https://biobot.io/biobots-wastewater-monitoring-the-omicron-... indicates they use PCR. How does PCR testing return a quantitative result? I thought the purpose was to amplify (reproduce) proteins to enable detection, and this precludes finding original concentrations.
The cycle threshold (Ct) is the quantitative value from PCR. This is mapped to counts per volume based on results in https://pubmed.ncbi.nlm.nih.gov/32607521/ I believe.
Yes. I think the device used is a bit more sophisticated than simply obtaining the cycle number where it crosses the threshold. There's a variation of PCR called quantitative PCR (qPCR) that measures a fluorescence signal more or less continuously and the growth rate allows one to work backwards to the initial count. Here's a basic description from the maker of the device they used (Taqman) https://www.thermofisher.com/blog/ask-a-scientist/what-is-qp...
There's a lot of ways you can get fancier and more precise quantitative results, sure. The basics is the cycle threshold. The next step further is just to try and come up with a fractional cycle number through interpolation-- e.g. if cycle 20 was not-quite-positive-but-very-close and cycle 21 was strongly positive, that implies a value close to 20, versus if cycle 20 was very far from positive and 21 was just barely over the threshold, that implies the real value is just under 21.
And there's further, but diminishing gains from fitting the fluorescence curves.
You can measure how efficient a PCR is by how long it takes to get a positive result. PCR requires a loop of different temperatures to cause different steps in the reaction to occur. This loop is usually repeated 30-40 times. You measure if its positive by looking for a (continuous) light signal. The light signal increases each time you loop through the temperatures. When the light signal passes a pre-determined threshold, that cycle is said to be the one where you got the positive result. The more virus DNA/RNA in the sample, the less loops you need for a positive result.
Perhaps, but there have been reports of varying veracity hinting that COVID-19 was already in Western sewage, blood and autopsy samples in 2019. Who knows if that was contamination, flawed equipment, geopolitical shenanigans or legitimate data though.
The reason why these are mostly believed to be false positive is that all current covid-19 lineages (sequences) can be traced back to a single clone that (based on mutation rate estimates) appeared somewhere in late 2019. There may have been other lineages before that, but we seem to have no RNA sequence of those lineages, so we cannot put them in relation to any existing strain. One has to wonder, where are those 'alternative' lineages now, if they existed in the first place? Sure, they may have gone extinct in the great lockdown. But then one has to ask why did those went extinct while so many other virusses didn't. An a simple (occams razor) explaination is: they never existed.
We can look at excess deaths (https://www.cdc.gov/nchs/nvss/vsrr/covid19/excess_deaths.htm) and the speed and locations it spread around the world and be fairly certain that if the virus were here in significant quantities in 2019 we'd have seen signs of it.
I'm entertained by the idea that somewhere out there, the CCP sent Chinese James Bond to swipe archived wastewater with covid infected ones to prove that it wasn't in Wuhan, but nobody has tested it yet.
That makes me wonder… where does the Covid in the wastewater go? Do we successfully filter it out of the wastewater before recycling it back into the ecosystem? Where specifically does filtered wastewater go, and how confident are we in the filtering process?
It's often done more for political reasons than technical ones, because it's easier for the public to understand and trust UV disinfection than the other, much more complex processes that are typically used.
Cobb County GA is an example of a plant that has large scale UV treatment right before discharge into the Chattahoochee River. But it's effluent is cleaner than the water getting pumped into their water supply.
I thought direct chlorination played a larger role, it seems it doesn't.
(Heavy chlorination of water does result in post-treatment chlorine compounds being present, these are themselves an environmental concern. The bulk of the chlorine evaporates or is reacted relatively quickly. Chlorine also negatively impacts "digestors" which process residual organic matter in wastewater.)
UV, oxygenation, sunlight, filtration, and dilution are all utilised as well.
Viruses tend not to survive long periods of environmental exposure outside a host in most circumstances, though I'm not knowledgeable on specifics or exceptions.
Not sure what the water treatment plant steps are downstream, but I can tell you I've been processing SARS-CoV-2 positive wastewater samples for ages and managed not to catch COVID. Most of the gene fragments tested for in these studies are just that, fragments. The virus itself degrades pretty quickly under environmental stress (UV, heat, evaporation, etc).
I wouldn't be too worried about catching COVID from the water.
