Lancet: COVID-19 causes long term brain damage

Yeh, let it spread because Scummo says we should. Via The Lancet:

Abstract

Background

Increasing evidence supported the possible neuro-invasion potential of SARS-CoV-2. However, no studies were conducted to explore the existence of the micro-structural changes in the central nervous system after infection. We aimed to identify the existence of potential brain micro-structural changes related to SARS-CoV-2.

Methods

In this prospective study, diffusion tensor imaging (DTI) and 3D high-resolution T1WI sequences were acquired in 60 recovered COVID-19 patients (56.67% male; age: 44.10 ± 16.00) and 39 age- and sex-matched non-COVID-19 controls (56.41% male; age: 45.88 ± 13.90). Registered fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) were quantified for DTI, and an index score system was introduced. Regional volumes derived from Voxel-based Morphometry (VBM) and DTI metrics were compared using analysis of covariance (ANCOVA). Two sample t-test and Spearman correlation were conducted to assess the relationships among imaging indices, index scores and clinical information.

Findings

In this follow-up stage, neurological symptoms were presented in 55% COVID-19 patients. COVID-19 patients had statistically significantly higher bilateral gray matter volumes (GMV) in olfactory cortices, hippocampi, insulas, left Rolandic operculum, left Heschl’s gyrus and right cingulate gyrus and a general decline of MD, AD, RD accompanied with an increase of FA in white matter, especially AD in the right CR, EC and SFF, and MD in SFF compared with non-COVID-19 volunteers (corrected p value <0.05). Global GMV, GMVs in left Rolandic operculum, right cingulate, bilateral hippocampi, left Heschl’s gyrus, and Global MD of WM were found to correlate with memory loss (p value <0.05). GMVs in the right cingulate gyrus and left hippocampus were related to smell loss (p value <0.05). MD-GM score, global GMV, and GMV in right cingulate gyrus were correlated with LDH level (p value <0.05).

Interpretation

Study findings revealed possible disruption to micro-structural and functional brain integrity in the recovery stages of COVID-19, suggesting the long-term consequences of SARS-CoV-2.

Introduction

Coronavirus Disease 2019 (COVID-19), an illness caused by the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), is an on-going viral pandemic and has spread to the whole world. To date, it has been spreading globally with nearly 4,700,000 active infections and the total death toll was over 560,000 [1]. As a member of the coronavirus family, SARS-CoV-2 shares a 77.2% amino acid identity, 72.8% sequence identity and structural similarity with Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) [2,3]. With high affinity of the receptor-binding domain of Angiotensin Converting Enzyme-2 (ACE-2), SARS-CoV-2 invades human cells in the same way as SARS-CoV [4,5]. In light of the neurological invasion of SARS-CoV proved by abundant studies, it is plausible to hypothesize that SARS-CoV-2 has the potential to attack the central nervous system (CNS) as well [6].

Increasing evidence supported the neuro-invading potential of SARS-CoV-2. According to the first-hand evidence from Wuhan, 36.4% of COVID-19 patients presented neurological symptoms such as dizziness, headache and impaired consciousness during hospitalization. Furthermore, the percentage and extensiveness were higher in severe patients [7]. Except the frequent olfactory and gustatory dysfunctions in mild-to-moderate COVID-19 patients recorded by 12 European hospitals, scattered cases of various neurological diseases including encephalitis, stroke, micro-hemorrhage, hemorrhage posterior reversible encephalopathy and cerebral venous embolism were also reported in hospitalized patients [8, 9, 10]. Additionally, it was documented that the specific SARS-CoV-2 RNA was detected in the cerebral-spinal fluid (CSF) of a COVID-19 patient [11]. Although no definite description of the pathological findings has been recorded, all the aforementioned evidence indicated SARS-CoV-2 was neuro-invasive just like SARS-CoV [12].

