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COVID-19 (coronavirus disease-2019) is caused by a novel strain, the SARS-CoV-2. Mounting of antiviral immunity towards SARS-CoV-2 was greatly impaired among patients with coronary artery disease (CAD). Thus, the main aim of the study is to investigate the preexisting antiviral innate and adaptive immune status among CAD patients. In addition, functional alterations with cellular immune responses under the influence of SARS-CoV-2 spike proteins are being investigated, underscoring the fact that CAD patients are more vulnerable to COVID-19 due to underlying chronic inflammation, which dysregulates the antiviral immune mechanisms. For this purpose, blood samples from 30 CAD patients and 15 older and 15 younger normal controls are examined for the immunophenotypic characterization of a) expression patterns of SARS-CoV-2 cognate receptors (ACE2 and CD147) on blood monocytes, lymphocytes and granulocytes; b) blood circulating frequencies of MAIT cells expressing migration markers (CCR5 and CCR6) and ACE2, b) blood circulating frequencies of CD8⁺ T cells and their activation (CD25, CD69) and exhaustion markers (PD-1, Tim-3). Furthermore, functional outcome of CD4⁺, CD8⁺ and MAIT cells in response to titrated SARS-CoV-2 spike proteins are being investigated in a Chandler loop system, simulating the extracorporeal blood circulation, in terms of a) T cell proliferation, b) apoptosis and c) cytokine and chemokine production.We have observed decreased MAIT cells and increased CD8^- MAIT cells among CAD patients in comparison with normal controls. Of note, ACE2 expression is minimal in lymphocytes, followed by granulocytes and highly expressed in monocytes. Importantly, functional cellular immune responses to SARS-CoV-2 spike proteins are currently being investigated.