Peek-a-Boo Flu
Is viral interference between SARS-CoV-2 and the flu a myth? And if we don’t believe the PCR test can diagnose the presence of SARS-CoV-2 why should we trust it to diagnose the absence of influenza?
A previous WATN (Where Are The Numbers) post looked into the global disappearance of the flu virus. It found that flu had not actually disappeared but had actually been playing hide-and-seek and could be found hiding in the Hindu-Kush or sunning itself in Haiti. It clearly wasn’t hanging around to witness the craziness of the West’s response to the new ‘novel and deadly’ interloper.
This post examines another part of the puzzle - the near-universal acceptance of the explanation for the disappearance of the flu: that it was out-competed by SARS-CoV-2 from Spring 2020 and failed to return until the end of 2021, just after the arrival of the SARS-CoV-2 Omicon variant. It reappeared just as quickly as it disappeared. And it did so globally and with a high degree of synchronicity across multiple countries.
Based on published empirical evidence we think that the explanation that flu disappeared because of competition from SARS-CoV-2 is wrong and, given this fact, we need to look elsewhere for an explanation for flu’s disappearance.
Viral Interference
The disappearance of the flu supposedly rests on a well-accepted theory, called viral interference, whereby the circulation patterns of flu, and other viruses, fluctuate and change from year to year and hemisphere to hemisphere. Under this theory we are told to accept that this is the single and only plausible explanation for what happened to flu and that, after many decades of absolute respiratory viral dominance by flu, SARS-CoV-2 was just too fit and potent a competitor for flu to win the fight to occupy people’s respiratory systems. This relationship between flu and SARS-CoV-2 has been likened to a see-saw.
As a result, flu disappeared and only returned after the circulation of the SARS-CoV-2 Omicron variant. This did not just happen with flu but was reported to have occurred with rhinovirus and RSV, which also absconded with the flu but then returned.
The biological mechanisms for viral interference look plausible and have been around since the 1960s. A good review of the various interference mechanisms can be found here, along with a review of results from epidemiological, ex vivo and in vivo studies, which show that sequential or co-infection with one virus can interfere with, and reduce the propensity of, infection by another. It is posited that production of a strong immune response to the first virus prevents other viruses from setting in.
However, it should be noted that even if this phenomenon is accepted as credible (and we do question its evidential basis below), it is surely a huge stretch to suggest that something which appears to happen at an individual level can result in synchronized population-wide suppression of influenza globally, and it doesn't explain how it bounced back.
Empirical evidence for viral interference with SARS-CoV-2
What empirical evidence do we have that viral interference occurs between the flu, rhinoviruses (RV), respiratory syncytial virus (RSV) and SARS-CoV-2?
Piret and Boivin report on two experiments involving sequential infection of flu and SARS-CoV-2 in Syrian hamsters and ferrets but concluded that there was no detectable sign of viral interference. They concluded:
……previous infection with SARS-CoV-2 did not affect pH1N1 load in the lungs compared with a single infection…….further studies are needed to clarify the interactions between SARS-CoV-2 and influenza viruses.
Fage et al looked at the replication kinetics and interactions between SARS-CoV-2, A(H1N1) flu, and RSV and concluded that:
Our results showed that during simultaneous infection, SARS-CoV-2 interferes with RSV-A2 but not with A(H1N1)pdm09 replication. The prior infection of nasal HAE with SARS-CoV-2 reduces the replication kinetics of both respiratory viruses. SARS-CoV-2 replication is decreased by a prior infection with A(H1N1)pdm09 but not with RSV-A2.
Replication of influenza A was reduced in the presence of prior infection by SARS-CoV-2 and vice-versa. So, both viruses had some ability to interfere with each other but there is no evidence that it was predominately one way, favouring the dominance of SARS-CoV-2.
Essaidi-Laziosi et al investigated dual infections involving SARS-CoV-2 with RV and Influenza A and B viruses (IAV and IBV), using reconstituted repository airway epithelial cells and stated that:
We found that SARS-CoV-2 replication was impaired by primary, but not secondary, rhino- and influenza virus infection. In contrast, SARS-CoV-2 had no effect on the replication of these seasonal respiratory viruses.