Based on previous researches, coronaviruses can cause demyelination, neurodegeneration, and cellular senescence which accelerate brain aging and exacerbate neurodegenerative pathology [4,13, 14, 15, 16]. However, only scattered neurological cases in COVID-19 patients were collected to document the neurological changes during the acute infection period and so far, no long-term observation has been conducted to explore possible structural changes in the CNS. Despite satisfactory recovery in the majority of COVID-19 patients, they will have a great burden if there are neurological consequences. Therefore, it was necessary to investigate the long-term impact of SARS-CoV-2 infection on the CNS, especially on the structures easily attacked by virus and the structures highly-expressing ACE-2 [3,17].

In contrast to the pathological methods, in-vivo Magnetic Resonance Imaging (MRI) could reflect the cerebral structures non-invasively. The possible micro-structural damage in CNS could be detected by structural MRI and diffusion tensor imaging (DTI). Axial diffusivity (AD), radial diffusivity (RD), mean diffusivity (MD) and fractional anisotropy (FA) can be calculated using track-based spatial statistics (TBSS) [18]. Together with volumetric analysis, DTI is widely used in a large scale of neuro-radiological studies to detect micro-structural changes in patients with cerebral viral infections, Human Immunodeficiency Virus (HIV) and Herpes Simplex Virus (HSV), etc [19,20]. So far, no researches have been found to describe the cerebral changes after SARS-CoV-2 infection.
Therefore, in the current study, we aimed to apply volumetric and diffusion measurements in recovered COVID-19 patients to identify the existence of potential long-term brain structural changes related to SARS-CoV-2, which could provide better insights to understand the impact of SARS-CoV-2 on the CNS.

Discussion

In this prospective work, we recorded the detailed cerebral volumetric, DTI metrics 3 months after SARS-CoV-2 infection by applying DTI and 3D T1WI in 60 recovered COVID-19 patients and 39 age- and sex-matched normal volunteers. Overall, these recovered COVID-19 patients were more likely to have enlarged olfactory cortices, hippocampi, insulas, Heschl’s gyrus, Rolandic operculum and cingulate gyrus, and a general decline of MD, AD, RD accompanied with an increase of FA in white matter, especially AD in the right CR, EC and SFF, and MD in SFF compared with non-COVID-19 volunteers. Global GMV, GMVs in left Rolandic operculum, right cingulate, bilateral hippocampus, left Heschl’s gyrus, and Global MD of WM were found to correlate with memory loss. GMVs in right cingulate gyrus and left hippocampus were related to smell loss. MD-GM score, global GMV, and GMV in right cingulate gyrus were correlated with LDH level.
Given the olfactory and gustatory dysfunction in COVID-19 patients and evidence of olfactory epithelium invasion by SARS-CoV, the olfactory gyrus was thought to be the first functional area in CNS to be infected by SARS-CoV-2 [26]. To avoid cross-infection, patients were unable to undertake MRI scans during the acute phase, but we are still curious about whether any micro-structural changes exist in the recovery stage of COVID-19 and whether any clues were left to suggest the probable intracranial infection route.

According to our results, significant enlarged volumes were observed in the bilateral olfactory cortices, hippocampi, insulas, left Heschl’s gyrus, left Rolandic operculum and right cingulate gyrus. All these structures mentioned above belonged to the central olfactory system. Among them, olfactory cortex, also named as piriform cortex, directly receives axonal projections from olfactory bulb (OB), is referred to as a part of ‘primary olfactory cortex’. Other structures are the cortical targets of primary olfactory cortex in the bilateral limbic lobe, temporal cortices, which were referred as ‘secondary olfactory cortex’ [27]. It was reported that the frequent olfactory loss during the course of upper respiratory tract infections (URTI) resulted in loss of stimulation and subsequent volume loss in the acute phase, while after olfactory recovery, the volumes of GM in the central olfactory system got enlarged subsequently [28,29]. We analyzed the GMV difference between patients with or without olfactory loss and found the GMVs of the central olfactory system were generally smaller in patients with persistent olfactory loss compared with those without olfactory problems which was aligned with previous similar studies (Supplementary Table 2) [28].

