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Covid The science behind Covid-19 - All you need to know

Regio X said:
Very interesting article.
"
Do Your Genes Predispose You to COVID-19?
Individual differences in genetic makeup may explain our susceptibility to the new coronavirus and the severity of the disease it causes
"
https://www.scientificamerican.com/article/do-your-genes-predispose-you-to-covid-19/
Click to expand...

Two other studies have recently come out, posted on the other thread, one of which looks at it in terms of "continental" groups, which shows the highest susceptibility to severity of result in East Asians, followed by Africans, followed by Europeans.

Another looks at it in terms of Europe and finds a higher susceptibility in Southern Europe versus Northern Europe.

This all mirrors previously discovered higher susceptibilities to HIV infection, which shares some coding with CoV-2, and perhaps also to plague.

Of course, this is all preliminary, and it would only be one factor, but if it turns out they're right, it would go some way to explaining differing outcomes in Europe, and also what is happening with black and Hispanic Americans, and what happened with the original SARS outbreak in Asia. At the slightest, earliest hint of a new virus in China East Asian countries rush to put on masks and isolate carriers. They've been down this road before.
 
I'm getting a bit skeptical of all the "miracle" claims for Vitamin D, but for what it's worth, this paper claims that low levels of Vitamin D correlate with more severe disease and death.

See:
http://www.irishhealth.com/article.html?id=27163#.VS-6DOWwQ_g.twitter

"Vitamin D may be an important factor in determining the severity of COVID-19 infections, new research from the Irish Longitudinal Study on Ageing (TILDA) at Trinity College Dublin has found.Vitamin D is known as the sunshine vitamin because it is produced in the skin by exposing the body to just 10-15 minutes per day of sunshine. Earlier this month, TILDA published a report which suggested that the vitamin plays an essential role in preventing respiratory infections, reducing antibiotic use, and boosting the immune system's response to infections.
According to these latest TILDA findings, there are major discrepancies in mortality rates related to vitamin D levels at different latitudes worldwide. Countries in the southern hemisphere, such as Australia, are recording relatively low COVID-related mortality, which the TILDA researchers state can no longer feasibly be related to the later appearance and spread of the virus.
They have pointed to the high prevalence of vitamin D deficiency in northern hemisphere countries, and the possible role of the vitamin in suppressing severe inflammatory responses seen in patients seriously ill with COVID-19.
The researchers explained that vitamin D deficiency correlates with poor sunlight exposure, increasing age, high blood pressure, diabetes, obesity and ethnicity. These are all features associated with an increased risk of severe COVID-19.
Currently, all countries that lie below a latitude of 35 degrees north have relatively low mortality from COVID-19. However, people in countries that lie 35 degrees north and above receive insufficient sunlight for adequate vitamin D levels in winter and spring. These include Italy and Spain, which have low population levels of vitamin D.
The researchers pointed out that mortality rates from COVID-19 are higher at these latitudes, with the exception of Nordic countries, where vitamin D supplementation is widespread and deficiency is much less common."

As a result of their findings, the researchers are recommending that all nursing home residents in Ireland take Vitamin D."

My confidence in this is a little shaken given that you'd think they'd know that Vitamin D is present in cheese as well as milk ONLY if the milk, from which the cheese is made, of course, has been fortified with VItamin D supplements. It's not present in milk naturally, or only in tiny amounts. Maybe they're assuming all the cheese is made with fortified milk, but I don't think that's a valid assumption.

On the other hand, black Americans have worse outcomes and numerous studies have shown they have chronically low Vitamin D levels, which makes sense given the color of their skin and the latitudes at which they currently live.

I avoid the sun because I always get terribly burned, and I never drink milk, both because I don't like it or am used to it, and because I became slightly latose intolerant in my thirties, so I've been prescribed Vitamin D supplements in the past, but I'm not taking them now.

I'm not convinced, but it can't hurt, so I guess I'll start again.
 