In the viral interference theory if SARS-CoV-2 was infected first and then followed by another, secondary, infectious agent, we would expect that the effect of primary infection by SARS-CoV-2 would decrease the presence of the secondary infection. However, Essaidi-Lazios’s experimental results did not match these theoretical expectations. As their charts show what they found was that primary infection by SARS-CoV-2 did not affect the infection trajectory of RV or flus at all.
Chart (B) SARS-CoV-2 replication in single infection versus tissues pre-infected by RV, IAV and IBV and mock solution: four experiments each involving secondary infection of SARS-CoV-2 preceded by primary infection by RV or Influenza A or B or a mock solution. The y-axis is the growth in the SARS-CoV-2 virus and the x-axis is calendar days.
Chart (I) RV, IAV and IBV replication in single Infection (dotted lines) and in the presence of SARS-CoV-2 pre-infection (solid lines): three experiments each involving primary infection of SARS-CoV-2 followed by a secondary infection of RV or Influenza A or B. Plus, three experiments with mock solution then infection by RV or Influenza A or B.
(Chart (B) x-axis is a typo in the original paper)
To hammer the point home, they concluded (my emphasis):
While infecting first with RV, IAV and IBV and then 48 h later with SARS-CoV-2 led to reduced SARS-CoV-2 replication even when inoculated with 2 logs higher multiplicity of infection (approximate MOI 0.1 for SARS-CoV-2 versus 0.001-0.002 for seasonal viruses), no such effect was seen when the order of infection was inverted, even when the incubation time between the two infections was shortened (in order to establish a co-infection during the exponential phase of SARS-CoV-2 infection). Our results indicate that the sequence of infection events influences the fate of SARS-CoV-2 infection. Regardless the order of infections …, no adaptation was observed in SARS-CoV-2 after co-infection (data not shown).
Bai et al, investigated coinfection between SARS-CoV-2 and found that preinfection with influenza A significantly promoted the infectivity of SARS-CoV-2, leading to more severe outcomes.
The upcoming flu season in the Northern Hemisphere merging with the current COVID-19 pandemic raises a potentially severe threat to public health. Through experimental coinfection with influenza A virus (IAV) and either pseudotyped or live SARS-CoV-2 virus, we found that IAV preinfection significantly promoted the infectivity of SARS-CoV-2 in a broad range of cell types. Remarkably, in vivo, increased SARS-CoV-2 viral load and more severe lung damage were observed in mice coinfected with IAV. Moreover, such enhancement of SARS-CoV-2 infectivity was not observed with several other respiratory viruses, likely due to a unique feature of IAV to elevate ACE2 expression. This study illustrates that IAV has a unique ability to aggravate SARS-CoV-2 infection, and thus, prevention of IAV infection is of great significance during the COVID-19 pandemic.
Finally, and perhaps most significantly, this Nature paper by Bai et al found that coinfection with influenza A (IAV) actually enhances SARS-CoV-2 infectivity! They tested whether IAV infection could affect the subsequent SARS-CoV-2 infection in both cultured cells and mice, stating that:
…..we found that IAV preinfection significantly promoted the infectivity of SARS-CoV-2 in a broad range of cell types. Remarkably, in vivo, increased SARS-CoV-2 viral load and more severe lung damage were observed in mice coinfected with IAV. Moreover, such enhancement of SARS-CoV-2 infectivity was not observed with several other respiratory viruses, likely due to a unique feature of IAV to elevate ACE2 expression. This study illustrates that IAV has a unique ability to aggravate SARS-CoV-2 infection….
So, is the theory that viral interference caused the eradication of the flu a myth?
Observational studies
An observational study by Stowe et al reported interactions between SARS-CoV-2 and influenza, and the impact of co-infection on disease severity. They used data for influenza and SARS-CoV-2 collected from England’s national surveillance systems between 20 January 2020 and 25 April 2020.
In their paper they conclude two things:
The risk of testing positive for SARS-CoV-2 was 58% lower among influenza-positive cases and
Patients with a co-infection had a risk of death of 5.92 (95% confidence interval: 3.21–10.91) times greater than those with neither influenza nor SARS-CoV-2. The odds of ventilator use, or death and intensive care unit admission or death were greatest among coinfected patients.
So here we see lower co-infection rates, but significant numbers of co-infections were indeed discovered. However, the study sampled people who were tested for both influenza and SARS-CoV-2 within 7 days of each other, without recording the order of the tests, so we can conclude little about whether previous infection with SARS-CoV-2 prevented infection by flu.