Several possible invasion routes of SARS-CoV-2 were raised including hematogenous, lymphatic and neuro retrograde routes, etc., yet the exact route was unknown. Based on our findings, the gray matter volumetric changes in the central olfactory system provided a speculation that SARS-CoV-2 might enter the CNS via an OB-mediated neuronal retrograde route. Two reasons were suspected to play a role in these GMV enlargement: the neurogenesis and functional compensation. Firstly, patients were suspected to experience neurogenesis. It is well accepted that neurogenesis in adults are restricted to two regions, the subventricular zone (SVZ) and the sub-granular layer of the dentate gyrus of the hippocampus [30]. The neuroblasts from SVZ migrate along the rostral migratory stream, enter olfactory cortex first and finally replace interneurons (e.g., periglomerular cells, granular cells) in the OB [30]. Therefore, the increasing neurons possibly resulted in the enlargement of the GMV in the olfactory system. Secondly, in order to compensate for impaired olfaction, the increased functional engagement of brain regions would be hypertrophy, which was proved to have enlarged neurons and increasing number of dendritic spines by experimental studies in sensory deprivation models [28]. These two reasons might be an explanation of the enlarged GMV, while further pathological exploration was needed.
In general, lower diffusivity parameters (MD, AD, RD) and higher FA values were recognized in the white matter from COVID-19 cohort. In addition, the diffusivity (MD and AD) of right CR, EC and SFF decreased significantly. The CR, consisting massive bundle of projection fibers, connects the cortex to the brainstem and the thalamus in afferent and efferent manners [31]. The EC and SFF are series of association fibers, connecting frontal, parietal, and temporal cortices. White matter was not the main target for neurotropic virus; however, the connecting fibers could act as the channel for intracranial viral transmission. Different from the elevated MD with compressed volume in fibers in hydrocephalus, the enlargement of white matter fibers, decreased MD values and elevated FA suggested a greater alignment of fibers and limited diffusion freedom, indicating a possible intrinsic re-construction (e.g. remyelination) process that occurred after infection [32].
It was interesting to notice that all the diffusivity abnormalities in the white matter restricted in the right hemisphere, without asymmetrical symptoms reported by COVID-19 patients. Since the blood flow rate and volume was higher in the hemisphere dominant for handedness, we hypothesized that the predominance of abnormal white matter diffusivities might be related to the difference of blood volume in bilateral hemispheres [33]. However, after comparing these abnormal diffusivity indices between lefthanded and righthanded patients, no difference was found (Supplementary Table 1). The asymmetrical phenomenon was detected in other studies as well [28,34]. The right-side predominance in odorant perception has been indicated by multiple olfactory functional studies which was not fully understood. The diffusivity changes on the right side might be related to the right-side odorant perception in which further exploration was needed [28].

