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posted by martyb on Monday August 03 2020, @04:04AM   Printer-friendly
from the quantify-*this*-in-dollars dept.

COVID-19 long-term effects: People report ongoing fatigue, brain fog and breathlessness, so what's happening in the body?:

As with many aspects of the new coronavirus, researchers are trying to pull together data to understand the medium-term health effects more fully.

[...] Its impact on the heart still isn't clear, Dr Gallo says, but studies published in recent weeks describe abnormalities in the hearts of patients who have completely cleared the virus.

"[The researchers] asked them about their just general wellbeing and a lot of the patients are commenting on just being generally exhausted and having shortness of breath, some of them having palpitations, atypical chest pain," she says.

What's more, many of these patients weren't that sick with COVID-19 — most of them had managed their illness at home, rather than needing hospital treatment.

[...] Other persistent symptoms people report have to do with the brain: "brain fog", sleeplessness and headaches.'

[...]Fatigue, which is more than just a feeling of tiredness, and can be associated with things like a "foggy" brain, slowed reflexes and headaches, is usually a useful response to infections.

"There's a good reason for that — mounting an immune response to fight an infection takes a huge amount of energy," Dr Landowski says.

"The body wants you to do as little as possible, so you can conserve energy and divert it to the immune system.

Then, once the infection is eliminated, the fatigue dissipates.

"However, in some people, the switch that returns the body back to normal seems to fail, resulting in chronic fatigue."

[...] "Regardless of which cells it's infecting, if it's infecting cells in the brain, it could be causing damage, which could have long-term consequences," Dr Lawson said.

Even if the virus doesn't infect brain cells directly, inflammation caused by the virus could also cause damage to the brain.

Some experts are concerned the medium-term effects on the brain might have consequences that reach further.

In an article in the Journal of Alzheimers Disease Reports, experts raise the question of whether people who've had COVID-19, particularly those whose symptoms included loss of taste or smell, will be at greater risk of conditions including Alzheimer's disease after they recover.

The last-linked article from above (which is open-access), is excerpted here with links sprinkled on some of the unusual terms:

Some of the earliest neurologic findings were in those experiencing COVID-19-related anosmia and dysgeusia [2]. Important to this equation is that COVID-19 may prove to be a risk factor for future neurodegenerative disorders, beyond that which would be expected in the context of other comorbidities and genetic predispositions. Anosmia and the biological processes resulting in this symptom contribute to grey matter loss in cortical regions [3], which is similar to where pathognomonic amyloid plaques are often discovered [4]. Olfactory dysfunction has also been found to be associated with the graduation from mild cognitive impairment (MCI) to AD, serving as a potential identifier for preclinical stages [5].

[...] It has become clear that many age-related conditions are found among those testing positive for COVID-19, though some of these are also related to lifestyle and family history. ... Systolic hypertension in midlife, rather than only late life, is associated with 18% and 25% increased risk of AD, respectively ... These cardiovascular risk factors are directly related to cerebrovascular consequences, such as hypoperfusion, a symptom strongly associated with MCI and AD [14]. Plasma exchange and albumin for AD patients with hypoperfusion, for example, has been shown to improve cognitive deficits and initiate cerebrospinal fluid (CSF) amyloid-β (Aβ)...

Journal Reference:
Jack C. Lennon. Neurologic and Immunologic Complications of COVID-19: Potential Long-Term Risk Factors for AlzheimerΓÇÖs Disease [open], Journal of Alzheimer's Disease Reports (DOI: 10.3233/ADR-200190)

Got it! The millennials surviving COVID-19 today may have higher chances of an early onset of dementia than the baby boomers of today.


Original Submission

 
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  • (Score: 0) by Anonymous Coward on Monday August 03 2020, @02:35PM (14 children)

    by Anonymous Coward on Monday August 03 2020, @02:35PM (#1030737)

    I'm sorry, but most "western" countries are doing fine. The US fucked up bad for some reason, but Canada and the EU are currently doing as well as can be expected as far as the disease is concerned. Yes, some countries in the EU are still having trouble, but most of the EU population is reasonably safe at the moment.
    by the way, I'm confused about what you mean by "western". I assume you mean Canada, USA, and the EEA countries.

    I'd add that some parts of the US are doing much better than others. Mostly the Northeast, because we got hit early (because of wide use of public transport and high population density) and saw the carnage that ensued.

    As such, while it's not everyone, *most* people are being really careful -- wearing masks, staying at least 2m away from others, and not gathering in groups *indoors*.

    The areas where we see low infection rates right now have large numbers of folks who see that we need to work together, protecting each other, not whinging about "muh rights!" and "gub'mint overreach!"

    No one can force you to care about your neighbors and fellow Americans. But like it or not, we share this country. And if we want to get this virus under control, we need to work together as Americans. For all of us.

    It makes me sad that many people only see it as "fuck you Jack! I'm all right," even though that will just extend and worsen this pandemic.

    More's the pity.

