Figure 2.

Viral entry and host response. (A) At the alveolar epithelial cell layer. Epithelial cells in the lungs express both angiotensin converting enzyme 2 (ACE2) receptors and transmembrane protease serine 2 (TMPRSS2), allowing for infection by SARS-CoV-2. Replication of the virus within these cells induces an intense immune response that attracts monocytes, T cells, and macrophages and, in some instances, can result in a cytokine storm. (B) Within nearby blood vessels. Cytokines produced by the epithelial cell layer are released into blood vessels supplying the infected tissue, which causes the recruitment of further immune cells to the area, driving the damaging inflammatory response further. Circulating cytokines also create a systemic inflammatory environment. (C) Adaptive immune response. Circulating lymphocytes carry viral antigens to lymph nodes and bone marrow to begin the adaptive immune system processes whereby B cells, and later antibodies, are activated. (D) SARS-CoV2 host replication. The SARS-CoV-2 virus uses the ACE2 receptor and TMPRSS2 to gain entry into human cells. Following release of the viral RNA within the host cell, the virus uses the host endoplasmic reticulum (ER) and Golgi apparatus to produce and manufacture new viral particles, which are released out of the cell to infect other cells and new hosts