If memory serves, there was a city in Italy I think where they were able to verify that Covid was present in the city some time before the first reported case because they keep samples of the sewer water for awhile, and that allowed them to retroactively test for it.
Not to nitpick but I don't think that's what's well known. The virus' "behavior" doesn't change in the Winter. What changes is human behavior. We're inside less and inside more, and that typically means we end up in closer (enclosed) quarters with others.
I think you have a valid theory, but... its not 100% clear if that's the only case.
Viruses could literally be affected by the lesser amounts of sun and shorter days. UV-rays kill the virus for instance, and we get less of them in the winter than during the summer.
Without knowing any more details on "why" there's a relationship between COVID and the winter (whether its human behavior that changes, or if its physically something associated with the virus / sun... like day length + UV rays or heat vs humidity), we just have to say the most generic thing possible to remain correct.
In this case: we know that COVID19 seems to spread more in the winter. We have lots of theories why this happens, but I personally haven't seen any "Mythbusters" style study that goes over all the theories and actually proves any of them.
The humidity inside buildings changes with the outdoor temperature, since cold air carries less water and heaters don't add that back unless you use a humidifier. Isn't that one of the theories behind transmission changing with the seasons?
Coronavirus typically has a spike that starts in December and lasts until February. There are many theories about why this happens, but reduced Vitamin D levels has substantial proof behind it.
Corona viruses are a family of viruses that extends far beyond the particular virus responsible for the current pandemic/epidemic.
Corona viruses are the #2 family responsible for the common (viral) cold, behind rhinoviruses (In the ballpark of 10-20% and 50-60% respectively, iirc, but definitely
rank #2 & #1).
So there is a great deal of historical knowledge about the corona family of viruses, just not necessarily specific to this corona virus and it's variants.
In the context of looking for seasonal patterns in respiratory viruses, it's the first place you'd look in trying to find common traits.
There is previous epidemiological history of other coronavirus variants, prior to the emergence of SARS-COV-2. That's what the comment above is referring to.
See for example:
"Epidemiology and Clinical Presentations of Human Coronavirus NL63 Infections in Hong Kong Children"
Authors: Ting Fan Leung, Chung Yi Li, Wai Yip Lam, Gary W. K. Wong, Edmund Cheuk, Margaret Ip, Pak Cheung Ng, and Paul K. S. Chan
ASM Journals,
Journal of Clinical Microbiology,
Vol. 47, No. 11
In the northern hemisphere? My theory is in spring/summer/fall people are hanging out outside, and as winter comes they think "I've been fine socializing the last few months, hanging out inside will be safe." and socialize indoors, where the lack of fresh air means the virus will spread...
This seems somewhat true based on spikes in the Southern US during the summer (people stay inside where there is AC), but doesn't seem to be the whole story. If that was the case, you would expect to see similar spikes in areas where there is say a week of rain (should be easy to measure in parts of Europe).
In my country - where for the last month we've basically had no sun, just clouds - there is a distinct spike around winter, which would follow nicely with the vitamin D theory. However in places like Southern Europe, which still has a good amount of sun during winter, there are similar spikes.
First, in case it's not clear, these are (indirect measurements of) concentrations not volumes. There is a strong seasonal effect here, but it also tells other stories based on variations outside of that. Still, the seasonal bit is not unexpected, but hugely significant.
Most respiratory viruses, like influenza and colds have greater prevalence during the local winter. We'd expect COVID to behave similarly. The reasons for that are still debated.
In wastewater collection system, I&I (Inflow & Infiltration) is a constant problem where excess water from the environment enters the waste treatment pipeline. It's costly because all that otherwise clean water has to get the full treatment. So, it's interesting to me, that, unless they have normalized for I&I somehow which is not apparent in their raw data, the true seasonal variation in concentration is actually understated.
> So, it's interesting to me, that, unless they have normalized for I&I somehow which is not apparent in their raw data, the true seasonal variation in concentration is actually understated.
Biobot says:
"We normalize the SARS-CoV-2 viral concentration to a fecal indicator, to account for differences in
dilution. We use PMMoV as this fecal indicator, which is an RNA virus that is commonly excreted in stool."
So they're effectively reporting on the ratio between SARS-CoV-2 and PMMoV concentration, which should be normalized for seasonal changes in dilution.
In some countries like Poland, covid looks like solely seasonal disease with nearly zero cases throughout the whole summer, and ramp up during autumn to peaks in winter and spring only broken with lockdowns, dropping back to near zero cases in the summer.