  • (Score: -1, Redundant) by Anonymous Coward on Monday August 03 2020, @03:36PM (13 children)

    by Anonymous Coward on Monday August 03 2020, @03:36PM (#1030759)

    Most people in the northeast are already immune. That is why it spreads slowly there now. Like 30-80% of people have pre existing t cell immunity, so only 10-20% of the population gets covid before herd immunity sets in.

    • (Score: 0) by Anonymous Coward on Monday August 03 2020, @04:46PM (1 child)

      by Anonymous Coward on Monday August 03 2020, @04:46PM (#1030787)

      I'd say more like 10-90% ballpark.

      • (Score: 0) by Anonymous Coward on Monday August 03 2020, @05:01PM

        by Anonymous Coward on Monday August 03 2020, @05:01PM (#1030791)

        Depends where you live.

        The teams also asked whether people who haven’t been infected with SARS-CoV-2 also produce cells that combat it. Thiel and colleagues analyzed blood from 68 uninfected people and found that 34% hosted helper T cells that recognized SARS-CoV-2. The La Jolla team detected this crossreactivity in about half of stored blood samples collected between 2015 and 2018, well before the current pandemic began. The researchers think these cells were likely triggered by past infection with one of the four human coronaviruses that cause colds; proteins in these viruses resemble those of SARS-CoV-2.

        https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients-bode-well-long-term-immunity [sciencemag.org]

        Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals, and validation of similarity to common cold human coronaviruses provided a functional basis for postulated heterologous immunity[9] in SARS-CoV-2 infection[10,11]

        https://www.researchsquare.com/article/rs-35331/v1%20 [researchsquare.com]

        Why are there so many anti-science retards on this site?

    • (Score: 0) by Anonymous Coward on Monday August 03 2020, @05:47PM (10 children)

      by Anonymous Coward on Monday August 03 2020, @05:47PM (#1030806)

      Most people in the northeast are already immune. That is why it spreads slowly there now. Like 30-80% of people have pre existing t cell immunity, so only 10-20% of the population gets covid before herd immunity sets in.

      And where did you get those numbers? AFAIK, *Antibody* testing isn't being done on any wide scale, nor is the much more involved (and accurate) T-Cell testing.

      The tests being done are viral tests to see if you are infected *right now*. And, just like the rest of the US, it's taking way too long to get results back. In some cases, 7-14 days. Which is, of course, worse than useless.

      So I ask again, where do you get these numbers to claim that 30-80% are immune? Other than from your rectal cavity?

      Please, do tell.

      • (Score: 0, Disagree) by Anonymous Coward on Monday August 03 2020, @05:55PM (9 children)

        by Anonymous Coward on Monday August 03 2020, @05:55PM (#1030812)

        The refs were posted here:
        https://soylentnews.org/comments.pl?noupdate=1&sid=38801&commentsort=0&mode=threadtos&threshold=-1&highlightthresh=-1&page=1&cid=1030791#commentwrap [soylentnews.org]

        Also, there are cross-reactive antibodies found in 5-10% of adults and much higher (up to 60%) of school children:

        In addition to its implications for serology assay development and interpretation or for the design of
        vaccination studies, potential cross-reactivity between seasonal HCoVs and the pandemic SARS-CoV-
        2 has important ramifications for natural infection. Thorough epidemiological studies of HCoV
        transmission suggest that cross-protective immunity is unlikely to be sterilising or long-lasting39,
        which is also supported by repeated reinfection of all age groups4, sometimes even with
        homologous HCoVs 47. Nevertheless, prior immunity induced by one HCoV has also been reported to
        reduce the transmission of homologous and, importantly, heterologous HCoVs, and to ameliorate
        the symptoms where transmission is not prevented1,4,5. A possible modification of COVID-19 severity
        by prior HCoV infection might account for the age distribution of COVID-19 susceptibility, where
        higher HCoV infection rates in children than in adults5,35,37, correlates with relative protection from
        COVID-1948 , and might also shape seasonal and geographical patterns of transmission.

        Public health measures intended to prevent the spread of SARS-CoV-2 will also prevent the spread of
        and, consequently, maintenance of herd immunity to HCoVs, particularly in children. It is, therefore,
        imperative that any effect, positive or negative, of pre-existing HCoV-elicited immunity on the
        natural course of SARS-CoV-2 infection is fully delineated.

        https://www.biorxiv.org/content/10.1101/2020.05.14.095414v2 [biorxiv.org]

        If all these lockdowns and other measures continue for long enough all this immunity is going away and the problem will be 2-5x worse than it was in April.