Very interesting article about re-using existing drugs to fight covid-19. Scientists identified 47 drugs with the potential to affect covid-19. Sent them to Pasteur Institute and Mount Sinai. Out of all of those these are the most promising:

Disrupting Translation

[FONT=&quot]The two compounds are called ternatin-4 and zotatifin. Both of these are currently used to treat multiple myeloma and seem to fight COVID-19 by binding to and inhibiting proteins in the cell that are needed for translation.[/FONT]
[FONT=&quot]Plitidepsin is a similar molecule to ternatin-4 and is currently undergoing a clinical trial to treat COVID-19. The second drug, zotatifin, hits a different protein involved in translation. We are working with the CEO of the company that produces it to get it into clinical trials as soon as possible.

Sigma receptors:

[/FONT]
[FONT=&quot]Our original map identified two promising MV cell receptors for drug treatments, SigmaR1 and SigmaR2. Testing confirmed our suspicions.[/FONT]
[FONT=&quot]We identified seven drugs or molecules that interact with these receptors. Two antipsychotics, haloperidol and melperone, which are used to treat schizophrenia, showed antiviral activity against SARS-CoV-2. Two potent antihistamines, clemastineand cloperastine, also displayed antiviral activity, as did the compound PB28 and the female hormone progesterone.

https://www.yahoo.com/news/found-tested-47-old-drugs-182645188.html

[/FONT]
[FONT=&quot]

[/FONT]
 
Clemastine is in Tavist, which I used to take and worded really well for me, but so far as I know it was taken off the market here. The only time I've seen Clemastine used is in medications for dogs. It's still on the market in Britain.

I think clemastine would be contraindicated for people with certain blood disorders where they have too many red blood cells.

I also don't know of any over the counter anti-histamines which contain cloperastine, but according to this, one of the antihistamines is pretty close in terms of the receptors.
https://www.selleckchem.com/products/cloperastine-hydrochloride.html
 
Pretty good analysis of IFR from all over the world...ranges between .2-4%. So, they settled on .8%. From what I remember Dr. Fauci's estimate at the very beginning was about 1%.


"[FONT=&quot]Summary:[/FONT][FONT=&quot] Estimation of infectiousness and fatality of the SARS-CoV-2 virus in the COVID-19 global pandemic is complicated by ascertainment bias resulting from incomplete and non-representative samples of infected individuals. We developed a strategy for overcoming this bias to obtain more plausible estimates of the true values of key epidemiological variables. We fit mechanistic Bayesian latent-variable SIR models to confirmed COVID-19 cases, deaths, and recoveries, for all regions (countries and US states) independently. Bayesian averaging over models, we find that the raw infection incidence rate underestimates the true rate by a factor, the case ascertainment ratio CARt that depends upon region and time. At the regional onset of COVID-19, the predicted global median was 13 infections unreported for each case confirmed (CARt = 0.07 C.I. (0.02, 0.4)). As the infection spread, the median CARt rose to 9 unreported cases for every one diagnosed as of April 15, 2020 (CARt = 0.1 C.I. (0.02, 0.5)). We also estimate that the median global initial reproduction number R0 is 3.3 (C.I (1.5, 8.3)) and the total infection fatality rate near the onset is 0.17% (C.I. (0.05%, 0.9%)). However the time-dependent reproduction number Rt and infection fatality rate as of April 15 were 1.2 (C.I. (0.6, 2.5)) and 0.8% (C.I. (0.2%,4%)), respectively. We find that there is great variability between country- and state-level values. Our estimates are consistent with recent serological estimates of cumulative infections for the state of New York, but inconsistent with claims that very large fractions of the population have already been infected in most other regions. For most regions, our estimates imply a great deal of uncertainty about the current state and trajectory of the epidemic."
[/FONT]https://sciencehouse.wordpress.com/2020/04/29/covid-19-paper/[FONT=&quot]

I saw an infection rate of 60% for Bergamo. That's approaching herd immunity.[/FONT]
 