Not sure what copies / mL means. Milliliter? The standardized abbreviation would be a small l.
Here in Finland they use a N2 PCR test published by the CDC (don't ask me how that works, I am a software developer...). However, the results are presented in millions of RNA copies per 1000 inhabitants per 24 hours.
I guess that leads to results unaffected by water consumption habits or rainfall (if the rains drains to the same system as household sewers, some location have dual systems).
Actually ISO mentions both. (Of course they don't define it because the standard unit would for volume would be m³.) So maybe usage really depends on country, I have lived and worked in several European countries, all of them use a small letter.
> Since 1979, the litre may exceptionally be written using either an uppercase "L" or a lowercase "l", a decision prompted by the similarity of the lowercase letter "l" to the numeral "1", especially with certain typefaces or English-style handwriting. The American NIST recommends that within the United States "L" be used rather than "l".
In European measurement contexts I've sometimes seen ℓ (with a script l), but I'm not sure I've seen plain l. (However, I live in the U.S. and might not have as much exposure to European references to liters.)
The rule is that units named by persons use a capital letter (Kelvin, Tesla, Newton, others use a small one (meter, gram). According to the rule liter was designated by a small l.
In 1979 the capital L was recognized by SI (as non-SI unit), too. (I don't know whether the script form was recognized at the same time). According the German Wikipedia capital L is used mainly in English speaking countries. Which makes sense because in handwriting the American (not so sure about the British) digit 1 and small letter l cannot really be distinguished. So 1 liter written as 1 l would be hard to read. In Germany the digit 1 nearly unviversally has a rising stroke on the left in handwriting, so 1 l is not a problem. German Wikipedia says capital L is not used by ISO.
We're working on it! Demultiplexing the signal is tricky though.
Currently, labs have two main tools available - RT-qPCR and tiled amplicon sequencing. RT-qPCR provides cycle threshold (Ct) values which quantify the amount of virus RNA in a sample. RT-qPCR is not practical for finding and quantifying de novo variants as it relies on standard primer sets. Sequencing based approaches are less quantitative but provide more insight into the diversity of RNAs and mutations present in a sample - and thus which variants are present.
https://www.gisaid.org/hcov19-variants/ has a variant dashboard based on sequencing data, including Omicron. It's not as quantitative qPCR, but still may be of interest.
Yes! Looking for gene target failure rates is a valid, albeit indirect way of quantifying variants. You will only be able to detect variants this way if the variant contains a mutation within the primer binding region and if that mutation happens to affect primer binding causing signal drop-off (a lot of 'ifs'!).
Both of these strategies leave much to be desired. For one, it's terribly costly to run multiple RT-qPCRs in parallel. It also fails to account for any novel variants whose mutations lie outside your primer binding region(s).
From what I've gathered, RT-qPCR is useful for quantifying what is already known while sequencing helps you discover what is unknown.
I guess if you had unlimited time and money you could order new primer/probe sets from IDT every time a new variant comes into play...kind of like a home-brew microarray? Honestly, I'm kind of surprised there aren't SARS-CoV-2 variant microarrays on the market yet...we're all just spitballing here.
Interesting, looks like the South Bay has some similar numbers: https://covid19.sccgov.org/dashboard-wastewater but I suppose having milder weather hasn't seen as serious an uptick as Massachusetts?
I think you’re looking at the ‘last six weeks’ charts? The ‘since tracking started in Oct / Nov 2020’ charts show current levels being way, way below last year, or even the July peaks.
Although, to be fair, last October didn’t look bad, and then there was a massive spike…
No I agree with that, I was looking at the 2020 peak to 2021 peak magnitude on the Boston Area plots and the same relative magnitude on the SCC plots and being somewhat surprised at how much of a difference there was between the two locations. As far as I understand we have roughly similar levels of vaccination although santa clara county is probably less dense so I would have guessed we'd have similar magnitude changes in positivity rate. (A good reminder I am in no way an epidemiologist)
Well I don't have positive PCR data for Boston specifically, but the data from Massachusetts generally has peaks at basically the same times over the last year and a half, so I'd say it's a valid measure.
I followed it pretty close until the spring. My recollection was that the data were noisy but over time seemed to have a strong correlation with what we saw in terms of case counts.
