I n the span of a few months, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was identified as the aetiological agent of coronavirus disease 2019 (COVID-19). Weeks later, viral diagnostic measures were deployed 1. This served to supplement the common disease signs and symptoms of COVID-19 of cough, fever and dyspnoea. As all are seen during seasonal upper respiratory tract infections 2 , precise diagnostic tests detect viral nucleic acids, viral antigens or serological tests are required to affirm SARS-CoV-2 infection 3. Chest computed tomography (CT) or magnetic resonance imaging (MRI) confirm disease manifestations 2,3. The signature of COVID-19 is the life-threatening acute respiratory distress syndrome (ARDS) 4. While the lung is the primary viral target, the cardiovascular, brain, kidney, liver and immune systems are commonly compromised by infection 5. Thus, due to significant COVID-19 morbidity and mortality, containment of viral transmission through contact tracing, clinical assessment and virus detection was implemented through social distancing, face masks, contact isolation and hand hygiene to limit SARS-CoV-2 transmission 6 .

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of coronavirus disease 2019 (COVID-19). SARS-CoV-2, is a positive-sense single-stranded RNA virus with epithelial cell and respiratory system proclivity. Like its predecessor, SARS-CoV, COVID-19 can lead to life-threatening disease. Due to wide geographic impact affecting an extremely high proportion of the world population it was defined by the World Health Organization as a global public health pandemic. The infection is known to readily spread from person-to-person. This occurs through liquid droplets by cough, sneeze, hand-to-mouth-to-eye contact and through contaminated hard surfaces. Close human proximity accelerates SARS-CoV-2 spread. COVID-19 is a systemic disease that can move beyond the lungs by bloodbased dissemination to affect multiple organs. These organs include the kidney, liver, muscles, nervous system, and spleen. The primary cause of SARS-CoV-2 mortality is acute respiratory distress syndrome initiated by epithelial infection and alveolar macrophage activation in the lungs. The early cell-based portal for viral entry is through the angiotensin-converting enzyme 2 receptor. Viral origins are zoonotic with genomic linkages to the bat coronaviruses but without an identifiable intermediate animal reservoir. There are currently few therapeutic options, and while many are being tested, although none are effective in curtailing the death rates. There is no available vaccine yet. Intense global efforts have targeted research into a better understanding of the epidemiology, molecular biology, pharmacology, and pathobiology of SARS-CoV-2. These fields of study will provide the insights directed to curtailing this disease outbreak with intense international impact. Keywords Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coronavirus disease 2019 (COVID-19). Acute respiratory distress syndrome (ARDS). Angiotensin-converting enzyme 2 (ACE-2)

Emerging evidence demonstrates that adaptive immunity influences the pathobiology of neurodegenerative disorders. Misfolded aggregated self-proteins can break immune tolerance leading to the induction of autoreactive effector T cells (Teffs) with associated decreases in anti-inflammatory neuroprotective regulatory T cells (Tregs). An imbalance between Teffs and Tregs leads to microglial activation, inflammation and neuronal injury. The cascade of such a disordered immunity includes the drainage of the aggregated protein antigens into cervical lymph nodes serving to amplify effector immune responses. Both preclinical and clinical studies demonstrate transformation of this altered immunity for therapeutic gain. We posit that the signs and symptoms of common neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases, amyotrophic lateral sclerosis, and stroke can be attenuated by boosting Treg activities. Graphical Abstract

We investigated the effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on behavioral and pathological outcomes in Alzheimer's disease (AD) and non-transgenic mice. GM-CSF treatment in AD mice reduced brain amyloidosis, increased plasma Aβ, and rescued cognitive impairment with increased hippocampal expression of calbindin and synaptophysin and increased levels of doublecortin-positive cells in the dentate gyrus. These data extend GM-CSF pleiotropic neuroprotection mechanisms in AD and include regulatory T cell-mediated immunomodulation of microglial function, Aβ clearance, maintenance of synaptic integrity, and induction of neurogenesis. Together these data support further development of GM-CSF as a neuroprotective agent for AD.

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