Susceptibility of the Elderly to SARS-CoV-2 Infection: ACE-2 Overexpression, Shedding, and Antibody-dependent Enhancement (ADE)

Author(s)

Jean Pierre Schatzmann Peron ; Helder Nakaya ^[2]

• Document type: Journal article
• Source: Clinics; v. 75, 2020-05-15.

Abstract

The world is currently facing a serious SARS-CoV-2 infection pandemic. </mac_aq>This virus is a new isolate of coronavirus, and the current infection crisis has surpassed the SARS and MERS epidemics</mac_aq> that occurred in 2002 and 2013, respectively. SARS-CoV-2 has currently infected more than 142,000 people, causing </mac_aq>5,000 deaths and spreading across more than 130 </mac_aq>countries worldwide. The spreading capacity of the virus clearly demonstrates the potential threat </mac_aq>of respiratory viruses to human health, thereby reiterating to the governments around the world that preventive </mac_aq>health policies and scientific research are pivotal to overcoming the crisis. Coronavirus disease (COVID-19) causes flu-like symptoms in most cases. However, approximately 15% of the patients need hospitalization, and 5% require assisted ventilation, depending on the cohorts studied. What is intriguing, however, is the higher susceptibility of the elderly, especially individuals who are older than 60 years of age, and have comorbidities, including hypertension, diabetes, and heart disease. In fact, the death rate in this group may be up to 10-12%. Interestingly, children are somehow less susceptible and are not considered as a risk group. Therefore, in this review, we discuss some possible molecular and cellular mechanisms by virtue of which the elderly subjects may be more susceptible to severe COVID-19. Toward this, we raise two main </mac_aq>points, i) increased ACE-2 expression in pulmonary and heart tissues in users of chronic angiotensin 1 </mac_aq>receptor (AT1R) blockers; and ii) antibody-dependent enhancement (ADE) after previous exposure to other circulating coronaviruses. We believe that these points are pivotal for a better understanding of the pathogenesis of severe COVID-19, and must be carefully addressed by physicians and scientists in the field. (AU)

• FAPESP's process: 12/19278-6 - Systems biology of long non-coding RNAs
• Grantee: Helder Takashi Imoto Nakaya
• Support Opportunities: Research Grants - Young Investigators Grants
• FAPESP's process: 18/21934-5 - Network statistics: theory, methods, and applications
• Grantee: André Fujita
• Support Opportunities: Research Projects - Thematic Grants
• FAPESP's process: 17/22504-1 - TAM receptors and their ligands Gas6 and Pros1 on the ZIKV Congenital Syndrome in Experimental Models
• Grantee: Jean Pierre Schatzmann Peron
• Support Opportunities: Regular Research Grants
• FAPESP's process: 17/50137-3 - Long noncoding RNA interplay with the host microbiome may determine mucosal influenza vaccine immunogenicity
• Grantee: Helder Takashi Imoto Nakaya
• Support Opportunities: Regular Research Grants
• FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
• Grantee: Fernando de Queiroz Cunha
• Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
• FAPESP's process: 18/14933-2 - Integrative biology applied to human health
• Grantee: Helder Takashi Imoto Nakaya
• Support Opportunities: Research Grants - Young Investigators Grants - Phase 2
• FAPESP's process: 17/26170-0 - Neuroimmunology in experimental models of Autoimmune Encephalomyelitis and Congenital Zika Syndrome: physiopathogenesis, susceptibility, cellular therapy, vaccination
• Grantee: Carolina Demarchi Munhoz
• Support Opportunities: Research Projects - Thematic Grants