Coronavirus - General Chat - No statistics

[bruncher]

I guess this is why it is spreading so widely.

So what?

And what do you seek? Another lockdown? So that people like me won't have mild symptoms and a minor inconvenience?

What I appreciate is that people who are unwell take themselves out of circulation for a few days, to avoid spreading infection.

[servodude]

So what?

And what do you seek? Another lockdown? So that people like me won't have mild symptoms and a minor inconvenience?

What I appreciate is that people who are unwell take themselves out of circulation for a few days, to avoid spreading infection.

Not every one covers their mouth when they sneeze, or cough, or washes their hands after the toilet.
If they've made it to adult hood as entitled and thick selfish twats it's unlikely they'll ever learn
... they'll be around until they die out.
Just cross the road and walk on

[Lootman]

So what?

And what do you seek? Another lockdown? So that people like me won't have mild symptoms and a minor inconvenience?

What I appreciate is that people who are unwell take themselves out of circulation for a few days, to avoid spreading infection.

Not everyone has the luxury of taking themselves out of circulation. People have jobs, families, responsibilities. Every time I take a train there is someone on my carriage coughing and sneezing, and this is summer.

And so each individual has to use their judgement on matters like this. The larger point being made here is that Covid has effectively been demoted to something like the common cold. And most people do not stop their life because they have a cold. At this point it is a matter of personal judgement rather than government mandate, and 2020 seems like a long time ago now.

[Charlottesquare]

What I appreciate is that people who are unwell take themselves out of circulation for a few days, to avoid spreading infection.

Not everyone has the luxury of taking themselves out of circulation. People have jobs, families, responsibilities. Every time I take a train there is someone on my carriage coughing and sneezing, and this is summer.

And so each individual has to use their judgement on matters like this. The larger point being made here is that Covid has effectively been demoted to something like the common cold. And most people do not stop their life because they have a cold. At this point it is a matter of personal judgement rather than government mandate, and 2020 seems like a long time ago now.

And employers carry a legal duty of care to their other staff and are responsible for creating a safe working environment

Ten/fifteen years ago staff regularly came in to work and infected their colleagues but these days those that are ill with something infectious are encouraged not to come into work by most sensible employers.

My other half is vulnerable, luckily now retired, but if tradesmen/contractors etc are coming in and out of my office coughing and spluttering etc, they get told not to enter/to leave, if they argue then they likely can kiss goodbye to any more work from us. (One we use regularly possibly had Covid last week- my discussions with him were outside in the car park six feet apart- think he picked up from his wife who picked up from school age son- children, like rats, seem to be spreading the current outbreaks)

[Dicky99]

So what?

And what do you seek? Another lockdown? So that people like me won't have mild symptoms and a minor inconvenience?

What I appreciate is that people who are unwell take themselves out of circulation for a few days, to avoid spreading infection.

I tested positive for covid yesterday. The symptoms came on Monday evening and are milder than the average cold. I took an extra anti histamine that evening thinking it may be pollen related.

Since I had reasons to go to Savers, and out of curiosity, I bought a single test kit and tested positive. This morning symptoms are I'd say minimal such that had I not tested yesterday I'd have forgotten about it by now and put it down to hayfever or a mild summer cold.

So you may appreciate people taking themselves out of circulation but with such mild short lived symptoms, for every person like me who tests there will be (pick a number) of people who don't test because they've no idea they have it.

[Hallucigenia]

This is a good review of Long Covid in the Lancet by Greenhalgh et al.

Long COVID: a clinical update
https://doi.org/10.1016/S0140-6736(24)01136-X

People with long COVID typically recount an initial acute illness that was either paucisymptomatic (ie, with one or a few symptoms—perhaps cough, fever, and breathlessness) or multisymptomatic (ie, with multiple symptoms, which might include shortness of breath, chest pain, cognitive impairment, loss of smell and taste, profound fatigue, muscle and joint pain, gastrointestinal upset, headache, and rashes), although long COVID has also been documented after asymptomatic COVID-19. Following acute COVID-19 infection, people might describe partial or even complete—but temporary—recovery before developing a set of symptoms, either similar to or different from the original illness, which some individuals describe as “strange”, energy-sapping and, in many but not all cases, fluctuating. The underlying pathological mechanisms driving these symptoms are complex and described in panel 2.

