A novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) causing lethal acute respiratory disease emerged in December 2019. The World Health Organization named this disease “COVID-19” and declared it a pandemic on March 11, 2020. Many studies have shown that mesenchymal stem cells (MSCs) and their exosomes (MSCs-Exo), which are isolated from allogenic bone marrow stem cells, significantly lower the risk of alveolar inflammation and other pathological conditions associated with distinct lung injuries. For example, in acute respiratory distress syndrome (ARDS) and pneumonia patients, MSCs-Exo and MSCs provide similar healing properties and some clinical trials have used cell-based inhalation therapy which show great promise. MSCs and MSCs-Exo have shown potential in clinical trials as a therapeutic tool for severely affected COVID-19 patients when compared to other cell-based therapies, which may face challenges like the cells’ sticking to the respiratory tract epithelia during administration. However, the use of MSCs or MSCs-Exo for treating COVID-19 should strictly adhere to the appropriate manufacturing practices, quality control measurements, preclinical safety and efficacy data, and the proper ethical regulations. This review highlights the available clinical trials that support the therapeutic potential of MSCs or MSCs-Exo in severely affected COVID-19 patients.

There are regular reports of extrapulmonary infections and manifestations related to the ongoing COVID-19 pandemic. Coronaviruses are potentially neurotropic, which renders neuronal tissue vulnerable to infection, especially in elderly individuals or in those with neuro-comorbid conditions. Complaints of ageusia, anosmia, myalgia, and headache; reports of diseases such as stroke, encephalopathy, seizure, and encephalitis; and loss of consciousness in patients with COVID-19 confirm the neuropathophysiological aspect of this disease. The brain is linked to pulmonary organs, physiologically through blood circulation, and functionally through the nervous system. The interdependence of these vital organs may further aggravate the pathophysiological aspects of COVID-19. The induction of a cytokine storm in systemic circulation can trigger a neuroinflammatory cascade, which can subsequently compromise the blood-brain barrier and activate microglia- and astrocyte-borne Toll-like receptors, thereby leading to neuronal tissue damage. Hence, a holistic approach should be adopted by healthcare professionals while treating COVID-19 patients with a history of neurodegenerative disorders, neuropsychological complications, or any other neuro-compromised conditions. Imperatively, vaccines are being developed at top priority to contain the spread of the severe acute respiratory syndrome coronavirus 2, and different vaccines are at different stages of development globally. This review discusses the concerns regarding the neuronal complications of COVID-19 and the possible mechanisms of amelioration.

In this article, we discuss the nontuberculous mycobacterial pulmonary disease in a 40-yearold HIV-seropositive female patient. The patient has a history of pulmonary tuberculosis, experienced two years ago. At the time, she was treated successfully with anti-tuberculous therapy. A chest x-ray (CXR) and computed tomography (CT) scan of the chest showed a thinwalled cavitary lesion in the right lung. In addition, the tree-in-bud sign, indicative of airway obstruction, was present on CT imaging. Fluorescence microscopy using auramine staining showed acid-fast bacilli (AFB) in sputum smears on more than two samples. Mycobacterium tuberculosis was not detected in the nucleic acid amplification test in the same sample. The AFB identified were mycobacteria other than tubercle bacilli, i.e., nontuberculous mycobacteria, that cause cavitary lung disease. Culture in liquid media and subsequent molecular analysis showed Mycobacterium avium complex (MAC). The patient is now being treated with a multidrug regimen of antibiotics and has improved, with documented sputum conversion.

Diabetes is managed to keep the blood sugar in normal range. This involves liver as glucose metabolizing organ and sensitization of somatic cells to utilize this glucose for daily energy requirements. The management is subjected to the rhythmic glucose intake as diet and liver circadian cycles that runs parallel to this zeitgeber. COVID-19 patients having diabetes as comorbid condition face the challenges of inflammatory cytokine management along with the organization of glucose. Increased blood glucose level during the cytokine storm further aggravates the pathophysiology of COVID-19 patients leading to high morbidity and mortality in such patients. Clinical treatment of these patients requires multidimensional approach involving circadian variation of hepatic physiology, glucose intake, and inflammatory cytokine release.