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Now tracking the new emerging South Africa Omicron Variant

Is it possible? - Event Date: February 03 2020 - February 04 2020

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Usk View Drop Down
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    Posted: February 03 2020 at 8:34am
Does anyone in this forum know if it is possible to engineer a virus to target a specific ethnic group?
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 03 2020 at 8:35am
As far as I know no one has done it yet, but yes.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Lonewolf Quote  Post ReplyReply Direct Link To This Post Posted: February 03 2020 at 9:26am
Along this conspiracy i was reading about how asians lungs were genetically different and the severity of pneumonia could be different. Camt remember where i saw this.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote arirish Quote  Post ReplyReply Direct Link To This Post Posted: February 03 2020 at 10:27pm
USK- I think in the right hands anything is possible with the CRISPR technology!


CRISPR technology is a simple yet powerful tool for editing genomes. It allows researchers to easily alter DNA sequences and modify gene function. Its many potential applications include correcting genetic defects, treating and preventing the spread of diseases and improving crops. However, its promise also raises ethical concerns.

In popular usage, "CRISPR" (pronounced "crisper") is shorthand for "CRISPR-Cas9." CRISPRs are specialized stretches of DNA. The protein Cas9 (or "CRISPR-associated") is an enzyme that acts like a pair of molecular scissors, capable of cutting strands of DNA.

CRISPR technology was adapted from the natural defense mechanisms of bacteria and archaea (the domain of single-celled microorganisms). These organisms use CRISPR-derived RNA and various Cas proteins, including Cas9, to foil attacks by viruses and other foreign bodies. They do so primarily by chopping up and destroying the DNA of a foreign invader. When these components are transferred into other, more complex, organisms, it allows for the manipulation of genes, or "editing."

Until 2017, no one really knew what this process looked like. In a paper published Nov. 10, 2017, in the journal Nature Communications, a team of researchers led by Mikihiro Shibata of Kanazawa University and Hiroshi Nishimasu of the University of Tokyo showed what it looks like when a CRISPR is in action for the very first time.


https://www.livescience.com/58790-crispr-explained.html
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Post Options Post Options   Thanks (1) Thanks(1)   Quote CRS, DrPH Quote  Post ReplyReply Direct Link To This Post Posted: February 03 2020 at 11:29pm
Originally posted by Usk Usk wrote:

Does anyone in this forum know if it is possible to engineer a virus to target a specific ethnic group?


Only on TV. The actual genetic differences between all humans is actually very, very small.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: February 04 2020 at 12:51am
Thank you all for your reply. I saw on the news that as yet unverified corona virus lab at hopkins noted that this virus seems to be worse in people with ACE1(?) enzyme code. Which happens to primarily in Asian populations
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: February 04 2020 at 12:53am
If true does that mean targeted gene splice or country of origin nature splice?
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Lonewolf Quote  Post ReplyReply Direct Link To This Post Posted: February 04 2020 at 1:34am
https://www.rndsystems.com/resources/articles/ace-2-sars-receptor-identified

   That was it. Ace÷2 pneumonia asians and sars coromavirus. Could have to do with asian susceptibility.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: February 04 2020 at 9:58pm
Yes. Ace2 enzyme.
ABSTRACT

In response to infectious and, in some instances, noninfectious insults, the affected tissues/cells of the host undergo inflammation. However, uncontrolled inflammation could be detrimental to the host, resulting in inflammatory disease, such as inflammatory lung disease. Although the etiology of the disease is well defined, the underling pathogenesis is still incompletely understood. The renin–angiotensin system (RAS), one of the primary cardiovascular regulatory systems, has been proposed to be involved in the pathogenesis of inflammatory lung disease. In particular, the RAS has been implicated as advances in the understanding of the multifunctionality of individual components of the system have been made, and by the fact that the RAS acts not only systemically, but also locally in a variety of tissues, including the lung. Angiotensin-converting enzyme 2 (ACE2), a relatively new member of the RAS, has drawn extensive attention since 2003, because of the findings that ACE2 is the receptor for SARS Corona virus and that maintenance of normal ACE2 levels in the lung is beneficial for the host to combat inflammatory lung disease. Nevertheless, the mechanism through which ACE2 plays a role in inflammatory lung disease has not been clearly identified. In an attempt to summarize current literature findings and progress made in uncovering the role of ACE2 in inflammatory lung disease, this review will focus on recent studies examining pulmonary ACE2 biology, its roles in inflammatory lung disease pathogenesis and possible underlying mechanisms. Finally, we will discuss pulmonary ACE2 as a potential therapeutic target for inflammatory lung disease.
And part of abstract from 2008 virologist


