Molecular immune pathogenesis and diagnosis of COVID-19

Abstract

Coronavirus disease 2019 (COVID-19

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): An overview of viral structure and host response

“…In fact, based on findings in patients who recovered six year after coronavirus infection, T cell memory was still able to hit the peptide spike when the first exposure occurred [33]. This further explains and directs researchers to the development of vaccines against the corona virus, especially to SARS-COV-2, which is now a pandemic outbreak in the worldwide [28].…”

“…JAK1 and TYK2 kinases further phosphorylate STAT1 and 2 followed by its complexation with IRF9, and together they migrate into the nucleus to initiate the transcription of IFN-stimulated genes (ISGs) and lead to suppression of viral replication and prevent the severity of the disease [25]. However, excess releasing of pro-inflammatory cytokines such as IFN-α, IFN-γ, IL-1β, IL-6, IL-12, IL-18, IL-33, TNF-α, TGFβ, and chemokines CCL2, CCL3, CCL5, CXCL8, CXCL9, CXCL10 from immune effector cells causes hyperinflammation which will eventually lead to ARDS [28,29].…”

“…Next, activation of Th1 cells could stimulate CD8 + T cells, which are one of the effectors of T cells that will target and kill cells infected with CoV. At the same time, CD4 T cells could stimulate humoral immune responses by producing antigen-specific antibodies via activating T-dependent B cells [15,28,30].…”

“…The antibodies produced are generally IgM and IgG which have a unique presence pattern in response to the presence of coronavirus [28]. Generally, this infection will produce a specific IgM that can only last 12…”

“…Generally, viruses including coronavirus have number of avoidance ways from onslaught of immune system cells to better survive and infect host cells [28,30]. The strategy can be applied to various processes, both at the time of introduction (before entering the cell) and when it has entered the host cell.…”