Question

COVID-19 is a disease caused by SARS-CoV-2. This coronavirus infection results in an acute respiratory infection that can lead to viral pneumonia and end-organ failure. CoV-2 is a RNA virus (single stranded RNA genome) that specifically targets cells in the lungs that express the ACE2 receptor. Answer the three related questions regarding a mucosal immune response to SARS-CoV-2:

1. Which antibody class would you expect to encounter CoV-2 and which T effector T cell would activate B cells? As the lungs are part of the respiratory tract, where would you expect this antibody class to encounter CoV-2? What B cell effector function would inhibit CoV-2?

2. Last, once the adaptive immune response together with cells of the innate immune system come together to clear CoV-2 from the lungs how does the adaptive immune system function to then remove this response and prevent any long-term damage to the respiratory tract and the host, overall.

Answer 1

1.Severe acute respiratory syndrome coronavirus (SARS-CoV) virus-like particles (VLPs) can be assembled using a recombinant baculovirus (rBV) expression system and such VLPs induce specific humoral and cellular immune responses after subcutaneous injection.

VLPs are capable of inducing B-cell-mediated immune responses and are highly effective in stimulating CD4 T cell proliferation and cytotoxic T lymphocyte (CTL) responses.

2. SARS CoV mainly targets lung tissues and the clinical syndrome of SARS indicates that the host immune system is greatly damaged. Dendritic cells (DCs) are antigen-presenting cells that play key role in innate and adaptive immunity. Exposure of DCs to infectious SARS CoV leads to the phenotypic and functional maturation of DCs, including costimulatory molecule expression, T cell-stimulation and cytokine production. In addition, UV-inactivated SARS CoV also activates immature DCs. BVLPs, morphologically and antigenically similar to the native virus, exhibited stimulating ability in DCs and induced DC maturation by enhancing the expression of cell-surface costimulatory molecules including those essential for optimal activation of T cells: CD40, CD86, CD80 and CD83. Phenotypic maturation of DCs exposed to BVLPs was similar to those observed in DCs incubated with lipopolysaccharide (LPS), a well-known stimulator of DCs maturation. In contrast, heat-denatured BVLPs lost the ability to enhance the expression of cell surface molecules and the secretion of cytokine, suggesting that the specific structure of viral proteins might significantly contribute to the immune modulating activity. The baculovirus derived-BVLPs can interact with human DCs to induce DC maturation and activation.