Although in different groups, the coronaviruses severe acute respiratory syndrome-coronavirus (SARS-CoV) and NL63 use the same receptor, angiotensin converting enzyme (ACE)-2, for entry into the host cell. Despite this common receptor, the consequence of entry is very different; severe respiratory distress in the case of SARS-CoV but frequently only a mild respiratory infection for NL63. Using a wholly recombinant system, we have investigated the ability of each virus receptor-binding protein, spike or S protein, to bind to ACE-2 in solution and on the cell surface. In both assays, we find that the NL63 S protein has a weaker interaction with ACE-2 than the SARS-CoV S protein, particularly in solution binding, but the residues required for contact are similar. We also confirm that the ACE-2-binding site of NL63 S lies between residues 190 and 739. A lower-affinity interaction with ACE-2 might partly explain the different pathological consequences of infection by SARS-CoV and NL63.

Severe acute respiratory syndrome (SARS) and NL63 coronaviruses (CoV) are two new members of the family Coronaviridae that have received considerable attention since their recent discovery (Drosten et al., 2003; Kuiken et al., 2003; Li et al., 2003; Pyrc et al., 2007; Sloots et al., 2008; van der Hoek et al., 2004). Infection by SARS-CoV causes severe acute respiratory syndrome with high levels of morbidity and mortality (Drosten et al., 2003; Feng & Gao, 2007; Kuiken et al., 2003), while infection by NL63 rarely requires hospitalization despite being commonly associated with lower respiratory tract infection and croup (van der Hoek, 2007; van der Hoek et al., 2005; Wu et al., 2008). Both viruses use angiotensin converting enzyme (ACE)-2 as the viral receptor (Hofmann et al., 2005; Li et al., 2003), raising the interesting possibility that the difference in pathology is (in part) the result of differential receptor engagement. Virus-mediated downregulation of ACE-2 has been suggested to underlie the pathology of SARS-CoV infection (Imai et al., 2005; Kuba et al., 2005) and it is unclear why this should not also be the case for NL63. Following engagement with ACE-2, the cellular pathways of internalization of the two viruses also appear to be different with SARS-CoV requiring the presence of the lysosomal cysteine protease cathepsin L to infect susceptible cells, while NL63 has no such requirement (Huang et al., 2006). These data suggest that although both viruses utilize ACE-2 as the receptor, the consequences of receptor binding differ, although the reasons for this remain unclear. Using NL63 pseudotyping and soluble S binding to ACE-2-expressing mammalian cells, Hofmann et al. (2005) showed that while ACE-2 leads to efficient NL63 S-mediated entry, the binding of NL63 S was apparently lower than that of SARS-CoV S. They later suggested that this may be the consequence of NL63 S protein binding to a different region of ACE-2 (Hofmann et al., 2006). In contrast, following the definition of a minimum receptor-binding domain (RBD) within NL63 S, residues 301–749, Li et al. (2007) showed that incubation of a tagged form of the RBD with cell lines expressing a number of natural and synthetic ACE-2 variants indicated that the ACE-2 contact residues critical for binding both SARS-CoV and NL63 S overlap (Li et al., 2007).
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 05 2020 at 3:32am
Usk, Please can you post the link to that article. I would love to read all of it.
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http://xf.timebomb2000.com/xf/index.php?threads/single-cell-rna-expression-profiling-of-ace2-corona-targets-asian-men.567434/

omparison between eight individual samples demonstrated that the Asian male one has an extremely large number of ACE2-expressing cells in the lung. This study provides a biological background for the epidemic investigation of the 2019-nCov infection disease, and could be informative for future anti-ACE2 therapeutic strategy development.

