receptor activity of ACE2 from 14 mammal species and found that ACE2 from multiple species can support the infectious entry of lentiviral particles pseudotyped with the wild-type or furin cleavage site deficient S protein of SARS-CoV-2. ACE2 of human/rhesus monkey and rat/mouse exhibited the highest and lowest receptor activity, respectively. Among the remaining species, ACE2 from rabbit and pangolin strongly bound to the S1 subunit of SARS-CoV-2 S protein and efficiently supported the pseudotyped virus infection. These findings have important implications for understanding potential natural reservoirs, zoonotic transmission, human-to-animal transmission, and use of animal models.
Anyone who work with animal showing ACE2 receptor activity is more at risk to SARS-CoV-2 infection. Is this your hypothesis?
Mahmoud Elkazzaz grateful for you Serrtia marcescens (ACE2) & Bacillus cereus (ACE4)
They have several applications in the fields of genetic engineering and genetic expression now also with corona virus
Mahdi Movahed-Abtahi Yes, the virus is transmitted from animals to humans because of the same receptors in both
The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body that is essential for the regulation of blood pressure and fluid balance. The system is mainly comprised of the three hormones renin, angiotensin II and aldosterone. Primarily it is regulated by the rate of renal blood flow.
Angiotensin-converting enzyme 2 (ACE2)[5] is an enzyme attached to the outer surface (cell membranes) of cells in the lungs, arteries, heart, kidney, and intestines. ACE2 lowers blood pressure by catalysing the hydrolysis of angiotensin II (a vasoconstrictor peptide) into angiotensin (1–7) (a vasodilator). ACE2 counters the activity of the related angiotensin-converting enzyme (ACE) by reducing the amount of angiotensin-II and increasing Ang(1-7)[ making it a promising drug target for treating cardiovascular diseases.ACE2 also serves as the entry point into cells for some coronaviruses including Severe acute respiratory syndrome coronavirus 2. The human version of the enzyme is often referred to as hACE2.
Yes, this is the correct explanation for the ACE2 pathway in viral infections the full-length ACE2 on the cell membrane by the meta lloprotease ADAM17 and then released into the extracellular environment . The type II transmembrane serine protease, TMPRSS2 was found to compete withADAM17 for ACE2 shedding but cleaves ACE2 di erently. Both ADAM17 and TMPRSS2 remove ashort C-terminal fragment from ACE2. Arginine and lysine residues within amino acids 652 to 659 arecritical for ADAM17 shedding, whereas arginine and lysine residues within amino acids 697 to 716 areessential for TMPRSS2 shedding. Only cleavage by TMPRSS2 results in augmented SARS-CoV cellentry . There are two ways for SARS-CoV to enter the target cell: endocytosis, and fusion of the viral membrane with a membrane of the target cell, which is 100 times more ecient than endocytosis for viral replication. With the help of TMPRSS2, ADAM17-regulated ectodomain shedding of ACE2 could induce SARS-CoV cell entry through endocytosis [however, ADAM17 activity is not required for SARS-CoV cell entry through fusion . As the N-terminal domain is the coronavirus binding site, circulating ACE2 also binds to the virus. Iwata-Yoshikawa et al. infected both wild type (WT) and TMPRSS2 knockout (KO) mice with SARS-CoV. Their results showed that compared to WT mice, SARS-CoV-infected TMPRSS2 KO mice expressed lower viral replication in the lungs with muchlighter alveolar damage and less cytokines release . Recently, two research groups demonstrated
that intra cellular entry of SARS-CoV-2 also depends on TMPRSS2-shed ACE2 TMPRSS2 is highly expressed in large populations of epithelial cells (prostate > colon > small intestine > pancreas >kidney > lung > liver) and is upregulated by androgen In human respiratory and intestinal cells, less than 10% of the cells (including lung type II pneumocytes, ileal absorptive enterocytes, andnasal goblet secretory cells) co-express ACE2 and TMPRSS2 . This evidence indicates that for successful SARS-CoV-2 infection, cellular ACE2 and TMPRSS2 are necessary and male sex hormones may contribute to the infectibility of the host (a recent clinical study reported that among 191
COVID-19 inpatients, 62% were male; among non-survivors 70% were male . In contrast, the major shedding enzyme, ADAM17-shedded ACE2 (circulating ACE2) is believed to protect lungs from theviral infection . Evidence has shown that the expression of TMPRSS2 inhibits ADAM17-shedding of ACE2 . However, it is unclear how TMPRSS2 transcends ADAM17 to cleave ACE2 during SARS-CoV or SARS-CoV-2 infection.
God has granted you all the wishes that you wish in your scientific field and in all areas of life
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Preprint Broad and differential animal ACE2 receptor usage by SARS-CoV-2
SARS-CoV-2 spike protein (S1) enters host cells by binding to ACE2 receptors