A common symptom in long COVID is fatigue, which classically becomes worse following physical or mental exertion (post-exertional symptom exacerbation). Fatigue might be associated with sleep disturbance (especially, unrefreshing sleep and a sensation of being too tired to sleep), exacerbations of pain, and blunting of cognitive function (ie, brain fog), particularly in relation to memory and higher order functions such as multitasking and making complex judgements. People who were admitted to hospital (most usually for acute respiratory distress) or seen in an emergency department during their acute COVID-19 illness are more likely to go on to develop persistent respiratory symptoms, especially breathlessness, although these symptoms might occur in any patient. There might be a characteristic pattern of respiratory symptoms—a constricting or burning sensation in the chest, a sense of not getting enough air in, not being able to fully breathe out, and feeling “gaspy”. Some but not all such cases could fit what clinicians call breathing pattern disorder.

Accompanying allergic symptoms can include rashes (eg, hives), streaming eyes, or blocked nose. Throat and upper gastrointestinal symptoms include altered voice, difficulty swallowing, and nausea, which, combined with persistent inability to smell or taste food, can lead to altered eating patterns, loss or gain in weight, and nutritional deficits; lower gastrointestinal symptoms can include bloating and diarrhoea. Dizziness with hypotension on standing (orthostatic hypotension) or tachycardia without hypotension (postural orthostatic tachycardia syndrome) can be traced back to disturbed autonomic function (dysautonomia). Anxiety and depression often accompany long COVID, especially if multisymptomatic, and teasing out whether the mental health condition or conditions preceded or followed the physical manifestations can be difficult. Older people might present atypically and non-specifically. Sarcopenia can accompany persistent long COVID in people of any age.

A striking characteristic of long COVID is functional impairment: individuals find they cannot do what they could previously do. Many cannot work a full 8-hour day, resulting in withdrawal from the workforce if adjustments and phased returns cannot be accommodated. In severe cases, people are unable to undertake activities of daily living such as washing and dressing, or they find these basic activities so draining they require rest afterwards. The course of long COVID varies. Recovery can progress at different rates, and some people experience periods of apparent recovery followed by relapse. The chance of recovery is highest in people who had a less severe acute illness, are in the first 6 months after that illness, and were vaccinated; people whose illness has lasted between 6 months and 2 years are less likely to fully recover. There is little published research on people who have had long COVID for 2 years or more, but their chances of full recovery appear low. At this stage, the condition typically relapses and remits with compromised quality of life. People with persistent long COVID face substantial economic burden from their inability to work, either at their premorbid level or at all.

Long COVID can be caused or complicated by organ damage or systemic stress that occurred in the acute phase or emerges anew in the post-acute phase (eg, pulmonary embolism, stroke, myocardial infarction, acute kidney injury, hepatobiliary injury, Guillain-Barré syndrome, or sepsis). Compared with people who were not infected, the risk of death or hospitalisation is increased for at least 12–24 months after the acute illness, especially but not exclusively in people who were hospitalised or had severe symptoms during their initial COVID-19 illness. Clinicians should be alert to the increased risk of organ damage, including clot formation and downstream acute infarction consequences, in the subsequent months and even years, especially in the context of multiple SARS-CoV-2 reinfections. New symptoms that emerge with time might reflect respiratory, cardiovascular, neurological, musculoskeletal, autoimmune, and generic (eg, myalgic-encephalomyelitis-like) sequelae or the effect of reinfection. Some people will also have long-term sequelae of medical trauma (eg, post-intensive care syndrome and post-traumatic stress disorder)....

Three main clusters of primary mechanisms are strongly supported by current evidence. The first comprises virus-related mechanisms that include persistence of the SARS-CoV-2 (replication-competent) virus or, more probably, its components (proteins S and N) in tissues, which would directly damage target tissues and organs, and reactivation of other viruses such as Epstein-Barr and other herpesviruses; this persistence could be caused by ineffective immunity or other mechanisms. The second comprises immunoinflammatory mechanisms that include dysregulated immune response (eg, exhausted T-helper cells, elevated cytotoxic T cells, elevated cytokines, and the appearance of aberrant immune cell subsets) and consequent immunopathology, which destroys or injures bystander tissues or autoimmunity with its consequences. The third includes endothelial inflammation and immune thrombosis. Both immunoinflammatory mechanisms and endothelial inflammation and immune thrombosis can cause or exacerbate dysregulation of the complement cascade and complement-mediated tissue injury.