Where it was less useful was when people would cite it day by day. All kinds of examples where it'd contradict what we were seeing in the actual COVID data when using it that way.
By "actual COVID data", do you mean positive tests? All things considered, I would assume that wastewater data to be a lot less suspectible to biases (eg who gets tested) and random fluctuations (testing on weekends, holidays, etc).
Should have mentioned that the data I was referring to I found here, at John Hopkins' Univ. github, which they are pulling from a variety of sources: https://github.com/CSSEGISandData/COVID-19
Stepping up for the pedants of my adopted hometown, I note the proper name of that institution is The Johns Hopkins University, named for its likewise plurally christened founder.
Around here we mostly just call it Hopkins or JHU.
Be careful interpreting this. Delta and now Omicron are more contagious than the original virus precisely because they have higher peak viral loads and shed more virus from infected patients. Hence, the virus in wastewater per infected individual has been changing along with the number of infected individuals.
Wow that is SICK! I think if I had to read viral particles in wastewater for many different diseases at a sewage treatment plant I would go crazy and move to the countryside!
Has that been proven or are you just speculating? I don't think increased viral load/shedding is the only mechanism by which a virus becomes more contagious.
Delta has been documented to result in higher viral loads and this is thought to be a factor behind the increased transmissibility.
I don't think anyone knows about the kinetics of Omicron yet. I think the increasing prevalence of Omicron may have a lot more to do with its ability to escape immunity from past infection and increased probability of vaccine breakthrough than any inherent higher transmissibility to those who are immunologically naive.
>Delta has been documented to result in higher viral loads and this is thought to be a factor behind the increased transmissibility.
has it ? I've seen this claim made over and over, w/out documentation.
I've seen documentation of higher nasal swab loads, but not higher systemic circulating virus. Higher upper respiratory loads (e.g. mucosal) would also lead to increased transmissibility, but not higher waste water levels.
> I've seen documentation of higher nasal swab loads, but not higher systemic circulating virus.
You'll have almost no reports of "systemic circulating virus" load, because there's not really an accepted definition for how this measurement would be taken. Plasma concentrations don't appear to be particularly meaningful except in late stages of critical disease.
> higher waste water levels.
My understanding of the evidence is that fecal loads of Delta are higher than other variants, but not as elevated in comparison to how much throat and nose swabs are elevated. I.e. both statements appear true (higher loading overall, and even higher loading in upper respiratory tissue).
> You'll have almost no reports of "systemic circulating virus" load, because there's not really an accepted definition for how this measurement would be taken.
> Viral load, also known as viral burden, is a numerical expression of the quantity of virus in a given volume of fluid, including biological and environmental specimens.
> Viral load, also known as viral burden, is a numerical expression of the quantity of virus in a given volume of fluid
Yes, in a specific fluid. Grandparent doesn't like viral load data coming from upper respiratory swabs-- preferring some kind of "higher systemic load" number.
Well, there's no magical "real systemic" load. You can measure it in the nose; you can measure it (sometimes) in the bloodstream (but this is sporadic and small even in severe cases, though it has prognostic value in critical care). You can measure it in feces, etc.
> To better understand the coronavirus’s journey from one person to another, a team of 50 scientists has for the first time created an atomic simulation of the coronavirus nestled in a tiny airborne drop of water.
> To create the model, the researchers needed one of the world’s biggest supercomputers to assemble 1.3 billion atoms and track all their movements down to less than a millionth of a second. This computational tour de force is offering an unprecedented glimpse at how the virus survives in the open air as it spreads to a new host.
And they look at things like how mucins, water, and calcium atoms interact with the proteins of the virus particle.
> This discovery may help explain how the Delta variant became so widespread. Delta’s spike proteins have a more positive charge than those on earlier forms of the coronavirus. As a result, mucins huddle more closely around them. That attraction could potentially make the mucins a better shield.
Delta undoubtedly has many advantages, and disadvantages, over earlier variants that it outcompeted. That's why I said viral load is "a factor".
One thing that's interesting to me is how the selective pressures on pathogens change. Early on, adaptations that cause higher viral loads are often highly advantageous because they aid transmission-- this tends to be correlated with higher virulence, too. Later, as a smaller portion of the population is susceptible, and adaptations that are less virulent, have longer incubation periods, etc, can win.
