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The Neuro-Invasive Potential of SARS-CoV2 Contributes to Respiratory Failure in COVID-19

The 2019 novel coronavirus (2019‐nCoV  [COVID-19]) epidemic, the third known zoonotic coronavirus disease after severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) is now know to be caused by coronavirus 2 (SARS‐CoV‐2). The SARS‐CoV‐2 virus probably originated in bats from which it transmitted to humans. Epidemic transmission is caused by human-to-human transmission. The virus attaches to the angiotensin‐converting enzyme 2 (ACE2) receptor expressed on alveolar epithelial cells of the lungs. 

The common symptoms of COVID‐19 related fever, dry cough and shortness of breath at onset is followed in many by respiratory distress necessitating intensive unit care (ICU) and ventilator support, which have been the most lethal and challenging health care systems nationwide.  The reason for this uncertainty appears to be direct neuronal involvement of respiratory centers of the brainstem by SARS‐CoV‐2. 

The exact route by which SARS‐CoV enters the nervous system is still unknown. However, an experimental mouse model of MERS1 found that intranasal administration of SAR-CoV crosses into the central nervous system along nerve terminal junctions leading to widespread infection in the brain. In humans, the intranasal penetration at the onset of infection is probably the first and most important moment for early brain involvement. The neurotrophic affinity of the CoV for brainstem respiratory centers puts individuals at risk for respiratory failure, in conjunction with dysregulated cytokine and chemokine production due to post-infectious autoimmunity leading to destruction of lung tissue.  

There is no vaccine and treatment is empiric awaiting the results of clinical trials of a variety of potential therapies. In the absence of effective treatments, the best way to deal with the SARS‐CoV‐2 epidemic is to control the sources of infection through early diagnoses, case reporting, isolation of infected persons, supportive treatments. Protective measures include improving personal hygiene, wearing medical masks, adequate rest, and keeping rooms well ventilated. 

However, attention to symptoms of nervous system involvement may be an important early indicator of the need for ICU monitoring and transient ventilator support. This was the case for U.K. Prime Minister Boris Johnson who survived worsening respiratory symptoms of SARS‐CoV‐2 with meticulous ICU monitoring but not ventilator support.  His case highlights the need for evidence-based neurological and pulmonary indicators for patients entering the hospital to gauge their expected level of care and the need for ICU and ventilator support.