During SARS-CoV-2 infection, 41/60 (68.33%) patients had neurological symptoms and over 50% recovered patients still had symptoms 3 months later. It was interesting to find the GMV in hippocampi (a key part in the organization of memory) and cingulate gyri (an important part of limbic system) were negatively related to loss of smell during infection and loss of memory 3 month later, which could support our hypothesis of neurogenesis in these regions mentioned above. Tremor was found to be negatively related to FA_WM score both in the acute stage and at the 3-month follow-up point which indicated a destruction of WM fibers in both hemispheres, possibly resulted from SARS-CoV-2 induced cytokine storm [35].
According to WHO guideline, COVID-19 patients were divided into mild, severe and critical types based on their clinical information and laboratory results [21]. No significant difference was observed between severe and non-severe groups. But the clinical types were positively related to MD values in bilateral cingulate gyri (r=0.271 and 0.272, p=0.035 and 0.036 respectively), implying the more severe the case was, the higher the MD value of bilateral cingulate gyri was presented. Cingulate gyrus usually plays an important role in attention, motivation, decision making, learning, and cost-benefit calculation, as well as conflict and error monitoring, which is frequently affected in limbic encephalitis [36]. Therefore, the dysregulated cytokine response was speculated in severe cases [35].
After exploring the relationship between laboratory data and DTI metrics, the global GMV was significantly but slightly correlated with the LDH concentration in COVID-19 patients. LDH is one of the key enzymes in the glycolytic pathway, highly expressed in cells from kidney, heart, liver and brain [37]. Elevated concentrations of LDH are observed in patients with encephalitis, ischemic stroke and head injuries [37]. Higher concentration of serum LDH always follows tissue breakdown and is closely linked to the deterioration and poor outcome [38]. The decreased global GMV in LDH-elevated patients might indicate an atrophy due to a severe inflammatory response.
Since the hemostatic abnormalities, including disseminated intravascular coagulation (DIC) and severe inflammatory response, were frequently observed in COVID-19 patients, individuals may predispose to cerebral-vascular events caused by infection and treatment [39]. An index score system was introduced into our study to investigate the existence of micro-structural abnormalities due to micro-vessel diseases. The ischemic changes are known to be accompanied with lower FA value and higher MD value in the ischemic lesions. However, our findings showed that FA-WM score was higher, MD-GM and MD-WM scores were lower in the COVID-19 group compared with the control group, and the differences were insignificant. Thus, no obvious evidence of micro-vessel diseases was found.

It is important to investigate the relationship between abnormal anatomical brain areas and ACE-2 distribution. It is clarified that SARS-CoV-2 enters the host cell by attaching with ACE-2 via Spike (S) glycoprotein. Therefore, the more expression of ACE-2 might bring more severe abnormalities. The distribution of ACE2 was non-equivalent over the brain and was most frequently expressed in substantia nigra, followed by spinal cord, hippocampus, basal ganglia, limbic system and frontal cortex [17]. Our results suggested that various components in the limbic system were affected structures sharing possible high ACE-2 expression, which were partly aligned with the proposed ACE-2-riched regions. Although we were not able to observe the DTI metrics in substantia nigra since it was not included in the brain atlas we used, it was still very hard to support any relationship between ACE2 expression and affected brain areas.

At the time of writing, there was still no research to detect the cerebral micro-structural changes after SARS-CoV-2 infection from imaging or pathological aspects. Our study gave a hint to possible neurological changes after SARS-CoV-2 infection. The limitations of our study were listed as follows: 1) we did not enroll enough patients with neurological dysfunction or olfactory loss, therefore the relationship between GMV/diffusivity changes and olfactory symptoms would be missed; 2) as a single-centered study, a selection bias might result from limited ethnical and regional characteristics of the participants, and possible mutants of SARS-CoV-2 in other countries, and limit the generalization of the study; 3) the atlas we applied did not contain the structure in brainstem, therefore, we failed to obtain the volumetric and DTI information about the nucleus in brainstem, some of which were quite important, especially the solitary nuclei.
In this prospective study, volumetric and micro-structural abnormalities were detected mainly in the central olfactory cortices, partial white matter in the right hemisphere from recovered COVID-19 patients, providing new evidence to the neurological damage of SARS-CoV-2. The abnormalities in these brain areas might cause long-term burden to COVID-19 patients after recovery, which was thus worth public attention.

6. Contributors

Yiping Lu, Bo Yin and Daoying Geng conceived and designed the research. Yiping Lu, Anling Xiao, Xuanxuan Li, Nan Mei, Yajing Zhao and Dongdong Wang contributed to data collection and interpretation. Yiping Lu, Xuanxuan Li, Pu-Yeh Wu, Chu-Chung Huang and Tianye Jia contributed to statistical analysis. Yiping Lu, Xuanxuan Li and Nan Mei contributed to draft and revise the manuscript. Anling Xiao and Bo Yin supervised the whole research. Yiping Lu, Xuanxuan Li, Daoying Geng and Nan Mei contributed equally to this study. All authors gave final approval for the version to be published.

