Can ACE2 Receptor Polymorphism Predict Species Susceptibility to SARS-CoV-2?

Devaux, Christian; Pinault, Lucile; Osman, Ikram Omar; Raoult, Didier

doi:10.3389/fpubh.2020.608765

Cited by 38 publications

(53 citation statements)

References 89 publications

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“…During the past year, in vitro and in silico studies allowed to analyze interactions between SARS-CoV-2 and ACE2 (48)(49)(50). This has led many clinical research teams to hypothesize that soon after infection of people, SARS-CoV-2 is likely to trigger a dysfunction of ACE2 and subsequently variations in the balance between Ang II and Ang-(1-7), contributing to worsening hypertension and releasing of proinflammatory cytokines, especially IL-6, thereby accelerating -atherogenesis (35,51).…”

Section: Discussionmentioning

confidence: 99%

Expression of ACE2, Soluble ACE2, Angiotensin I, Angiotensin II and Angiotensin-(1-7) Is Modulated in COVID-19 Patients

et al. 2021

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The etiological agent of COVID-19 SARS-CoV-2, is primarily a pulmonary-tropic coronavirus. Infection of alveolar pneumocytes by SARS-CoV-2 requires virus binding to the angiotensin I converting enzyme 2 (ACE2) monocarboxypeptidase. ACE2, present on the surface of many cell types, is known to be a regulator of blood pressure homeostasis through its ability to catalyze the proteolysis of Angiotensin II (Ang II) into Angiotensin-(1-7) [Ang-(1-7)]. We therefore hypothesized that SARS-CoV-2 could trigger variations of ACE2 expression and Ang II plasma concentration in SARS-CoV-2-infected patients. We report here, that circulating blood cells from COVID-19 patients express less ACE2 mRNA than cells from healthy volunteers. At the level of circulating cells, this ACE2 gene dysregulation mainly affects the monocytes, which also show a lower expression of membrane ACE2 protein. Moreover, soluble ACE2 (sACE2) plasma concentrations are lower in prolonged viral shedders than in healthy controls, while the concentration of sACE2 returns to normal levels in short viral shedders. In the plasma of prolonged viral shedders, we also found higher concentrations of Ang II and angiotensin I (Ang I). On the other hand, the plasma levels of Ang-(1-7) remains almost stable in prolonged viral shedders but seems insufficient to prevent the adverse effects of Ang II accumulation. Altogether, these data evidence that the SARS-CoV-2 may affect the expression of blood pressure regulators with possible harmful consequences on COVID-19 outcome.

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Section: Discussionmentioning

confidence: 99%

Expression of ACE2, Soluble ACE2, Angiotensin I, Angiotensin II and Angiotensin-(1-7) Is Modulated in COVID-19 Patients

et al. 2021

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“…Six RBD amino acids from the SARS-CoV S1 have been shown to be critical for binding to ACE2, namely L455, F486, Q493, S494, N501, and Y505 in SARS-CoV-2 (Andersen et al, 2020). The polymorphism of the ACE2 receptor at amino acid positions 31, 41, 82, 90, and 353 (with the most favorable residues being K31, Y41, N82, N90, K353) was used to estimate species susceptibility to SARS-CoV-2 (Devaux et al, 2021). Species such as Macaca mulatta, Felis catus, Rhinolophus sinicus, M. javanica, or Pelodiscus sinensis have been shown to be susceptible to SARS-CoV-2 infection.…”

Section: A Matter Of Compatibilitymentioning

confidence: 99%

“…Regarding SARS-CoV-2, several animal species were considered to be possible intermediaries, i.e. susceptible hosts which can be infected and are directly involved in the transmission to humans, besides pangolin, including cat, dog, cow, buffalo, goat, sheep, swine, civet, hamster, turtle, and pigeon (Devaux et al, 2021;Luan et al, 2020;Qiu et al, 2020).…”