Strangely i think it might be tje opposite. I saw an article that said ace2 was lower in older malea and those are the ones with higher mortality. More rrsearch is required but it would lend credibility to tje whole possibility of this threads viability

Also saw a page somewhere about zinc in the process. Then rememnered zinc lowers the effects and duration of the common cold
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Lonewolf Quote  Post ReplyReply Direct Link To This Post Posted: February 05 2020 at 7:29am
If the above article got it in reverse and it is less deadly to asians than Caucasians. And if it was a bio made virus. That would lead presidence to the possibility that it was being made in canada under bioweapon research (looking for a vaccine to a possible weapon. And stolen by the chinese in wuhan and accidently released from their lab.
   Welcome to the arms race.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 05 2020 at 8:00am
Not Peer Reviewed - yet


New Results 16 comments
Single-cell RNA expression profiling of ACE2, the putative receptor of Wuhan 2019-nCov
Yu Zhao, Zixian Zhao, Yujia Wang, Yueqing Zhou, Yu Ma, Wei Zuo
doi: https://doi.org/10.1101/2020.01.26.919985
This article is a preprint and has not been certified by peer review [what does this mean?].

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Abstract

A novel coronavirus (2019-nCov) was identified in Wuhan, Hubei Province, China in December of 2019. This new coronavirus has resulted in thousands of cases of lethal disease in China, with additional patients being identified in a rapidly growing number internationally. 2019-nCov was reported to share the same receptor, Angiotensin-converting enzyme 2 (ACE2), with SARS-Cov. Here based on the public database and the state-of-the-art single-cell RNA-Seq technique, we analyzed the ACE2 RNA expression profile in the normal human lungs. The result indicates that the ACE2 virus receptor expression is concentrated in a small population of type II alveolar cells (AT2). Surprisingly, we found that this population of ACE2-expressing AT2 also highly expressed many other genes that positively regulating viral reproduction and transmission. A comparison between eight individual samples demonstrated that the Asian male one has an extremely large number of ACE2-expressing cells in the lung. This study provides a biological background for the epidemic investigation of the 2019-nCov infection disease, and could be informative for future anti-ACE2 therapeutic strategy development.

Severe infection by 2019-nCov could result in acute respiratory distress syndrome (ARDS) and sepsis, causing death in approximately 15% of infected individuals1,2. Once contacted with the human airway, the spike proteins of this virus can associate with the surface receptors of sensitive cells, which mediated the entrance of the virus into target cells for further replication. Recently, Xu et.al., modeled the spike protein to identify the receptor for 2019-nCov, and indicated that Angiotensin-converting enzyme 2 (ACE2) could be the receptor for this virus3. ACE2 is previously known as the receptor for SARS-Cov and NL634–6. According to their modeling, although the binding strength between 2019-nCov and ACE2 is weaker than that between SARS-Cov and ACE2, it is still much higher than the threshold required for virus infection. Zhou et. al. conducted virus infectivity studies and showed that ACE2 is essential for 2019-nCov to enter HeLa cells7. These data indicated that ACE2 is likely to be the receptor for 2019-nCov.

The expression and distribution of the receptor decide the route of virus infection and the route of infection has a major implication for understanding the pathogenesis and designing therapeutic strategies. Previous studies have investigated the RNA expression of ACE2 in 72 human tissues8. However, the lung is a complex organ with multiple types of cells, and such real-time PCR RNA profiling is based on bulk tissue analysis with no way to elucidate the ACE2 expression in each type of cell in the human lung. The ACE2 protein level is also investigated by immunostaining in lung and other organs8,9. These studies showed that in normal human lung, ACE2 is mainly expressed by type II and type I alveolar epithelial cells. Endothelial cells were also reported to be ACE2 positive. However, immunostaining analysis is known for its lack of signal specificity, and accurate quantification is also another challenge for such analysis.