It'll be interesting to learn about Omicron virulence and transmissibility. I wouldn't be surprised if it's less, like early reports hint at. However, disentangling this from partial immune escape, etc, is hard.
Couldn’t that potentially be explained by the lag between infection and symptoms with many people being asymptomatic early on while still shedding virus at significant levels? If that’s theory is true, we should see many more tests and identifications of omicron in the coming week.
Still, I think it means we’re likely in the early/mid stages of the exponential curve. I saw estimate of ~5 day doubling time. Meaning that even if 3 weeks ago there were 100 people with Omicron in Boston, there are still only like 800 now. Takes another month or three for it to explode to a large case load.
MA does massive amounts of surveillance testing of people who don’t have symptoms. So infections should be picked up by both wastewater testing and PCR tests at about the same time
But Delta has been the only game in town for a while now (>99% of cases since late August), so this recent rise in the wastewater viral levels shouldn’t be attributable to a change in the proportion of variants (TBD on Omicron?).
The current situation is a handful of confirmed Omicron cases in the US, and a (useless) travel ban to prevent additional cases. Either this data is noise, or that genie isn't just out of the bottle, but ransacked the house while we're arguing over the cork. With a doubling time around 3-5 days and very effective spread to both previously infected and vaccinated, the exact position on that curve is a difference of days.
If we're lucky, it's a mild strain - this doesn't have strong evidence yet. If we're unlucky, and it's similar to other strains, we have around a month before things get very bad indeed.
Lots of good points here! Viral loads and variants are important to keep in mind when interpreting wastewater data.
That said, our current best guess is that the rising SARS-CoV-2 concentration in Boston wastewater reflects a real increase in cases.
Delta has higher nasal shedding than other variants, but not necessarily higher fecal shedding--the ratio of wastewater concentrations to clinical cases seems pretty constant in our data over time (see our blog post on this topic here: https://biobotanalytics.medium.com/mass-vaccination-delta-an...)
We know much less about omicron, but it's probably still only a small minority of cases. We're currently sequencing samples of Boston wastewater, so we'll know more about omicron levels in wastewater very soon!
And yes! Our testing represents every individual in the community that has used a toilet connected to a sewer, independent of where they live, whether they experience symptoms, or whether they have the time, money or access to clinical testing. It's helped public officials stay informed and make decisions even with limited or inconsistent individual testing data.
Doesn't look like there's anything like this for where I live, so I submitted a FOIA request to my local water agency to get that data. If anyone's curious about submitting one for their own city, here's the kinda sloppy language I used for Chicago (IANAL):
Pursuant to IL FOIA, please provide me with records sufficient to show all non-exempt fields of information from the COVID-19 water sampling that's described at: https://mwrd.org/sites/default/files/documents/Sewage%20Surveillance_FS_210119.pdf. The document mentions that MWRD already shares this surveillance information with academic partners, so I believe it should be relatively easy to collect these records.
As the statute allows a requester to specify a file format, please provide me the records in excel format.
Please reach out to me if you have any questions about this request.
Slighly off topic, but it would be interesting to see what other activities have increased or decreased as well. For example, what's happened with legal and illegal pharmaceuticals? What about foods (e.g., sugar)?
Folks have been testing wastewater for legal and illegal drugs for years (https://score-cost.eu has an interesting report if you're interested).
There's been talk amongst Police Departments in whether investing in wide scale wastewater monitoring could help locate drug dealers/labs. Personally, I think this is a huge invasion of privacy, but since wastewater is a "public good" police currently can do whatever they want with it (source: I work in a wastewater testing facility).
Prudence might be as big a concern. If the public gets used to reports on waste streams, it would be an easy target for those who wish to create fear and panic among the populace.
As easy as one bad actor flushing the wrong/right stuff a few times (stuff that is known to be monitored, say a specific infectious agent) in a few public toilets across a city, and waiting for the reports to trickle in. More of a fanning the flames rather than starting a panic, since the threat would have been well-known enough to have been monitored in the first place.
So maybe keep those waste reports on a need-to-know basis, rather than broadcasting a public “daily waste report”.
It's so refreshing to click on a page and just see the answer to the question in the url.
I've gotten very conditioned when urls contain a question, to expect a bloated, ad-ridden , 5-page editorial, focusing on a tangentially related long sob story of a guy and their dog, with the answer to the question barely hinted at, buried inconspicuously somewhere around page 4.