Maciamo said:
Another paper says that at lower temperatures, the virus could survive on a stainless steel surface from 5 to 28 days. It lasted longest in very cold and dry conditions: at 4°C and 20% humidity. So the environmental conditions play a role too.
Click to expand...
Here is another study, this one about this particular coronavirus, confirming the findings:
[h=1]Temperature significantly changes COVID-19 transmission in (sub)tropical cities of Brazil[/h]
[FONT=&quot]Cumulative data with the daily number of confirmed cases was collected from February 27 to April 1, 2020, for all 27 state capital cities of Brazil affected by COVID-19. A generalized additive model (GAM) was applied to explore the linear and nonlinear relationship between annual average temperature compensation and confirmed cases. Also, a polynomial linear regression model was proposed to represent the behavior of the growth curve of COVID-19 in the capital cities of Brazil.[/FONT]
[FONT=&quot]The GAM dose-response curve suggested a negative linear relationship between temperatures and daily cumulative confirmed cases of COVID-19 in the range from 16.8 °C to 27.4 °C. Each 1 °C rise of temperature was associated with a −4.8951% (t = −2.29, p = 0.0226) decrease in the number of daily cumulative confirmed cases of COVID-19. A sensitivity analysis assessed the robustness of the results of the model. The predicted R-squared of the polynomial linear regression model was 0.81053.[/FONT]
[FONT=&quot]In this study, which features the tropical temperatures of Brazil, the variation in annual average temperatures ranged from 16.8 °C to 27.4 °C. Results indicated that temperatures had a negative linear relationship with the number of confirmed cases. The curve flattened at a threshold of 25.8 °C. There is no evidence supporting that the curve declined for temperatures above 25.8 °C. The study had the goal of supporting governance for healthcare policymakers.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182516/[/FONT]

 
Prediction of mortality in COVID 19 patients ten days in advance.

https://www.nature.com/articles/s42...anic&utm_campaign=NGMT_USG_JC01_GL_NRJournals

"The sudden increase in COVID-19 cases is putting high pressure on healthcare services worldwide. At this stage, fast, accurate and early clinical assessment of the disease severity is vital. To support decision making and logistical planning in healthcare systems, this study leverages a database of blood samples from 485 infected patients in the region of Wuhan, China, to identify crucial predictive biomarkers of disease mortality. For this purpose, machine learning tools selected three biomarkers that predict the mortality of individual patients more than 10 days in advance with more than 90% accuracy: lactic dehydrogenase (LDH), lymphocyte and high-sensitivity C-reactive protein (hs-CRP). In particular, relatively high levels of LDH alone seem to play a crucial role in distinguishing the vast majority of cases that require immediate medical attention. This finding is consistent with current medical knowledge that high LDH levels are associated with tissue breakdown occurring in various diseases, including pulmonary disorders such as pneumonia. Overall, this Article suggests a simple and operable decision rule to quickly predict patients at the highest risk, allowing them to be prioritized and potentially reducing the mortality rate."

Anyone know the snps for these so they could be checked in raw data?
 
APOE e4 genotype predicts severe COVID-19 in the UK Biobank community cohort

Not one I would have predicted, that's for sure...