The recently developed single-cell RNA sequencing (scRNA-Seq) technology enables us to study the ACE2 expression in each cell type and give quantitative information at single-cell resolution. Previous work has built up the online database for scRNA-Seq analysis of 8 normal human lung transplant donors10. In current work, we used the updated bioinformatics tools to analyze the data. In total, we analyzed 43,134 cells derived from normal lung tissue of 8 adult donors. We performed unsupervised graph-based clustering (Seurat version 2.3.4) and for each individual, we identified 8~11 transcriptionally distinct cell clusters based on their marker gene expression profile. Typically the clusters include type II alveolar cells (AT2), type I alveolar cells (AT1), airway epithelial cells (ciliated cells and Club cells), fibroblasts, endothelial cells and various types of immune cells. The cell cluster map of a representative donor (Asian male, 55-year-old) was visualized using t-distributed stochastic neighbor embedding (tSNE) as shown in Fig. 1b and his major cell type marker expressions were demonstrated in Fig.2.
Figure 1.

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Figure 1. Single-cell analysis of normal human lung.

a. Characteristics of lung transplant donors for single-cell RNA-Seq analysis.

b. Cellular cluster map of the Asian male. All 8 samples were analyzed using the Seurat R package. Cells were clustered using a graph-based shared nearest neighbor clustering approach and visualized using a t-distributed Stochastic Neighbor Embedding (tSNE) plot.
Figure 2.

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Figure 2. Violin plots of expression for ACE2 and select cell type-specific marker genes significantly upregulated in distinct lung cell clusters of the Asian male donor.

AGER, type I alveolar cell marker; SFTPC (SPC), type II alveolar cell marker; SCGB3A2, Club cell marker; TPPP3, ciliated cell marker; CD68, macrophage marker; PTPRC(CD45), pan-immune cell marker.

Next, we analyzed the cell-type-specific expression pattern of ACE2 in each individual. For all donors, ACE2 is expressed in 0.64% of all human lung cells. The majority of the ACE2-expressing cells (averagely 83%) are AT2 cells. Averagely 1.4±0.4% of AT2 cells expressed ACE2. Other ACE2 expressing cells include AT1 cells, airway epithelial cells, fibroblasts, endothelial cells, and macrophages. However, their ACE2-expressing cell ratio is low and variable among individuals. For the representative donor (Asian male, 55-year-old), the expressions of ACE2 and cell-type-specific markers in each cluster are demonstrated in Fig.2.

To further understand the special population of ACE2-expressing AT2, we performed gene ontology enrichment analysis to study which biological processes are involved with this cell population by comparing them with the AT2 cells not expressing ACE2. Surprisingly, we found that multiple viral process-related GO are significantly over-presented, including “positive regulation of viral process” (P value=0.001), “viral life cycle” (P value=0.005), “virion assembly” (P value=0.03) and “positive regulation of viral genome replication” (P value=0.04). These highly expressed viral process-related genes in ACE2-expressing AT2 include: SLC1A5, CXADR, CAV2, NUP98, CTBP2, GSN,HSPA1B,STOM, RAB1B, HACD3, ITGB6, IST1,NUCKS1,TRIM27, APOE, SMARCB1,UBP1,CHMP1A,NUP160,HSPA8,DAG1,STAU1,ICAM1,CHMP5,D EK, VPS37B, EGFR, CCNK, PPIA, IFITM3, PPIB, TMPRSS2, UBC, LAMP1 and CHMP3. Therefore, it seems that the 2019-nCov has cleverly evolved to hijack this population of AT2 cells for its reproduction and transmission.

We further compared the characteristics of the donors and their ACE2 expressing patterns. No association was detected between the ACE2-expressing cell number and the age or smoking status of donors. Of note, the 2 male donors have a higher ACE2-expressing cell ratio than all other 6 female donors (1.66% vs. 0.41% of all cells, P value=0.07, Mann Whitney Test). In addition, the distribution of ACE2 is also more widespread in male donors than females: at least 5 different types of cells in male lung express this receptor, while only 2~4 types of cells in female lung express the receptor. This result is highly consistent with the epidemic investigation showing that most of the confirmed 2019-nCov infected patients were men (30 vs. 11, by Jan 2, 2020).

We also noticed that the only Asian donor (male) has a much higher ACE2-expressing cell ratio than white and African American donors (2.50% vs. 0.47% of all cells). This might explain the observation that the new Coronavirus pandemic and previous SARS-Cov pandemic are concentrated in the Asian area.