David Llewellyn-Smith
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Comments

    • This is a novel (new) virus, and as such we really do not know a lot about it yet. We’re learning more all the time, and it’s not looking good. There are long term sequelae that were not anticipated. There is multisystem damage. This is not the flu, it’s much, much worse.

      I know it’s all terribly inconvenient for some people, and ideologically enraging for some, but the only sensible path forward is to eliminate this virus whenever possible in anticipation of 1) a vaccine and/or 2) effective antivirals or other medications.

      • ErmingtonPlumbingMEMBER

        “We aimed to identify the existence of potential brain micro-structural changes related to SARS-CoV-2.”

        Structural changes that allow for the control of peoples Brains using the 5G network!!!!!
        Brain control is so much more powerful than that old fashioned and unscientific “Mind control” hocus-pocus

        https://youtu.be/pGoMgkjbl2Q

        https://youtu.be/zbHFgQ419Qs

      • So it’s basically just a really bad flu
        I mean I got the flu badly maybe 10 years ago, and I obviously have brain damage because I still barrack for the Melbourne Football Club

        • FUDINTHENUDMEMBER

          Well if it’s just a catastrophically and horrendously bad flu then let’s just carry on as normal shall we?

    • What about Boris Johnson? Or Balsinaro in Brazil?

      They weren’t the brightest to start with.

      Anyway, soon they’ll look good because they’ll be compared to geriatric Joe Biden.

    • I doubt alcohol can do it because of 1 night binge. covid seems can do it with 1 infection. If alcohol was that bad I would have been a plant many years ago.

    • Yeah, but on the upside, alcohol consumption also makes people sexier!
      .
      .
      .
      “Ohh, she’s a seven-pinter, that one!”

      • Too true — thankfully I’ve never had a 7-pinter. 4 perhaps.

        Still, there’s always next week … or the next. One should aim to have as many experiences as possible in life.

  1. This neither surprises or overly alarms me. My reading is that it was found in the recovery phase. Longer term effects would be more concerning.

      • That is not what the paper says.
        I would hazard that almost nobody here would have any idea what this paper means let alone its clinical implications. My partner is a radiologist and I reckon she will shrug her shoulders when I show it to her.
        I used to subscribe to a business site. If I want gonzo medical information I can go and talk to the medical students and interns.

        • BaldbadgerMEMBER

          Start complaining when you resubscribe. You might be listened to then. Otherwise feel free to go elsewhere.

        • Does being a radiologist confer knowledge of the brain?

          Or is this general medicine/research knowledge we’re talking about

          So, go show her and report back please?

        • Being a radiologist will help you interpret what this image-based data means in comparison to variation in other diseases. You might also be surprised at the expertise in the room. I have a prediction. Covid 19 will cause changes (decrease) in bone density.

        • Just to be clear I expect changes. I still think we should be treating covid with great caution.

        • Jevons ghostMEMBER

          I read through that paper. I noticed a number of design flaws on a cursory first pass. Apparently no base-line MRI data for either group and apparently no screening of the control group for asymptomatic SARS-2-CoV infection. Prospective study??? High tech bumph. And if we get much more of this sort of stuff out there the health system will be bankrupted by an avalanche of the essentially asymptomatic worried well wanting MRI scans because they might have tested positive for SARS-2-CoV.

      • Technically they mostly loose the mylin sheaths that cote the nerve cells rather than the brain cells being killed. This causes reduced conductivity resulting brain fog and chronic mental fatigue with recovery taking minimum 12 months to years.