It is notable that in Spring 2020 there was up to a 10-times higher risk of death in people with a SARS-CoV-2 co-infection with flu. And this correlated with ventilator use. However, with hindsight we now know that, as a matter of protocol rather than genuine health needs, many covid patients were unnecessarily put on ventilators leading to increased risk of their death.
Of course, tracking of both flu and SARS-CoV-2 was routinely performed worldwide by national health bodies. The independent newspaper reported for Public Health England (PHE):
…of the 685,243 samples that have been reviewed at PHE’s laboratories since the first week of January, not a single one has tested positive for influenza. In the week up to 31 December 2020, just one case of flu was confirmed by laboratory analysis.
Think about this. Nearly seven hundred thousand tests and they are all negative, except one. And that single positive was confirmed to be a true positive. So, there was not one single FALSE positive test result. This just is not possible for any test, as it implies a specificity of 100%, zero chance of cross contamination and perfect laboratory conditions, which we know cannot possibly be true.
Next, in October 2022 the CDC published a paper on circulation of human coronaviruses (HCoVs) and found that the cold season had shifted in 2020:
They also reported evidence of coinfection of HCoVs and flu in data collected from 2014 until 2021:
From this study it is clear that HCoVs can happily coinfect with flu and other coronaviruses, showing that people might carry a nexus of infections by a host of different viruses. Given that SARS-CoV-2 is simply another coronavirus there is no reason to suppose that it behaves any differently from the others.
Another study, published in Nature Communications, by Butler et al used shotgun transcription to test for many kinds and strains of virus extant in the initial spring wave in New York City (NYC) in Spring 2020:
So, during the NYC deadly Spring wave, when SARS-CoV-2 was rampant, over 23% of patients being admitted to hospital were found to have influenza A. Bearing in mind that in a typical peak flu season we might see 20-40% of ILIs testing positive for flu this shows that in March-May 2023 the flu season was in full swing in NYC despite a co-occurring peak in SARS-CoV-2 prevalence.
They also observed a coinfection rate of around 3% between SARS-CoV-2 and other viruses:
Lastly, Dao et al conducted a meta-analysis of dozens of studies reporting rates of coinfection and found wide variability in rates in many studies, but some very high rates in some:
This Chinese paper by Yue et al reports on 307 SARS-CoV-2 infected patients, finding significant levels of coinfection:
Unexpectedly, there were only 42.7% (131) of SARS-CoV-2 single positive patients. Most of the SARS-CoV-2 infected patients were also positive for influenza viruses, including influenza A (49.8%) and influenza B (7.5%), taking up 57.3% (176/307) in total. Notably, early patients with COVID-19 were almost all coinfected with influenza B virus while influenza A virus infection has become prominent in the co-infection patients since 28 January onwards, which indicated that the two types of influenza viruses appeared a competing relationship.
It should be noted that the rate of coinfection found in all of these studies will depend on the testing process and potential influence of testing protocols, procedures and the effect of quarantines, as described by us here, hence we should not be surprised by such wide variability in these results.
The Twindemic
The return of flu was presaged by a sequence of significant events:
In August 2021 New York Times warned of the possibility of an upcoming Twindemic of flu and SARS-CoV-2.
The omicron variant of SARS-CoV-2 emerged in South Africa on 24 November 2021 and was said to have then spread at an unprecedented rate thereafter.
Then in January 2022 something odd happened:
Israel reported the first coinfections of flu and SARS-CoV-2, referred to as flurona.
The Washington Post reported that flurona coinfections were increasing as omicron surged.
Given the omicron variant was said to be milder and had outcompeted all other SARS-CoV-2 variants prevailing beforehand, this was presented as the main reason for relaxing lockdowns and quarantines throughout the world. Omicron came just in time to enable flu to reappear and then for coinfection of flu and SARS-CoV-2 to become possible, whereas before it was considered impossible. And with amazing prescience the New York Times predicted that a twindemic was imminent at a time when co-infection was deemed highly improbable, because flu had disappeared.
PCR Testing
We are all painfully aware of the inaccuracy of using PCR to test for SARS-CoV-2, and a useful review of SARS-CoV-2 PCR can be found here:
Another recent publication by Collateral Global highlights the PCR scandal in the UK. Our interpretation of their conclusions is that PCR testing in the UK is not effectively regulated, and that PCR testing is effectively as opaque as a black box.