Altogether, in the current study, we report the RNA expression profile of ACE2 in the human lung at single-cell resolution. Our analysis suggested that the expression of ACE2 is concentrated in a special population of AT2 which expresses many other genes favoring the viral process. This conclusion is different from the previous report which observed abundant ACE2 not only in AT2, but also in endothelial cells8. In fact, to our knowledge, endothelial cells sometimes can be non-specifically stained in immunohistochemical analysis. The abundant expression of ACE2 in a population of AT2 explained the severe alveolar damage after infection. The demonstration of the distinct number and distribution of ACE2-expressing cell population in different cohorts can potentially identify the susceptible population. The shortcoming of the study is the small donor sample number, and that the current technique can only analyze the RNA level but not the protein level of single cells. Furthermore, it remains unknown whether there is any other co-receptor responsible for the 2019-nCov infection, which might also help to explain the observed difference of transmission ability between SARS-Cov and 2019-nCov. Future work on the ACE2 receptor profiling could lead to novel anti-infective strategies such as ACE2 protein blockade or ACE2-expressing cell ablation.
Methods

Public datasets (GEO: GSE122960) were used for bioinformatics analysis. Firstly, we used Seurat (version 2.3.4) to read a combined gene-barcode matrix of all samples. We removed the low-quality cells with less than 200 or more than 6,000 detected genes, or if their mitochondrial gene content was > 10%. Genes were filtered out that were detected in less than 3 cells. For normalization, the combined gene-barcode matrix was scaled by total UMI counts, multiplied by 10,000 and transformed to log space. The highly variable genes were identified using the function FindVariableGenes. Variants arising from number of UMIs and percentage of mitochondrial genes were regressed out by specifying the vars.to.regress argument in Seurat function ScaleData. The expression level of highly variable genes in the cells was scaled and centered along each gene, and was conducted to principal component analysis.

Then we assessed the number of PCs to be included in downstream analysis by (1) plotting the cumulative standard deviations accounted for each PC using the function PCElbowPlot in Seurat to identify the ‘knee’ point at a PC number after which successive PCs explain diminishing degrees of variance, and (2) by exploring primary sources of heterogeneity in the datasets using the PCHeatmap function in Seurat. Based on these two methods, we selected the first top significant PCs for two-dimensional t-distributed stochastic neighbor embedding (tSNE), implemented by the Seurat software with the default parameters. We used FindClusters in Seurat to identify cell clusters for each sample. Following clustering and visualization with t-Distributed Stochastic Neighbor Embedding (tSNE), initial clusters were subjected to inspection and merging based on the similarity of marker genes and a function for measuring phylogenetic identity using BuildClusterTree in Seurat. Identification of cell clusters was performed on the final aligned object guided by marker genes. To identify the marker genes, differential expression analysis was performed by the function FindAllMarkers in Seurat with Wilcoxon rank sum test. Differentially expressed genes that were expressed at least in 25% cells within the cluster and with a fold change more than 0.25 (log scale) were considered to be marker genes. tSNE plots and violin plots were generated using Seurat.
Acknowledgements

This work was funded by National Key Research Program to W. Zuo (2017YFA0104600), National Science Foundation of China (81770073 to W. Zuo, 81570091 to W. Zuo), Youth 1000 Talent Plan of China to W. Zuo, Tongji University (Basic Scientific Research-Interdisciplinary Fund and 985 Grant to W. Zuo), Shanghai Science and Technology Talents Program (19QB1403100 to W. Zuo), and Shanghai East Hospital Annual Grant to W. Zuo.

Source:   https://www.biorxiv.org/content/10.1101/2020.01.26.919985v1.full

Published by Cold Spring Harbour - looks legit - Despite Chinese sources.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Lonewolf Quote  Post ReplyReply Direct Link To This Post Posted: February 05 2020 at 8:34am
Hey technophobe. Could you possibly just summerize with a link and a few short applicable quotes from the article like i did above. Thats a lot to swim through. And skimming through this i fo would be easier. Not trying to be mean. Thanks for the info. It is appreciated
Also i need to look into the zinc as a possible methode of easing the severity of this virus. If it plays out it could be paramount. Im at work so it will be a few before i get to that point. It appears as though it might have the science backing it up. Thanks for the help and work in following this.