https://www.medrxiv.org/content/10.1101/2020.05.07.20094409v2

The apolipoprotein E (ApoE) gene makes a protein which, when combined with fat, becomes a lipoprotein. The lipoprotein ApoE is a very low-density lipoprotein, responsible in part for removing cholesterol from the bloodstream. Variations in ApoE affect cholesterol metabolism, which in turn alter your chances of having heart disease and in particular a heart attack or a stroke. Variations in ApoE are also associated with altered odds of having Alzheimer's disease and other diseases.
There are three relatively common allelic variants of ApoE, as defined by two SNPs, rs429358 and rs7412 known as ApoE-ε2, ApoE-ε3, and ApoE-ε4. The proteins produced by these genes are called ApoE2, ApoE3, and ApoE4. The most common variant overall is the "standard" ApoE-ε3, and therefore more people inherited one ApoE-ε3 from each parent than any other of the possible pairs of variants. Note that each of these types can actually have additional changes too, so there are different subtypes as well.
[TABLE="class: wikitable"]
[TR]
[TH="align: center"]Common name[/TH]
[TH="align: center"]Genoset[/TH]
[TH="align: center"]Magnitude[/TH]
[TH="align: center"]rs429358[/TH]
[TH="align: center"]rs7412[/TH]
[TH="align: center"]Comment[/TH]
[/TR]
[TR]
[TD]Apo-ε1/ε1[/TD]
[TD]gs267[/TD]
[TD]6[/TD]
[TD](C;C)[/TD]
[TD](T;T)[/TD]
[TD]the rare missing allele[/TD]
[/TR]
[TR]
[TD]Apo-ε1/ε2[/TD]
[TD]gs271[/TD]
[TD]2.5[/TD]
[TD](C;T)[/TD]
[TD](T;T)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε1/ε3[/TD]
[TD]gs270[/TD]
[TD]2.6[/TD]
[TD](C;T)[/TD]
[TD](C;T)[/TD]
[TD]ambiguous ε2/ε4 or ε1/ε3[/TD]
[/TR]
[TR]
[TD]Apo-ε2/ε4[/TD]
[TD]gs270[/TD]
[TD]2.6[/TD]
[TD](C;T)[/TD]
[TD](C;T)[/TD]
[TD]ambiguous ε2/ε4 or ε1/ε3[/TD]
[/TR]
[TR]
[TD]Apo-ε1/ε4[/TD]
[TD]gs272[/TD]
[TD]2.5[/TD]
[TD](C;C)[/TD]
[TD](C;T)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε2/ε2[/TD]
[TD]gs268[/TD]
[TD]4[/TD]
[TD](T;T)[/TD]
[TD](T;T)[/TD]
[TD]good; lowest risk[/TD]
[/TR]
[TR]
[TD]Apo-ε2/ε3[/TD]
[TD]gs269[/TD]
[TD]2[/TD]
[TD](T;T)[/TD]
[TD](C;T)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε3/ε3[/TD]
[TD]gs246[/TD]
[TD]2[/TD]
[TD](T;T)[/TD]
[TD](C;C)[/TD]
[TD]the most common[/TD]
[/TR]
[TR]
[TD]Apo-ε3/ε4[/TD]
[TD]gs141[/TD]
[TD]3[/TD]
[TD](C;T)[/TD]
[TD](C;C)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε4/ε4[/TD]
[TD]gs216[/TD]
[TD]6[/TD]
[TD](C;C)[/TD]
[TD](C;C)[/TD]
[TD]~11x increased Alzheimer's risk
[/TD]
[/TR]
[/TABLE]


A rare form of the ApoE3 allele, rs121918393, also known as the Christchurch (R136S) mutation, appears to convey a significant amount of resistance to PSEN1-based form of autosomal dominant Alzheimer’s, according to a 2019 study.[1]

There's more. Ancestry apparently does a lousy job with this and the results might be inaccurate.

For me:

rs429358:TT

rs7412:CT

Well, I guess I'm E2/E3.

Not the worst.

Another bad one:rs4420638
I'm AA. GG is trouble.

I wonder if this is about whether it affects your heart or just gives you pneumonia.

At any rate, take it all with a grain of salt. This is not yet exact science.
 
Angela said:
APOE e4 genotype predicts severe COVID-19 in the UK Biobank community cohort

Not one I would have predicted, that's for sure...