Much of the discussion in the Daily Beagle focused on cycle thresholds which might determine whether there is SARS-CoV-2 in the sample or not. But focusing on this alone side-steps questions of cross-reactivity, non-specificity, cross contamination or some outcome synergistic with high amplification. These are central to whether we can determine whether another pathogen (such as flu) might be the actual cause of a false positive test result for SARS-CoV-2.
This article noted that the possibility of cross reactivity with flus, other coronaviruses and bacterial contamination was actually the reality, and this reality was recognised as far back as 2020. However, it appears that the magnitude of the problem was underappreciated and misunderstood at the time.
There is so much PCR kit heterogeneity that it can be difficult to know which PCR test kits can be trusted and which cannot. Some PCR kits claim to be perfectly accurate, with no cross reactivity, such as GeneXpert , GenMark and BioFire. However, in June 2020 this Australian validation of the Beijing Genomics Institute (BGI) test kit reveals a specificity of 97.5% at one laboratory. Also, this study that appeared in the Journal of Clinical Virology looked at the accuracy of the Australian Diagnostics multiplex kit, which also tests for flus, and found a specificity of 92%.
We should be wary of taking PCR manufacturer data at face value when we know that viruses continually mutate and are a moving target. As they mutate the potential for cross reaction and non-specificity obviously increases and the test, invented at a particular point in time, inevitably become progressively less trustworthy.
The central question about PCR is therefore this:
If we don’t believe the PCR test can diagnose the presence of SARS-CoV-2
why should we trust it to diagnose the absence of influenza?
Australia in 2020 is used by some as the basis to claim that SARS-CoV-2 PCR kits are perfect as they had a long stretch of 1:10K positivity off-season1. In response to an FOI request the ONS deployed the same lazy logic with regards PCR testing in the UK:
“We know the specificity of our test must be very close to 100% as the low number of positive tests in our study over the summer of 2020 means that specificity would be very high even if all positives were false.”
The ONS are claiming that because the number of PCR positives were so low in the summer, when SARS-CoV-2 was not circulating, then the tests must therefore be perfectly specific. However, this claim only makes logical sense if the PCR tests undertaken were actually subject to challenge by other circulating viruses or bacteria that had the capacity to trigger a non-specific false positive result. In the absence of a competing challenge then a negative test result would be inevitable and proves nothing2. Further, given that both SARS-CoV-2 and the flu circulate during winter then the absence of both in summer would logically lead to a high rate of true negative PCR test results in summer.
To put it another way if SARS-CoV-2 PCR cross reacts with flu then when flu is present during the winter this will generate PCR false positives for SARS-CoV-2. If flu is absent in the summer but other non-seasonal pathogens or contaminants were circulating, that caused false positives, we would observe a high false positive rate during the summer season. The fact that we did not see high false positive rates during the summer logically means that the kits are predominately picking up flu in the winter when it is circulating. We could use similar arguments for cross reaction with other competing winter coronaviruses (which as far as we know continued to circulate and were unaffected by viral interference).
Back in December 2020 we raised the issue of the role of confirmatory testing being done in the summer but not in the winter flu season in the UK. By performing confirmatory testing for SARS-CoV-2 during a period of low prevalence the false positive rate would depress case rates to make the PCR testing look accurate and, when confirmatory testing ceases, it will inflate the SARS-CoV-2 case rate.
In the early part of the pandemic doctors were incentivised to diagnose SARS-CoV-2, where the symptoms are indistinguishable from flu, for symptoms which would have hitherto been attributed to Influenza-like-illnesses (ILIs). That incentive was achieved by a combination of authoritative diktat by the WHO, who mandated that a respiratory death could be certificated as covid-19 deaths on the flimsiest of grounds, and the all-pervasive fear caused by the ceaseless propaganda about a novel and deadly virus. And this despite the fact that the UKHSA (Health Security Agency) had ruled that SARS-CoV-2 was not a High Consequence Infectious Disease.
PCR Multiplex kits
In early 2020 we assume influenza and SARS-CoV-2 testing was performed by different PCR kits but by July 2020 the CDC approved the first multiplex (multi-virus) kits under EUA to detect both influenzas and SARS-CoV-2. After their near universal global roll-out flu disappeared over winter 2020/21. This may be a coincidence.