  2. Display NameMEMBER

    There are far too many reports of people with various types of organ damage after getting covid for it to be “just like flu”. Clearly these people are a minority and from my reading it appears not to be comorbidity as the cause of additional damage but perhaps genetic susceptibility. We will not know for sure for a while. Sounds like Russian Roulette to me.

    • thinking same.. it will take time before we learn true impact and no one knows for sure if it’s going to be really bad or not to bad for most people. For now, best to not get infected at all but it will be hard to pull it off – unless you are harry.

  3. If I understand the situation correctly, there is no long term immunity, just like the common cold.

    One dose of Covid might damage the brain and vital organs a little bit. 5 doses over ten years will leave people as shambling brain damaged wrecks with significant and widespread organ damage.

    If you catch the first dose at age 20, by 30 you’ll be fcked.

    Average human lifespans are going to go into decline worldwide.

    Thank you so very very much, CCP cnts.

    • If I understand the situation correctly, there is no long term immunity, just like the common cold.

      Antibodies fade fast, but the experts argue that T-cells and other immune cells provide immunity.

      The answer is we don’t really know how long immunity lasts. This question will be answered within a year, in my estimation.

      If it returns annually, slightly mutated, like that other famous coronavirus (the common cold), we are in a very deep hole full of manure.

      • This is not true of any other Coronavirus, so this is hope at best (or vested interests looking to get the worker bees back in the hive at worst), not science.

  4. How is this a problem for Australia? A high IQ is not a prerequisite to be a real estate agent or Deliveroo rider.

  5. GunnamattaMEMBER

    Lancet: COVID-19 causes long term brain damage

    Enough to motivate people to…….

    A. Attend an anti mask rally planned for this weekend
    B. Feel that being asked to self isolate or quarantine, have a COVID19 test (or wear a mask) is a breach of their civil liberties
    C. Think that policing a pandemic management need is akin to incipient Nazi stormtroopers, global elite government, and 24/7 big brother observation for every individual, and somehow more than Google, Ebay, Amazon are already capable of (not to Mention the Chinese)
    D. Enough to think the Australian economy (the very quintessence of a bubble economy, lovingly hand crafted by corrupted political interests over the course of a generation) is somehow more affected by a hard lockdown for however long it takes than an ongoing and rolling series of half lockdowns
    E. All of the above

    • F. Turn this headline “Cerebral Micro-Structural Changes in COVID-19 Patients – An MRI-based 3-month Follow-up Study”
      into a long term brain damage headline that would make a Newscorp tabloid blush.

      • GunnamattaMEMBER

        Well i am seeing in the lancet spiel …..

        Interpretation
        Study findings revealed possible disruption to micro-structural and functional brain integrity in the recovery stages of COVID-19, suggesting the long-term consequences of SARS-CoV-2.

        I dont think anyone at MB need blush too much

    • I believe them because if it is shown to be fake they will retract it. That point is a bit too subtle for some.

    • The Lancet has retracted 34 papers out of over 10,000 issues published (each issue contains many papers). The math is against you

      • Former editors of both the Lancet and the New England Journal of Medicine have claimed that over half of published medical science is simply untrue
        [PubMed] Skeptical of medical science reports?. As a followup, one of the most cited papers in medicine is [PLOS] Why Most Published Research Findings Are False. That second paper should be a wake-up call to anyone who ventures into the medical literature without a highly sceptical attitude to any purported finding.

        A significant body of “medical science” is almost certainly wrong, and in a significant number of cases, deliberately corrupt. Sorting out the what is true & false is even more difficult, no journal is immune, despite it’s impact factor.

        • This is almost entirely restricted to research that has commercial motives, IOW drug trials etc. The pure science side of medical research does not suffer nearly as much

          • Nah, there are huge numbers of dodgy studies published all the time. Probably a lot more should end up retracted than ever do. Publication bias means that this study finding something made it far more likely to be published, and published in a prestigious journal, than if it had found nothing. There are also lots of people ‘juking the stats’ or just plain fabricating data or even entire studies (there have been some good statistical techniques developed recently to spot some of these studies). No single study should ever have too much faith placed in it for this reason. Unfortunately there’s not a lot of career glory in replicating science that has already been done so not a lot of replication work gets done.