https://www.medrxiv.org/content/10.1101/2020.05.07.20094409v2

The apolipoprotein E (ApoE) gene makes a protein which, when combined with fat, becomes a lipoprotein. The lipoprotein ApoE is a very low-density lipoprotein, responsible in part for removing cholesterol from the bloodstream. Variations in ApoE affect cholesterol metabolism, which in turn alter your chances of having heart disease and in particular a heart attack or a stroke. Variations in ApoE are also associated with altered odds of having Alzheimer's disease and other diseases.
There are three relatively common allelic variants of ApoE, as defined by two SNPs, rs429358 and rs7412 known as ApoE-ε2, ApoE-ε3, and ApoE-ε4. The proteins produced by these genes are called ApoE2, ApoE3, and ApoE4. The most common variant overall is the "standard" ApoE-ε3, and therefore more people inherited one ApoE-ε3 from each parent than any other of the possible pairs of variants. Note that each of these types can actually have additional changes too, so there are different subtypes as well.
[TABLE="class: wikitable"]
[TR]
[TH="align: center"]Common name[/TH]
[TH="align: center"]Genoset[/TH]
[TH="align: center"]Magnitude[/TH]
[TH="align: center"]rs429358[/TH]
[TH="align: center"]rs7412[/TH]
[TH="align: center"]Comment[/TH]
[/TR]
[TR]
[TD]Apo-ε1/ε1[/TD]
[TD]gs267[/TD]
[TD]6[/TD]
[TD](C;C)[/TD]
[TD](T;T)[/TD]
[TD]the rare missing allele[/TD]
[/TR]
[TR]
[TD]Apo-ε1/ε2[/TD]
[TD]gs271[/TD]
[TD]2.5[/TD]
[TD](C;T)[/TD]
[TD](T;T)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε1/ε3[/TD]
[TD]gs270[/TD]
[TD]2.6[/TD]
[TD](C;T)[/TD]
[TD](C;T)[/TD]
[TD]ambiguous ε2/ε4 or ε1/ε3[/TD]
[/TR]
[TR]
[TD]Apo-ε2/ε4[/TD]
[TD]gs270[/TD]
[TD]2.6[/TD]
[TD](C;T)[/TD]
[TD](C;T)[/TD]
[TD]ambiguous ε2/ε4 or ε1/ε3[/TD]
[/TR]
[TR]
[TD]Apo-ε1/ε4[/TD]
[TD]gs272[/TD]
[TD]2.5[/TD]
[TD](C;C)[/TD]
[TD](C;T)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε2/ε2[/TD]
[TD]gs268[/TD]
[TD]4[/TD]
[TD](T;T)[/TD]
[TD](T;T)[/TD]
[TD]good; lowest risk[/TD]
[/TR]
[TR]
[TD]Apo-ε2/ε3[/TD]
[TD]gs269[/TD]
[TD]2[/TD]
[TD](T;T)[/TD]
[TD](C;T)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε3/ε3[/TD]
[TD]gs246[/TD]
[TD]2[/TD]
[TD](T;T)[/TD]
[TD](C;C)[/TD]
[TD]the most common[/TD]
[/TR]
[TR]
[TD]Apo-ε3/ε4[/TD]
[TD]gs141[/TD]
[TD]3[/TD]
[TD](C;T)[/TD]
[TD](C;C)[/TD]
[TD][/TD]
[/TR]
[TR]
[TD]Apo-ε4/ε4[/TD]
[TD]gs216[/TD]
[TD]6[/TD]
[TD](C;C)[/TD]
[TD](C;C)[/TD]
[TD]~11x increased Alzheimer's risk[/TD]
[/TR]
[/TABLE]


A rare form of the ApoE3 allele, rs121918393, also known as the Christchurch (R136S) mutation, appears to convey a significant amount of resistance to PSEN1-based form of autosomal dominant Alzheimer’s, according to a 2019 study.[1]

There's more. Ancestry apparently does a lousy job with this and the results might be inaccurate.

For me:

rs429358:TT

rs7412:CT

Well, I guess I'm E2/E3.

Not the worst.

Another bad one:rs4420638
I'm AA. GG is trouble.

I wonder if this is about whether it affects your heart or just gives you pneumonia.

At any rate, take it all with a grain of salt. This is not yet exact science.
Click to expand...

Me:

[TABLE="width: 500"]
[TR]
[TD]# rsid[/TD]
[TD]chromosome[/TD]
[TD]position[/TD]
[TD]genotype[/TD]
[/TR]
[TR]
[TD]rs429358[/TD]
[TD]19[/TD]
[TD]45411941[/TD]
[TD]CT[/TD]
[/TR]
[TR]
[TD]rs7412[/TD]
[TD]19[/TD]
[TD]45412079[/TD]
[TD]CC[/TD]
[/TR]
[/TABLE]

Apo-E3/E4 - Magnitude 3

Average Risk or Low risk ??? :grin:

PS: rs121918393 missing from my raw data.
 
Duarte said:
Me:

[TABLE="width: 500"]
[TR]
[TD]# rsid[/TD]
[TD]chromosome[/TD]
[TD]position[/TD]
[TD]genotype[/TD]
[/TR]
[TR]
[TD]rs429358[/TD]
[TD]19[/TD]
[TD]45411941[/TD]
[TD]CT[/TD]
[/TR]
[TR]
[TD]rs7412[/TD]
[TD]19[/TD]
[TD]45412079[/TD]
[TD]CC[/TD]
[/TR]
[/TABLE]

Apo-E3/E4 - Magnitude 3

Average Risk or Low risk ??? :grin:
Click to expand...

Unfortunately, they don't categorize our risk, but given we get 3/4 "good" alleles, I'd say maybe at least "average"?