   
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Post Options Post Options   Thanks (1) Thanks(1)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 05 2020 at 8:44am
Summary: more deadly to Asians. The bit that stood out was: "We also noticed that the only Asian donor (male) has a much higher ACE2-expressing cell ratio than white and African American donors (2.50% vs. 0.47% of all cells). This might explain the observation that the new Coronavirus pandemic and previous SARS-Cov pandemic are concentrated in the Asian area."

This is not to say westerners can't get it, but it should be both more common and more deadly to Asians. (Westerners have the angiotensin converting enzyme type 2 as well, but not as much and that is the bit the virus sticks to. The epitope on the virus surface is the key for a lock Asian people have more of.)

It does suggest that the previous article DID get it the right way around.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 05 2020 at 8:46am
Bear in mind please, that article is out for peer-review, but has not yet been so. The cohort is also exceptionally small.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Lonewolf Quote  Post ReplyReply Direct Link To This Post Posted: February 05 2020 at 9:42am
https://www.researchgate.net/publication/7465952_Age-_and_gender-related_difference_of_ACE2_expression_in_rat_lung

Epidemiologic data suggested that there was an obvious predominance of young adult patients with a slight female proneness in severe acute respiratory syndrome (SARS). . .

. . In conclusion, the more elevated ACE2 in young adults as compared to aged groups may contribute to the predominance in SARS attacks in this age group.

So yes you are correct it would affect asians more which would answer the original question can a virus be engineered to affect a specific race
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Usk Quote  Post ReplyReply Direct Link To This Post Posted: February 06 2020 at 3:31am
Oh wow. Thank you both for this update as terrifying as it seems to be. My son in law is Chinese and I have two grandsons that are half Asian.   Thanks for helping me watch iver them and good that they live in the USA
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Lonewolf Quote  Post ReplyReply Direct Link To This Post Posted: February 06 2020 at 7:28am
Usk. YW. I wouldnt worry too much. It seems the younger people are ok and pull through it if they see a doctor. Just remember techno and i were just talking about it and it wasnt medical advice. Stay healthy and if they feel ill they should always see a doctor just in case. Best wishes.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 06 2020 at 7:45am
Agreed.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote DeepThinker Quote  Post ReplyReply Direct Link To This Post Posted: February 06 2020 at 8:38am
While I think is very difficult to create a targeted virus based on the genetics of who you want to get sick, I think there is a way to go about it.

You could create a virus that puts people with certain cultural norms, or certain dietary choices, at greatest risk.   It isn't a perfect solution but it would accomplish virtually the same thing.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Technophobe Quote  Post ReplyReply Direct Link To This Post Posted: February 07 2020 at 7:01am
Update to my previous summary

ACE2 is NOT an asian trait. It is expressed SPECIFICALLY in smokers. Nearly half of all Chinese men smoke and under 2% of women do.

Great medical video:   https://www.youtube.com/watch?v=GT3_A1bf9pU

It DOES seem to be the specific receptor for this virus.

Video also addresses the numbers in the Tencent leak and (like me previously) comes to some very unscientific conclusions.
How do you tell if a politician is lying?
His lips or pen are moving.
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Lonewolf View Drop Down
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Lonewolf Quote  Post ReplyReply Direct Link To This Post Posted: February 07 2020 at 8:25am
The treatment to it concerning asiams amd ace2 is

https://www.nature.com/articles/srep17253


Springer Nature is making Coronavirus research free. . . The primary endpoint was cough, which was recorded when participants were bothered by cough and respiratory symptoms during enalapril treatment. . . .
. . Common adverse reactions of ACE inhibitors include cough, increased serum creatinine, headache, dizziness, skin rash et al. Cough is the most common side effect of ACE-inhibitors and may occur within hours following the first dose of the medication11,12. The reported incidence of cough in patients prescribed with ACE inhibitors ranges from 5% (West) to as high as 50% or more (Chinese).
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