Introduction to Sars Cov 2 Tropism

What is/are Sars Cov 2 Tropism?

Sars Cov 2 Tropism - To gain insight into the molecular constituents that might influence SARS-CoV-2 tropism, we determined which additional host factors engage with the viral spike protein in disease-relevant human bronchial epithelial cells (16HBEo−). ^[1] SARS-CoV-2 tropism might occur by infecting monocyte-derived macrophages. ^[2] Therefore, this review sheds light on the possible mechanism of SARS-COV-2 infection in the GI system and its pathological symptoms raising a potential possibility of GI tract acting as a secondary site for SARS-CoV-2 tropism and infection. ^[3] To understand the reasons for the wide-spectrum complications and severe outcomes of COVID-19, we aimed to identify cellular targets of SARS-CoV-2 tropism and replication in various tissues. ^[4] SARS-CoV-2 tropism for the organs is associated with bilateral organ cross-talks as well as targeted dysfunctions, among which acute kidney injury (AKI) seems to be highly prevalent in infected patients. ^[5] SARS-CoV-2 tropism was not restricted to ACE2-expressing cells (e. ^[6] Therefore, these SARS-CoV-2 tropism data should be an essential resource for guiding clinical treatment and pathological studies, which should draw attention toward the prioritization of COVID-19 research in the future. ^[7] The upper respiratory tract is compromised in the early period of COVID-19, but SARS-CoV-2 tropism at the cellular level is not fully defined. ^[8] These components are assembled as an [ACE2: B0AT1]2 dimer-of-heterodimers quaternary complex that putatively steers SARS-CoV-2 tropism in the gastrointestinal (GI) tract. ^[9] Altogether, these findings suggest that CD147 is involved in SARS-CoV-2 tropism and represents a possible therapeutic target to challenge COVID-19. ^[10] However, the SARS-CoV-2 tropisms and the organ manifestations of COVID-19 are far more complex: in addition to the respiratory tract, several other organs and tissues are also permissive for SARS-CoV-2 replication, resulting in a variety of different types of COVID-19 [8, 17]. ^[11] It remains unknown whether atypical N-glycosylation of SGP modulates SARS-CoV-2 tropism for infections. ^[12]