It seems to us that single virus, rather than multi-virus test kits, that are sensitive and specific to a single organism, would surely reduce the risk of shared failure modes and common causes of error. Diverse types of PCR kits specialising in the diagnosis of separate and different viruses would reduce the risk of cross-contamination or confusion about whether a positive means a covid positive or an influenza positive or both.
Note that we have not discovered a smoking gun that exposes systemic problems with ALL multi-virus PCR kits. Some of the early PCR kits we know to be unreliable but after the CDC EUA approval of multi-viral kits many were declared to have perfect specificity. We have no idea how and why there was a step change in reliability for these kits, if indeed there was actually any real improvement. In any case, given the huge variety of kits available, of unknown provenance, we cannot simply assume perfection across the board.
The global downward trend in bacterial infections, as well as in virtually all other infections during spring 2020 is amply illustrated by this screenshot chart, from twitter. The chart was published by the BioFire syndromic trends reporting system and shows the percentage detection rate of pathogens, in the USA, by BioFire clinical diagnostic systems (PCR), from 2019 through to 2021. The reported rate of viral & bacterial pathogens detected at least halved after SARS-CoV-2 appears on the scene in the USA, UK and Europe in February 2020.
A drop in virtually all pathogens tracked by BioFire globally cannot be explained by viral or bacterial interference.
There are some potential failure modes worth investigating that might provide some insight into what might be going on:
Co-infection with both flu and SARS-CoV-2 may occur at the same time. Is a positive for SARS-CoV-2 somehow prioritised by the tests? Perhaps by SARS-CoV-2 masking the existence of flu or the tests showing this?
Often when people think of PCR they think of a biological/chemical reaction without considering that it takes place within a wider system involving technology, people, procedures and policies. Each and all of these have a potential role to play in generating results and are thus potential sources of systematic or random error. One potential vulnerability is that PCR equipment uses proprietary software algorithms and are connected to the internet. Yet we do not know whether the software is independently audited. Likewise, we do not know whether the chain of custody for samples, or their reporting, is respected. It is therefore not inconceivable that these, and more, vulnerabilities exist in this wider system that might be exploitable.
Clearly, we are speculating here. But things do not add up.
Flu and covid-19 cases in the USA from 2010 to 2021.
Sources: CDC and Our World in Data
Discussion
In theory there is no difference between theory and practice,
……while in practice there is.
Microbiology or virology theory is not our area of expertise hence we have not presented any arguments here rooted in theory. Instead, we have taken the sceptical option and asked - where is the empirical evidence? Anyone, no matter their credentials, can and should be able to ask this question.
We have found there is little empirical evidence that proves SARS-CoV-2 interferes with the flu in a dominant way. Therefore, there is no support for the widespread assumption that SARS-CoV-2 prevents flu’s transmission or infection. This is one of the central planks of the covid crisis and it looks to be wrong.
Flu did not globally disappear since we know it was playing hide-and-seek in some far-flung places. If we accept flu was in circulation, then we must entertain the possibility of alternative explanations, not for the disappearance of flu, but for the disappearance of positive flu test results, especially false positive results.
Also, recall that flu disappeared simultaneously just as SARS-CoV-2 appeared simultaneously across the globe. The omicron variant of SARS-CoV-2 appeared at the end of 2021, and it did so in near synchronicity across the globe. Coincidentally flu then reappeared and did so simultaneously globally with no evidence of transmission from place to place. The sequence of these events does not concord with another central plank of virology - the idea of viral spread. A seasonal trigger is often touted as an explanation for the synchronous appearance of flu at the end of 2021, yet this does not explain the fact that flu had not disappeared from Haiti, Afghanistan, Pakistan, Bangladesh and Laos.
Despite the similarity of the symptoms of flu with those of SARS-CoV-2 it was, at least initially, the infection fatality rate for SARS-CoV-2 that differentiated it from the flu - its novelty was dependant on its perceived elevated lethality. However, over time the infection fatality rates for SARS-CoV-2 have converged on that for the flu and now the deadliness of one is indistinguishable from the other. Why then do we, three years later, do we consider SARS-CoV-2 to be more novel than flu or any other respiratory viral infection? Given that the symptoms of both overlap to an extent which makes each completely indistinguishable from the other based on clinical presentation, legitimate questions have been raised as to the circumstances that led SARS-CoV-2 to be identified as a novel virus in the first place.