Did you check the last snp?

I know now why 23andme says slightly elevated risk of Alzheimer's: one damn "bad" version. Out of 9 children in my father's family who lived to middle age only one got Alzheimers. I guess through the roll of the genetic dice she somehow got a lot of the "bad" version.
 
Angela said:
Unfortunately, they don't categorize our risk, but given we get 3/4 "good" alleles, I'd say maybe at least "average"?

Did you check the last snp?

I know now why 23andme says slightly elevated risk of Alzheimer's: one damn "bad" version. Out of 9 children in my father's family who lived to middle age only one got Alzheimers. I guess through the roll of the genetic dice she somehow got a lot of the "bad" version.
Click to expand...

rs121918393 is missing from my raw data.
[TABLE="width: 500"]
[TR]
[TD]rs4420638[/TD]
[TD]19[/TD]
[TD]45422946[/TD]
[TD]AG[/TD]
[/TR]
[/TABLE]

Maybe all these are not too bad for me, I don't know :thinking:

PS: My father died with Alzheimer Disease at 84 years age.
 
Duarte said:
rs121918393 is missing from my raw data.
[TABLE="width: 500"]
[TR]
[TD]rs4420638[/TD]
[TD]19[/TD]
[TD]45422946[/TD]
[TD]AG[/TD]
[/TR]
[/TABLE]

Maybe all these are not too bad for me, I don't know :thinking:

PS: My father died with Alzheimer Disease at 84 years age.
Click to expand...

I don't think your results are "risky" at all.

Yes, that's about when my aunt died of it.

I want to emphasize this is speculative. As they point out in SNPedia, they are finding new snps all the time which swing the pendulum one way or another by modulating the effects of these particular snps.
 
Angela said:
I don't think your results are "risky" at all.

Yes, that's about when my aunt died of it.

I want to emphasize this is speculative. As they point out in SNPedia, they are finding new snps all the time which swing the pendulum one way or another by modulating the effects of these particular snps.
Click to expand...

For some reason they can't find my husband's rs429358

[TABLE="class: table collapsed-table-mobile table--borders marker-table js-marker-table, width: 982"]
[TR]
[TD]APOE[/TD]
[TD]rs7412[/TD]
[TD]45412079[/TD]
[TD]C or T[/TD]
[TD="class: genotype-label"]C / C[/TD]
[/TR]
[/TABLE]

[TABLE="class: table collapsed-table-mobile table--borders marker-table js-marker-table, width: 982"]
[TR]
[TD]intergenic[/TD]
[TD]rs4420638[/TD]
[TD]45422946[/TD]
[TD]A or G[/TD]
[TD="class: genotype-label"]A / A[/TD]
[/TR]
[/TABLE]


That's it; I don't want to make myself or anyone else crazy over something that may or may not be true.
 
... sorry for your loss ... :(


23andme V5 Raw-Data

rs429358 TT

rs7412 CC

... APOE E3/E3
 
Salento said:
... sorry for your loss ... :(
23andme V5 Raw-Data
rs429358 TT
rs7412 CC
... APOE E3/E3
Click to expand...

For myself, they're all gone, my father and all his brothers and sisters in the last 20 years or so, although they all lived relatively long lives, all reaching into their 80s except my father. (Meanwhile, I have great aunts in Italy in their mid 90s. Come back to aria tua one of them used to say to me.)

It's very sad making, particularly my parents, of course, but also my aunts and uncles. My nostalgia for my youth, when we would all gather together, with all my myriad cousins, is like a knife in my heart. When the last of them went, this particular aunt, it felt lonely, you know, and a bit scary. I'm definitely the adult now. :)

There's an old American movie called "How Green Was My Valley" which captures this kind of feeling like no other. I've seen it probably a dozen times and it reduces me to tears each and every time. John Ford directed it and the actors were all top notch as well.
 
Salento said:
... sorry for your loss ... :(
23andme V5 Raw-Data
rs429358 TT
rs7412 CC
... APOE E3/E3
Click to expand...

@Salento
:petrified::petrified::petrified: :grin:

@Angela
My condolences Angela :sad-2:
 
@Angela ...very sorry ....

@Duarte ... :petrified: I’ll totally outlive you :grin:
 
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