        • (Score: 0) by Anonymous Coward on Monday August 03 2020, @06:31PM (8 children)

          by Anonymous Coward on Monday August 03 2020, @06:31PM (#1030847)

          Except the references linked don't say what you think they do.
          https://www.sciencemag.org/news/2020/05/t-cells-found-covid-19-patients-bode-well-long-term-immunity [sciencemag.org]

          The results suggest “one reason that a large chunk of the population may be able to deal with the virus is that we may have some small residual immunity from our exposure to common cold viruses,” says viral immunologist Steven Varga of the University of Iowa. However, neither of the studies attempted to establish that people with crossreactivity don’t become as ill from COVID-19.

          https://www.researchsquare.com/article/rs-35331/v1 [researchsquare.com]

          This is a preprint. Preprints are preliminary reports that have not undergone peer review. They should not be considered conclusive, used to inform clinical practice, or referenced by the media as validated information.
          [...]
          No correlation between antibody titers directed against the nucleocapsid of human common cold coronaviruses (HCoV-229E, HCoV- NL63, HCoV-OC43), as determined by bead-based serological multiplex assays and the intensity of cross-reactive CD4+ and CD8+ T-cell responses in the SARS group, was detected (Extended Data Fig. 3c-h).
          [...]
          Neither the intensity of SARS-CoV-2-specific nor of cross-reactive T-cell responses to HLA class I or HLA-DR EC correlated with disease severity (Fig. 4g). Rather, diversity of T-cell responses in terms of recognition rate of SARS-CoV-2 T-cell epitopes was decreased in patients with more severe COVID-19 symptoms (Fig. 4h, Extended Data Fig. 4b), providing evidence that development of protective immunity requires recognition of multiple SARS- CoV-2 epitopes.

          What was that you were saying? Nothing useful or important.

          kthxbai.

          • (Score: -1, Redundant) by Anonymous Coward on Monday August 03 2020, @06:52PM (7 children)

            by Anonymous Coward on Monday August 03 2020, @06:52PM (#1030861)

            So now t-cell immunity doesnt confer protection either? Just like the WHO tweeted about antibodies... What is the point of it if not to confer protection like for every other virus?

            Also, no idea what the second quote is supposed to prove. Can you clarify what you think it says?

            • (Score: 0) by Anonymous Coward on Monday August 03 2020, @07:12PM (6 children)

              by Anonymous Coward on Monday August 03 2020, @07:12PM (#1030874)

              Also, no idea what the second quote is supposed to prove. Can you clarify what you think it says?

              Your semi-literacy is not my problem. It's yours.

              • (Score: 0) by Anonymous Coward on Monday August 03 2020, @07:24PM (5 children)

                by Anonymous Coward on Monday August 03 2020, @07:24PM (#1030884)

                Well you quoted something that says the cross reactive t-cells originally raised towards cold viruses are important for proper immune response. So, I guess you agree with me then...

                • (Score: 0) by Anonymous Coward on Monday August 03 2020, @07:52PM (4 children)

                  by Anonymous Coward on Monday August 03 2020, @07:52PM (#1030902)

                  No correlation between antibody titers directed against the nucleocapsid of human common cold coronaviruses (HCoV-229E, HCoV- NL63, HCoV-OC43), as determined by bead-based serological multiplex assays and the intensity of cross-reactive CD4+ and CD8+ T-cell responses in the SARS group, was detected

                  Neither the intensity of SARS-CoV-2-specific nor of cross-reactive T-cell responses to HLA class I or HLA-DR EC correlated with disease severity

                  English, motherfucker. Can you read it? Apparently not.

                  Your ignorance is stunning. Get a clue. If you can. I won't hold my breath.

                  • (Score: -1, Troll) by Anonymous Coward on Monday August 03 2020, @08:14PM (3 children)

                    by Anonymous Coward on Monday August 03 2020, @08:14PM (#1030914)

                    "Rather, diversity of T-cell responses in terms of recognition rate of SARS-CoV-2 T-cell epitopes was decreased in patients with more severe COVID-19 symptoms (Fig. 4h, Extended Data Fig. 4b), providing evidence that development of protective immunity requires recognition of multiple SARS- CoV-2 epitopes."

                    Whatever, you apparently have no idea what those words you quoted mean. I hope for your sake you are trolling instead of being profoundly stupid.

                    • (Score: 0) by Anonymous Coward on Monday August 03 2020, @11:57PM (2 children)

                      by Anonymous Coward on Monday August 03 2020, @11:57PM (#1031007)

                      Rather, diversity of T-cell responses in terms of recognition rate of SARS-CoV-2 T-cell epitopes was decreased in patients with more severe COVID-19 symptoms (Fig. 4h, Extended Data Fig. 4b), providing evidence that development of protective immunity requires recognition of multiple SARS- CoV-2 epitopes.

                      This means that while SARS COV2 *may* share epitopes [britannica.com] with other Coronaviruses, antibodies must be able to identify/connect to multiple epitopes, some that are unique to SARS COV2 in order to convey significant levels of immunity. Which fully supports what I said. Which is why I quoted it in the first place.

                      You're a troll and/or a moron. Don't care which. No more feeding for you, asshole. Get back under your bridge!

                      • (Score: -1, Troll) by Anonymous Coward on Tuesday August 04 2020, @12:30AM

                        by Anonymous Coward on Tuesday August 04 2020, @12:30AM (#1031026)

                        It means if you had prior immunity to other coronaviruses that cross react with sars2, then you have "diversity of T-cell responses", which is evidence for "protective immunity".

                        So no, that is not what you said.

                      • (Score: -1, Troll) by Anonymous Coward on Tuesday August 04 2020, @12:33AM

                        by Anonymous Coward on Tuesday August 04 2020, @12:33AM (#1031029)

                        Also it was about t-cells, not even about antibodies. It is so obvious you have no idea what you read.