Hi everyone, I’m the CEO of Biobot. I’m a computational biologist, passionate about leveraging wastewater data and analytics to improve human health. I’d be happy to answer any questions you have about the COVID-19 data that we’re generating at MWRA, what we’re up to at Biobot, or wastewater epidemiology generally.
107 comments
[ 2.5 ms ] story [ 166 ms ] threadhttps://www.kare11.com/article/news/local/breaking-the-news/...
And there's further, but diminishing gains from fitting the fluorescence curves.
We can look at excess deaths (https://www.cdc.gov/nchs/nvss/vsrr/covid19/excess_deaths.htm) and the speed and locations it spread around the world and be fairly certain that if the virus were here in significant quantities in 2019 we'd have seen signs of it.
But it's not really necessary most of the time.
It's often done more for political reasons than technical ones, because it's easier for the public to understand and trust UV disinfection than the other, much more complex processes that are typically used.
Cobb County GA is an example of a plant that has large scale UV treatment right before discharge into the Chattahoochee River. But it's effluent is cleaner than the water getting pumped into their water supply.
This paper discusses treatment and emergent pathogens:
"The Role of Wastewater Treatment in Protecting Water Supplies Against Emerging Pathogens"
https://www.jstor.org/stable/23803199
I thought direct chlorination played a larger role, it seems it doesn't.
(Heavy chlorination of water does result in post-treatment chlorine compounds being present, these are themselves an environmental concern. The bulk of the chlorine evaporates or is reacted relatively quickly. Chlorine also negatively impacts "digestors" which process residual organic matter in wastewater.)
UV, oxygenation, sunlight, filtration, and dilution are all utilised as well.
Viruses tend not to survive long periods of environmental exposure outside a host in most circumstances, though I'm not knowledgeable on specifics or exceptions.
I wouldn't be too worried about catching COVID from the water.
Because more people are getting sick with COVID19 at this time... it makes sense that more COVID19 samples will be found in wastewater.
Perhaps that's what you meant?
Viruses could literally be affected by the lesser amounts of sun and shorter days. UV-rays kill the virus for instance, and we get less of them in the winter than during the summer.
Without knowing any more details on "why" there's a relationship between COVID and the winter (whether its human behavior that changes, or if its physically something associated with the virus / sun... like day length + UV rays or heat vs humidity), we just have to say the most generic thing possible to remain correct.
In this case: we know that COVID19 seems to spread more in the winter. We have lots of theories why this happens, but I personally haven't seen any "Mythbusters" style study that goes over all the theories and actually proves any of them.
But yes, there was a spike in December 2019, and another spike in December 2020. So we all are expecting a spike in December 2021.
No, just a significant minority:
https://www.webmd.com/cold-and-flu/cold-guide/common_cold_ca...
Corona viruses are a family of viruses that extends far beyond the particular virus responsible for the current pandemic/epidemic.
Corona viruses are the #2 family responsible for the common (viral) cold, behind rhinoviruses (In the ballpark of 10-20% and 50-60% respectively, iirc, but definitely rank #2 & #1).
So there is a great deal of historical knowledge about the corona family of viruses, just not necessarily specific to this corona virus and it's variants.
In the context of looking for seasonal patterns in respiratory viruses, it's the first place you'd look in trying to find common traits.
ETA: WebMD says 10-40% Rhino, 20% Corona, 20% RSV/parainfluenza, and 20-30% "other".
See for example:
"Epidemiology and Clinical Presentations of Human Coronavirus NL63 Infections in Hong Kong Children"
Authors: Ting Fan Leung, Chung Yi Li, Wai Yip Lam, Gary W. K. Wong, Edmund Cheuk, Margaret Ip, Pak Cheung Ng, and Paul K. S. Chan
ASM Journals, Journal of Clinical Microbiology, Vol. 47, No. 11
https://doi.org/10.1128/JCM.00832-09
https://journals.asm.org/doi/10.1128/jcm.00832-09?permanentl...
In my country - where for the last month we've basically had no sun, just clouds - there is a distinct spike around winter, which would follow nicely with the vitamin D theory. However in places like Southern Europe, which still has a good amount of sun during winter, there are similar spikes.
Most respiratory viruses, like influenza and colds have greater prevalence during the local winter. We'd expect COVID to behave similarly. The reasons for that are still debated.
