GI-COVID: Are There COVID-19 Patients with Primary Gastrointestinal SARS-CoV-2 Infection and Symptoms?

Excerpt

Since its first outbreak in late 2019, the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has spread rapidly, ravaging industries and economies and claiming over a million lives worldwide. Approximately 1 year later, much has been learnt about this 29.9 kilobase pair, positive-sense, single-stranded RNA virus (ssRNA +). It is now understood that a lipid bilayer envelops the SARS-CoV-2 RNA and that its genome encodes the non-structural proteins (nsps) 1a and 1b, the trimeric glycoprotein spikes (S), the membrane proteins (M), the envelop proteins (E), and the nucleocapsid proteins (N). S is primed by host transmembrane serine protease 2 (TMPRSS2), and after its cleavage, the receptor binding domain (RBD) on the S1 subunit binds directly to the peptidase domain on angiotensin-converting enzyme 2 receptors (ACE2) in order to enable entry of the virus into host cells [1]. A D614G mutation in the S1 subunit has since led to a more virulent strain that is responsible for most COVID-19 cases worldwide. The S2 subunit assists with the fusion of the virus to the cell membrane, and once within the host cell, the E protein forms a cation-selective channel across the Endoscopic Reticulum-Golgi Intermediate Compartment (ERGIC) membrane, which plays an important role in the pathogenicity of SARS-CoV-2; the E protein is potentially a target for drug therapy [2]. Briefly, the end result is that the virus hijacks intracellular machinery in order to produce multiple copies of itself, subsequently triggering a deleterious cascade, including caspase-8 activation leading to cell death and tissue inflammation [3, 4]. Therefore, the distribution of ACE2 in tissue importantly influences disease symptomatology and pathophysiology. …