas 25% had Type 2 diabetes mellitus. Dyspnea, cough, and pyrexia were found to be very common in these patients. Majority of the patients had abnormal C-reactive protein, lymphopenia, neutrophilia along with bilateral consolidation, and ground-glass opacities. Two patients required admission to intensive care, both of whom unfortunately died along with one patient receiving ward based care. CONCLUSION: Our confirmed the presence of co-infection with M. pneumoniae and describes the clinical features, investigation results, clinical course, and outcomes for these patients. Further research is needed to review the role of procalcitonin in excluding bacterial co-infection and to assess the impact of co-infection of patients with COVID-19 on morbidity and mortality.
ABSTRACT
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the cause of Coronavirus Disease (COVID-19) that has resulted in a global pandemic. At the time of writing, approximately 16.06 million cases have been reported worldwide. Like other coronaviruses, SARS-CoV-2 relies on the surface Spike glycoprotein to access the host cells, mainly through the interaction of its Receptor Binding Domain (RBD) with the host receptor Angiotensin-Converting Enzyme2 (ACE2). SARS-CoV-2 infection induces a profound downstream pro-inflammatory cytokine storm. This release of the pro-inflammatory cytokines is underpinning lung tissue damage, respiratory failure, and eventually multiple organ failure in COVID-19 patients. The phosphorylation status of ERK1/2 is positively correlated with virus load and ERK1/2 inhibition suppressed viral replication and viral infectivity. Therefore, molecular entities able to interfere with binding of the SARS-CoV-2 Spike protein to ACE2, or damping hyperinflammatory cytokines storm, blocking ERK1/2 phosphorylation have a great potential to inhibit viral entry along with viral infectivity. Herein, we report that the FDA-approved non-peptide opioid antagonist drug, naltrexone suppresses high fat/LPS induced pro-inflammatory cytokine release both from macrophage cells and Adipose Tissue Macrophage. Moreover, Low Dose Naltrexone (LDN) also showed its activity as an ERK1/2 inhibitor. Notably, virtual docking and simulation data also suggest LDN may disrupt the interaction of ACE2 with RBD. LDN may be considered as a target as the treatment and (or) adjuvant therapy for coronavirus infection. Clinical toxicity measurements may not be required for LDN since naltrexone was previously tested and is an approved drug by the FDA.Communicated by Ramaswamy H. Sarma.