In wastewater collection system, I&I (Inflow & Infiltration) is a constant problem where excess water from the environment enters the waste treatment pipeline. It's costly because all that otherwise clean water has to get the full treatment. So, it's interesting to me, that, unless they have normalized for I&I somehow which is not apparent in their raw data, the true seasonal variation in concentration is actually understated.
Biobot says:
"We normalize the SARS-CoV-2 viral concentration to a fecal indicator, to account for differences in dilution. We use PMMoV as this fecal indicator, which is an RNA virus that is commonly excreted in stool."
So they're effectively reporting on the ratio between SARS-CoV-2 and PMMoV concentration, which should be normalized for seasonal changes in dilution.
Here in Finland they use a N2 PCR test published by the CDC (don't ask me how that works, I am a software developer...). However, the results are presented in millions of RNA copies per 1000 inhabitants per 24 hours.
I guess that leads to results unaffected by water consumption habits or rainfall (if the rains drains to the same system as household sewers, some location have dual systems).
https://www.thl.fi/episeuranta/jatevesi/jatevesiseuranta_vii...
https://web.archive.org/web/20170814094625/http://www.bipm.o...
The first random picture seems to confirm that in the US a capital L is used.
https://murraybrand.com/wp-content/uploads/2015/07/crystal_o...
> Since 1979, the litre may exceptionally be written using either an uppercase "L" or a lowercase "l", a decision prompted by the similarity of the lowercase letter "l" to the numeral "1", especially with certain typefaces or English-style handwriting. The American NIST recommends that within the United States "L" be used rather than "l".
In European measurement contexts I've sometimes seen ℓ (with a script l), but I'm not sure I've seen plain l. (However, I live in the U.S. and might not have as much exposure to European references to liters.)
In 1979 the capital L was recognized by SI (as non-SI unit), too. (I don't know whether the script form was recognized at the same time). According the German Wikipedia capital L is used mainly in English speaking countries. Which makes sense because in handwriting the American (not so sure about the British) digit 1 and small letter l cannot really be distinguished. So 1 liter written as 1 l would be hard to read. In Germany the digit 1 nearly unviversally has a rising stroke on the left in handwriting, so 1 l is not a problem. German Wikipedia says capital L is not used by ISO.
Eg, in the uk there’s less than 300 cases of it
SOURCE: I work in a leading U.S. wastewater testing lab.
Currently, labs have two main tools available - RT-qPCR and tiled amplicon sequencing. RT-qPCR provides cycle threshold (Ct) values which quantify the amount of virus RNA in a sample. RT-qPCR is not practical for finding and quantifying de novo variants as it relies on standard primer sets. Sequencing based approaches are less quantitative but provide more insight into the diversity of RNAs and mutations present in a sample - and thus which variants are present.
https://www.gisaid.org/hcov19-variants/ has a variant dashboard based on sequencing data, including Omicron. It's not as quantitative qPCR, but still may be of interest.
Some labs quantify amount of variant by running multiple RT-qPCRs using primers specific to mutations unique to each variant (see https://www.promega.com/products/pcr/qpcr-and-rt-qpcr/sars-c...).
Both of these strategies leave much to be desired. For one, it's terribly costly to run multiple RT-qPCRs in parallel. It also fails to account for any novel variants whose mutations lie outside your primer binding region(s).
From what I've gathered, RT-qPCR is useful for quantifying what is already known while sequencing helps you discover what is unknown.
I guess if you had unlimited time and money you could order new primer/probe sets from IDT every time a new variant comes into play...kind of like a home-brew microarray? Honestly, I'm kind of surprised there aren't SARS-CoV-2 variant microarrays on the market yet...we're all just spitballing here.
Although, to be fair, last October didn’t look bad, and then there was a massive spike…
Where it was less useful was when people would cite it day by day. All kinds of examples where it'd contradict what we were seeing in the actual COVID data when using it that way.
Around here we mostly just call it Hopkins or JHU.
I don't think anyone knows about the kinetics of Omicron yet. I think the increasing prevalence of Omicron may have a lot more to do with its ability to escape immunity from past infection and increased probability of vaccine breakthrough than any inherent higher transmissibility to those who are immunologically naive.
has it ? I've seen this claim made over and over, w/out documentation.
I've seen documentation of higher nasal swab loads, but not higher systemic circulating virus. Higher upper respiratory loads (e.g. mucosal) would also lead to increased transmissibility, but not higher waste water levels.