          • Publication bias means that this study finding something made it far more likely to be published, and published in a prestigious journal

            The Lancet is one of the most prestigious medical journals in the world. Only very occasionally do dud studies get through and need retraction (way less than 1%). So I find your skepticism odd. I prefer to err on the side of caution and assume that this is good science. You go ahead and scoff, good luck to you and your family.

          • No. I think it probably is good science. But I’ve seen enough good science be revised later to know not to make any important decisions based on just one study.
            Having said that, this study adds a lot of valuable weight to the “do whatever you can to not get this virus” point of view.

  6. Plenty of poorly designed studies out there. I wouldn’t be sweating about these results yet.

    • That could be true

      How many people here though understand risk and how to manage it

      Some, not so much

  7. All of which to say, the WuTangFlu ain’t nuttin to fk wit.
    Unless you’re DrX and other residents of the same thinking, in which case, please take yourselves and your children to the nearest known case and rub yourselves all over that person so you catch it. Report back at Weeks 1-5, months 1-4, then yearly. Cheers!

  8. Interesting that this is a China study, albeit 155 persons who survived Covid19 a modest number. A couple of months ago Caixin published a Covid19 Open Discussion with experts who treated patients during the Wuhan crisis. Well worth viewing. Doctors explored the diverse range of symptom presentation and extreme reactions particularly for those who were admitted to ICU: irreparable damage to lungs, blood vessels (including those of the brain), cytokine storms not dissimilar to those seen in end of life HIV patients where organ damage was extensive, etc. These experts provided treatment suggestions and speculated on the possible longterm outlooks for Covid19 survivors. Not one of them equated Covid19 with the influenza so variable was patient response. They took it very seriously and in China, still do.

    Although I’m broadly libertarian in outlook, China’s response to this virus informed my own. Caution required.

    ps One lifetime China-watcher/author’s personal calculations (via friends and colleagues ‘on the ground’) of deaths in China Hubei province ~300k. Of course we will never know. But they sure as hell shut the place down…

    • PalimpsestMEMBER

      The US experiment (Sweden with added liberty) will help inform assessments. Although, after Florida attempted to massage figures, and results were blocked from going to CDC, I’m not sure how reliable they are now either.

  9. So, they’re saying every disease is bad for you. Even COVID, it seems.
    Well, you learn something every day…

    • ZevombatMEMBER

      Inconvenient to those who made up their minds early to dismiss it as the flu, but there are studies coming out of different countries showing a range of physical and nervous system damage in survivors – even those who weren’t sick enough to be hospitalised

  10. Ronin8317MEMBER

    COVID-19 causes the blood plasma to ‘stick’ together, so they can’t supply enough oxygen to the brain. It’s a very nasty virus. The damage can be prevented if blood oxygen level is monitored and maintained, however since the patient is often unaware of the drop in oxygen level (known as Happy Hypoxia), people will literally drop dead in the street.

  11. Hate to keep banging on but the big sleeper is going to be the potential long term effects to kids youth toddlers etc esp the asymptomatic cases. and very little being done to research this but hey lets take the risk with our kids

    • This virus has the potential, if it keeps coming back like the common cold, to be civilization-ending. That’s not an exaggeration.

      We need a vaccine desperately. 😱

  12. Right so Covid-19 is clearing out all the aged care facilities, in order to open up lots of future capacity for the early onset dementia it will also generate.

    • But that, too, is the weaker members of society dying, is it not? Let’er’rip’s seem to be complacent that the old/weak get taken by the virus, so… wouldn’t it be “better” if the weak self-selected?

      Slippery slope, isn’t it?