Section: The Apparent "Multi-host Process" Of Coronavirus Emergencementioning

confidence: 99%

Emergence of Bat-Related Betacoronaviruses: Hazard and Risks

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The current Coronavirus Disease 2019 (COVID-19) pandemic, with more than 111 million reported cases and 2,500,000 deaths worldwide (mortality rate currently estimated at 2.2%), is a stark reminder that coronaviruses (CoV)-induced diseases remain a major threat to humanity. COVID-19 is only the latest case of betacoronavirus (β-CoV) epidemics/pandemics. In the last 20 years, two deadly CoV epidemics, Severe Acute Respiratory Syndrome (SARS; fatality rate 9.6%) and Middle East Respiratory Syndrome (MERS; fatality rate 34.7%), plus the emergence of HCoV-HKU1 which causes the winter common cold (fatality rate 0.5%), were already a source of public health concern. Betacoronaviruses can also be a threat for livestock, as evidenced by the Swine Acute Diarrhea Syndrome (SADS) epizootic in pigs. These repeated outbreaks of β-CoV-induced diseases raise the question of the dynamic of propagation of this group of viruses in wildlife and human ecosystems. SARS-CoV, SARS-CoV-2, and HCoV-HKU1 emerged in Asia, strongly suggesting the existence of a regional hot spot for emergence. However, there might be other regional hot spots, as seen with MERS-CoV, which emerged in the Arabian Peninsula. β-CoVs responsible for human respiratory infections are closely related to bat-borne viruses. Bats are present worldwide and their level of infection with CoVs is very high on all continents. However, there is as yet no evidence of direct bat-to-human coronavirus infection. Transmission of β-CoV to humans is considered to occur accidentally through contact with susceptible intermediate animal species. This zoonotic emergence is a complex process involving not only bats, wildlife and natural ecosystems, but also many anthropogenic and societal aspects. Here, we try to understand why only few hot spots of β-CoV emergence have been identified despite worldwide bats and bat-borne β-CoV distribution. In this work, we analyze and compare the natural and anthropogenic environments associated with the emergence of β-CoV and outline conserved features likely to create favorable conditions for a new epidemic. We suggest monitoring South and East Africa as well as South America as these regions bring together many of the conditions that could make them future hot spots.

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“…A number of recent computational studies comparing ACE2 protein sequences among different species or modeling the structure of the S protein:ACE2 complex to predict the breadth of potential viral hosts have suggested that, due to the high conservation of ACE2, many animals are vulnerable to infection by SARS-CoV-2 ( Ahmed et al, 2021 ; Damas et al, 2020 ; Devaux et al, 2020 ; Fischhoff et al, 2021 ; Huang et al, 2020b ; Kumar et al, 2021 ; Li et al, 2020b ; Liu et al, 2021 ; Melin et al, 2020 ; Rodrigues et al, 2020 ). Humans are likely to come into contact with 26 of these species in domestic, agricultural, or zoological settings ( Lam et al, 2020a ) ( Figure 3 ).…”

Section: Sars-cov-2 Phylogenetic Prediction Of Susceptible Speciesmentioning

confidence: 99%

“…In contrast, the highest similarity of the relative synonymous codon usage of SARS-CoV-2 and snakes led to the latter being hypothesized as a potential viral host ( Ji et al, 2020 ). However, bioinformatics approaches that are based on the analysis of their ACE2 receptor ( Luan et al, 2020 ; Zhang et al, 2020a ) argued against this assumption ( Devaux et al, 2020 ).…”

Section: Sars-cov-2 Phylogenetic Prediction Of Susceptible Speciesmentioning

confidence: 99%

Zoonotic and Reverse Zoonotic Transmissibility of SARS-CoV-2

et al. 2021

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The Coronavirus Disease 2019 (COVID-19) is the first known pandemic caused by a coronavirus. Its causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), appears to be capable of infecting different mammalian species. Recent detections of this virus in pet, zoo, wild, and farm animals have compelled inquiry regarding the zoonotic (animal-to-human) and reverse zoonotic (human-to-animal) transmissibility of SARS-CoV-2 with the potential of COVID-19 pandemic evolving into a panzootic. It is important to monitor the global spread of disease and to assess the significance of genomic changes to support prevention and control efforts during a pandemic. An understanding of the SARS-CoV-2 epidemiology provides opportunities to prevent the risk of repeated re-infection of humans and requires a robust One Health-based investigation. This review paper describes the known properties and the existing gaps in scientific knowledge about the zoonotic and reverse zoonotic transmissibility of the novel virus SARS-CoV-2 and the COVID-19 disease it causes.

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Can ACE2 Receptor Polymorphism Predict Species Susceptibility to SARS-CoV-2?

Cited by 38 publications

References 89 publications

Expression of ACE2, Soluble ACE2, Angiotensin I, Angiotensin II and Angiotensin-(1-7) Is Modulated in COVID-19 Patients

Expression of ACE2, Soluble ACE2, Angiotensin I, Angiotensin II and Angiotensin-(1-7) Is Modulated in COVID-19 Patients

Emergence of Bat-Related Betacoronaviruses: Hazard and Risks

Zoonotic and Reverse Zoonotic Transmissibility of SARS-CoV-2

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