Very early report on Delta, describing higher loads in oropharyngeal swabs: https://www.medrxiv.org/content/10.1101/2021.07.07.21260122v...
> I've seen documentation of higher nasal swab loads, but not higher systemic circulating virus.
You'll have almost no reports of "systemic circulating virus" load, because there's not really an accepted definition for how this measurement would be taken. Plasma concentrations don't appear to be particularly meaningful except in late stages of critical disease.
> higher waste water levels.
My understanding of the evidence is that fecal loads of Delta are higher than other variants, but not as elevated in comparison to how much throat and nose swabs are elevated. I.e. both statements appear true (higher loading overall, and even higher loading in upper respiratory tissue).
Wait, what? This seems completely at odds with the literal definition of viral load per https://en.wikipedia.org/wiki/Viral_load:
> Viral load, also known as viral burden, is a numerical expression of the quantity of virus in a given volume of fluid, including biological and environmental specimens.
Yes, in a specific fluid. Grandparent doesn't like viral load data coming from upper respiratory swabs-- preferring some kind of "higher systemic load" number.
Well, there's no magical "real systemic" load. You can measure it in the nose; you can measure it (sometimes) in the bloodstream (but this is sporadic and small even in severe cases, though it has prognostic value in critical care). You can measure it in feces, etc.
> To better understand the coronavirus’s journey from one person to another, a team of 50 scientists has for the first time created an atomic simulation of the coronavirus nestled in a tiny airborne drop of water.
> To create the model, the researchers needed one of the world’s biggest supercomputers to assemble 1.3 billion atoms and track all their movements down to less than a millionth of a second. This computational tour de force is offering an unprecedented glimpse at how the virus survives in the open air as it spreads to a new host.
And they look at things like how mucins, water, and calcium atoms interact with the proteins of the virus particle.
> This discovery may help explain how the Delta variant became so widespread. Delta’s spike proteins have a more positive charge than those on earlier forms of the coronavirus. As a result, mucins huddle more closely around them. That attraction could potentially make the mucins a better shield.
Delta undoubtedly has many advantages, and disadvantages, over earlier variants that it outcompeted. That's why I said viral load is "a factor".
One thing that's interesting to me is how the selective pressures on pathogens change. Early on, adaptations that cause higher viral loads are often highly advantageous because they aid transmission-- this tends to be correlated with higher virulence, too. Later, as a smaller portion of the population is susceptible, and adaptations that are less virulent, have longer incubation periods, etc, can win.
It'll be interesting to learn about Omicron virulence and transmissibility. I wouldn't be surprised if it's less, like early reports hint at. However, disentangling this from partial immune escape, etc, is hard.
https://covid.cdc.gov/covid-data-tracker/#variant-proportion...
If we're lucky, it's a mild strain - this doesn't have strong evidence yet. If we're unlucky, and it's similar to other strains, we have around a month before things get very bad indeed.
https://www.worldometers.info/coronavirus/country/us/
I definitely think there was going to be a major fourth surge that propelled the US death count to 1 million people from the holidays.
Who knows what omicron will do.
I wonder if this could be an effective way of determining COVID prevalence in areas where they are not doing enough testing?
And yes! Our testing represents every individual in the community that has used a toilet connected to a sewer, independent of where they live, whether they experience symptoms, or whether they have the time, money or access to clinical testing. It's helped public officials stay informed and make decisions even with limited or inconsistent individual testing data.
What else can our waste tell us?
There's been talk amongst Police Departments in whether investing in wide scale wastewater monitoring could help locate drug dealers/labs. Personally, I think this is a huge invasion of privacy, but since wastewater is a "public good" police currently can do whatever they want with it (source: I work in a wastewater testing facility).
As easy as one bad actor flushing the wrong/right stuff a few times (stuff that is known to be monitored, say a specific infectious agent) in a few public toilets across a city, and waiting for the reports to trickle in. More of a fanning the flames rather than starting a panic, since the threat would have been well-known enough to have been monitored in the first place.
So maybe keep those waste reports on a need-to-know basis, rather than broadcasting a public “daily waste report”.
I've gotten very conditioned when urls contain a question, to expect a bloated, ad-ridden , 5-page editorial, focusing on a tangentially related long sob story of a guy and their dog, with the answer to the question barely hinted at, buried inconspicuously somewhere around page 4.