Other mechanisms that have been invoked to explain long COVID pathogenesis include protein misfolding caused by viral proteins such as N and S and altered oral and gut microbiomes. Technically, however, these two mechanisms are more likely to be secondary manifestations of one of the three primary mechanistic clusters (misfolding as a consequence of virus-related mechanisms; altered microbiomes due to virus-related or immunoinflammatory mechanisms or both). The same is probable for other proposed mechanisms, including down-regulation of mitochondrial genes essential for energy metabolism (common in cytokine dysregulation disorders and in part responsible for fatigue), dysregulated circadian rhythms, autonomic dysregulation, deranged endocrine functions, dysfunctional neurological signalling (especially in the brainstem and vagus nerve), an imbalance of serotonin in the brain, vascular disruption in the blood–brain barrier, abnormalities in skeletal muscle structure, exercise-induced myopathy, and tissue infiltration of amyloid-containing deposits. Genetic susceptibility almost certainly plays some role, and there is a need for large-scale genomic sequencing studies to identify not only the genetic risk and protection factors, but also the underlying pathogenetic mechanisms. Immune abnormalities differ by sex (as does the propensity towards autoimmunity) and might explain some of the sex differences in long COVID symptomatology.

Importantly, the above mechanisms might coexist and feed into one another. A persistent reservoir of viral proteins or RNA, for example, could stimulate both innate and adaptive immunity, causing immunopathogenesis. Via tissue damage, it could further fuel autoimmunity in susceptible individuals, and inflammation could affect endothelial dysfunction, thrombosis, and altered metabolism. Viral molecules could further directly damage cell and tissue function, or cause protein misaggregation.

This is not a common cold.

[dealtn]

This is not a common cold.

So how is this different to other post-viral responses? Other than the scale and novelty of Covid-19 "long" illnesses have been established and recogised for viral infections, both corona and rhino versions (what many would refer to as "common colds") for many years.

I am one of those "victims", from 2017.

[servodude]

This is not a common cold.

So how is this different to other post-viral responses? Other than the scale and novelty of Covid-19 "long" illnesses have been established and recogised for viral infections, both corona and rhino versions (what many would refer to as "common colds") for many years.

I am one of those "victims", from 2017.

I'm a victim too but going back to 2004

One thing I've found interesting in the reading on long COVID is how the likelihood of sequelae has fallen since the start of the pandemic - it seems to be about half as likely as it was.

So just the fact this was a novel respiratory disease makes the investigation of the long term effects inherently interesting

[Harry23]

Sorry if this has been mentioned before (it's a long thread and I haven't read it all yet), but LC (long covid) does appear quite similar to CFS (chronic fatigue syndrome) / ME (myalgic encephalomyelitis). I know a couple of people who've suffered with CFS for years, which afaik was identified in the 1980s as 'yuppie flu' a post-viral condition. So I'm wondering if some of the research and treatment for CFS could be applicable to LC.

[Julian]

This is not a common cold.

So how is this different to other post-viral responses? ...

I don't mean to be glib, this is intended to be a genuine answer, but one difference that I can think of is that it's almost certainly(*) had a lot more research attention than other post-viral responses. Ultimately that could end up being a good thing if there are a decent number of points of commonality in terms of biological mechanisms at play so that research and discoveries about long Covid and its potential treatments might be able to be applied to other damaging post-viral responses.

- Julian

(*) I admit that is just a hunch but during the pandemic I did see a virologist (on a Vincent Racaniello podcast) quote some figures regarding the number of pre-print papers submitted for publication on Covid-related research vs previous years on all other viruses and the figures were dramatic. I assume an analysis could be done on papers either published or in review on Long Covid vs the established body of work on post-infection responses after other viral infections and I suspect that both the number of papers and the scale of many of the studies would be impressive vs what has been done before for other viruses. And even if the publication numbers aren't impressive I'd be pretty confident that the sample sizes on any large scale studies would be far greater for a big Covid study vs other post-infection studies for other viruses.