Given we cannot trust PCR tests for SARS-CoV-2, why should they be accepted as proof of the absence of flu? The evidence suggests that influenza and SARS-CoV-2 do not significantly interfere with each other, and given no false positives for flu were reported at all, how else can we explain the disappearance of flu except by changes in the PCR testing process? We know from the BioFire testing that all bacterial and viral pathogens except for SARS-CoV-2 decreased precipitously just when the pandemic was announced. This cannot be explained by viral or bacterial interference.
If flu has vanished there would surely be reduced evidence of zoonotic transmission of flu in animals, or from animals to humans via animal virus reservoirs (noted by “sl”). Dogs, cats and other animals all get flu and coronaviruses, yet we have no evidence that flu has been displaced by SARS-CoV-2 in these various animal populations.
Of course, non-pharmaceutical interventions, such as masks and social distance are also touted as the reason for the disappearance of the flu but there is zero empirical or theoretical evidence to support this either. Indeed, if they worked for the flu why did they not work to prevent the transmission of SARS-CoV-2, given that the primary mechanism for both appears to be aerosol transmission?
The fact that flu did return and co-existed with SARS-CoV-2 during the twindemics of 2021/22 and 2022/23 should be the nail in the coffin for the idea that flu disappeared because of viral interference from a novel interloper.
These are no doubt controversial conclusions but, given the evidence, a reasonable question to ask is: Was covid-19 disease actually entirely new, or is it simply caused by misattributing flu, or the myriad of other causes of respiratory illnesses, as SARS-CoV-2? Or is there some other unknown mechanism that generates one or the other or indeed both?
Private correspondence with Kevin McKernan
Kevin McKernan on PANDATA PCR Smoke and Mirrors twitter space 2nd April 2023 (from minute 37)
A lot to unpick here. There will no doubt be those who will claim that there was no SARS-CoV-2 virus at all and that all tests and all symptoms attributed to the presence of the 'novel' Covid virus were common colds, 'flu and viral and bacterial pneumonia. Then there will be those who claim that SARS-CoV-2 did not suddenly appear in Dec 2019 and the 'flu virus did not mysteriously disappear six months or so later - because viruses don't exist!
"Despite the similarity of the symptoms of flu with those of SARS-CoV-2 it was, at least initially, the infection fatality rate for SARS-CoV-2 that differentiated it from the flu - its novelty was dependant on its perceived elevated lethality. However, over time the infection fatality rates for SARS-CoV-2 have converged on that for the flu and now the deadliness of one is indistinguishable from the other. Why then do we, three years later, do we consider SARS-CoV-2 to be more novel than flu or any other respiratory viral infection? Given that the symptoms of both overlap to an extent which makes each completely indistinguishable from the other based on clinical presentation, legitimate questions have been raised as to the circumstances that led SARS-CoV-2 to be identified as a novel virus in the first place."
Its novelty was not just defined by the scary infection fatality rate put out by the WHO and others at the beginning of the so called 'pandemic'. It was also defined by some relatively mild, but very unusual symptoms described by people who caught 'something' - even as far back as autumn 2019. There are plenty of people who've had colds and 'flu who will attest to feeling that there was something quite unique about this 'new' infection. Its novelty was additionally defined by a seemingly very unusual, if not unique, pathology when it manifested as severe or fatal disease. Its novelty was also defined by the highly skewed vulnerability curve, where the very old and those with co-morbidities were at disproportionate risk, whilst (unlike with 'flu) much younger people were at statistically zero risk.
So personally, I think it is entirely possible, likely even, that 'flu positive tests and symptomatic 'flu cases were attributed to SARS-CoV-2, but I think the SARS-CoV-2 virus was still present and causing disease.
The influenza virus have not "disappeared", it never manifested on such scale to begin with. The influenza numbers were inflated artificially for decades via RT-PCR testing, to coerce the cattle into seasonal "flu shots". COVID-19 was perceived to be a similar source of revenue by mainstream vaccine manufacturers, who planned to roll out traditional vaccines on a usual schedule. However, the mRNA developers successfully interdicted via "Operation Warpspeed", and the situation became somewhat chaotic, as we can now see