The immunological profile of covid-19 patients

 The interaction between COVID-19 and the immune system participates in the dysfunction of the immune responses and disease advancement. Antibodies against the spike protein could prevent COVID-19 from binding with the angiotensin – converting enzyme 2 (ACE2) receptor on host cells. Blocking ACE2 interaction could avoid the virus from infecting the host cell. The generation of pro-inflammatory cytokines (including IL-6, IP-10, macrophage inflammatory protein 1α (MIP1α), MIP1β and MCP1) take place. These proteins magnetize monocytes, macrophages and T cells to the site of infection, elevating further inflammation (with the addition of IFNγ produced by T cells). Accumulation of immune cells in the lungs, causing increased synthesis of pro – inflammatory cytokines, which finally damages the lung. The resulting cytokine storm spreads to other organs, leading to the damage of many organs. Both T and B cell responses against SARS- CoV-2 are measured in the blood around 1 week after the beginning of COVID-19 symptoms. CD8+ T cells are important for directly attacking and killing virus- infected cells. CD4+ T cells are pivotal to prime both CD8+ T cells and B cells. CD4+ T cells are also responsible for cytokine production to drive immune cell induction. B cell responses typically arise first against the nucleocapsid (N) protein. Within 4–8 days after symptom onset, antibody responses to S protein are found. Neutralizing antibody responses, likely to the S protein, begin to develop by week 2, and most patients develop neutralizing antibodies by week 3. Antibodies are likely to be effective against SARS- CoV-2

Ref: The trinity of COVID-19: immunity, inflammation and intervention. Matthew Zirui Tay, Chek Meng Poh, Laurent Rénia, Paul A. MacAry and Lisa F. P. Ng  (2020) Nature reviews, Immunology