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Review
. 2021 Feb 7;22(4):1659.
doi: 10.3390/ijms22041659.

Viral Infection and Cardiovascular Disease: Implications for the Molecular Basis of COVID-19 Pathogenesis

Sarah Seeherman  1 , Yuichiro J Suzuki  2
Affiliations
Review

Viral Infection and Cardiovascular Disease: Implications for the Molecular Basis of COVID-19 Pathogenesis

Sarah Seeherman et al. Int J Mol Sci. .

Abstract

The current pandemic of coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While this respiratory virus only causes mild symptoms in younger healthy individuals, elderly people and those with cardiovascular diseases such as systemic hypertension are susceptible to developing severe conditions that can be fatal. SARS-CoV-2 infection is also associated with an increased incidence of cardiovascular diseases such as myocardial injury, acute coronary syndrome, and thromboembolism. Understanding the mechanisms of the effects of this virus on the cardiovascular system should thus help develop therapeutic strategies to reduce the mortality and morbidity associated with SARS-CoV-2 infection. Since this virus causes severe and fatal conditions in older individuals with cardiovascular comorbidities, effective therapies targeting specific populations will likely contribute to ending this pandemic. In this review article, the effects of various viruses-including other coronaviruses, influenza, dengue, and human immunodeficiency virus-on the cardiovascular system are described to help provide molecular mechanisms of pathologies associated with SARS-CoV-2 infection and COVID-19. The goal is to provide mechanistic information from the biology of other viral infections in relation to cardiovascular pathologies for the purpose of developing improved vaccines and therapeutic agents effective in preventing and/or treating the acute and long-term consequences of SARS-CoV-2 and COVID-19.

Keywords: ACE2; COVID-19; HIV; cardiovascular; coronavirus; dengue; heart; influenza; spike protein; virus.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
The spike protein downregulates ACE2 that in turn increases Ang II and decreases Ang (1–7), resulting in adverse effects. The spike protein also directly activates cell signaling through the ACE2 receptor, which may also promote adverse events.
Figure 2
Figure 2
The SARS-CoV-2 spike protein promotes severe COVID-19 conditions through ACE2 and possibly DPP4.
Figure 3
Figure 3
Influenza virus (through neuraminidase) and coronaviruses (through the spike protein) downregulate ACE2, increasing Ang II and decreasing Ang (1–7). The spike protein also elicits cell signaling through the ACE2 receptor.
Figure 4
Figure 4
HIV gp120 and the spike protein both activate receptor-mediated cell signaling at picomolar concentrations.
See this image and copyright information in PMC

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