Four years after infection, most people treated for long COVID in a specialist clinic still hadn’t returned to their previous level of health🧵
This prospective cohort study followed 3,590 people with long COVID for up to four years in a specialist post-COVID clinic in London.
Most patients were not hospitalised during their acute infection, the majority were working-age adults, and nearly two-thirds were women.
The most common symptoms were
fatigue (80%)
breathlessness (68%)
brain fog (54%)
muscle pain, sleep disturbance, and autonomic symptoms
Patients typically reported multiple symptoms at once (median = five).
Functional impact
About one-third of working patients were unable to work!
Quality of life scores were markedly reduced
The level of impairment was comparable to ME/CFS, and in some respects worse than chronic heart or lung disease
Only one-third of patients reached a level of health they considered at least 75% of their pre-illness baseline during follow-up.
Median time to recovery = 200 days
Non-hospitalised patients recovered more slowly than those who had been hospitalised
In other words, most patients did not fully recover, even after prolonged follow-up.
The strongest predictors of persistent illness were
severity of fatigue , autonomic / postural symptoms, muscle pain.
Patients with very high fatigue scores had the lowest likelihood of recovery over several years.
COVID-19 vaccination was associated with faster recovery, especially when given before infection.
This is an association, not proof of causation, but the signal was consistent.
Long COVID led to substantially increased healthcare utilisation.
After referral to the specialist clinic
emergency department visits decreased
outpatient visits increased
This suggests a shift from crisis-driven care to structured, ongoing management, rather than resolution of the condition.
Individuals aged ≥18 years with long covid (hospitalised and non-hospitalised) from April 2020 to March 2024.
Sum:
Long COVID is often prolonged, disabling, and resource-intensive, particularly in patients with severe fatigue.
Specialist services do not fix the condition quickly, but they reduce chaos, improve coordination of care, and reveal the scale of ongoing need.
Prashar at al., Trajectory, healthcare utilisation and recovery in 3590 individuals with long covid: a 4-year prospective cohort analysis. BMJ. bmjopen.bmj.com/content/16/1/e…
Nearly three-quarters of patients were never hospitalised, yet they had substantial functional impairment, recovered more slowly, made up the majority of long COVID workload.
This directly challenges the idea that long COVID is mainly a complication of severe acute disease.
A mild acute infection does not protect against long-term disability.
Fatigue severity was by far the strongest predictor of non-recovery.
This matters because it suggests -
fatigue reflects core pathophysiology, not secondary deconditioning
simple clinical tools (like fatigue scales) can meaningfully stratify risk
In practice, fatigue behaves almost like a functional biomarker for long COVID severity.
Nearly three-quarters of patients were never hospitalised, yet they had substantial functional impairment, recovered more slowly, made up the majority of long COVID workload.
This directly challenges the idea that long COVID is mainly a complication of severe acute disease.
A mild acute infection does not protect against long-term disability.
Fatigue severity was by far the strongest predictor of non-recovery.
This matters because it suggests -
fatigue reflects core pathophysiology, not secondary deconditioning
simple clinical tools (like fatigue scales) can meaningfully stratify risk
In practice, fatigue behaves almost like a functional biomarker for long COVID severity.
Patients with autonomic symptoms or prominent myalgia had significantly worse trajectories.
This supports the idea that long COVID is not one condition, but several overlapping phenotypes - some of which are much harder to recover from.
Referral to a long COVID service reduced emergency visits but increased planned outpatient care.
That tells us -
long COVID creates ongoing healthcare demand
specialist services convert crisis-driven care into managed, visible chronic care.
Not a failure - it’s a sign that long COVID is a chronic condition, not a transient complaint.
This study paints a consistent picture -
long COVID can be long-lasting and disabling
healthcare systems must plan for long-term management, not short-term reassurance
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A new study in Frontiers in Medicine analyzed 959 hospitalized COVID-19 patients (pre-vaccination).
It shows that T cell counts at admission strongly predict severe outcomes and mortality.
This isn’t just about inflammation - adaptive immunity is central🧵
Patients with CD3 T cells ≤ 666/mm³ had
2.3× higher risk of needing ventilatory support
2.4× higher risk of in-hospital death
CD4 ≤ 359/mm³ was associated with
2.8× higher risk of death
These associations remained independent after adjustment.
The study supports a model in which
T-cell responses (especially CD3/CD4) are weakened
Adaptive immunity fails to adequately control the virus
The body compensates through hyperactivation of innate immunity
The result is severe disease
This study suggests that in some patients, COVID-19 triggers a long-term process of vascular and cardiac injury that can gradually increase pulmonary pressure, strain the right ventricle, and raise the risk of death in the following years🧵
The study followed 480 hospitalized patients (240 moderate, 240 severe) for one year after discharge. It assessed heart function using echocardiography and measured biomarkers of vascular inflammation.
In severe COVID-19, right-ventricular function was already significantly worse at the first study examination. Over the following year, pulmonary artery pressure increased by 17.8% in severe cases and 7.1% in moderate cases!
If normal population plasma truly carries more low-grade inflammation, this study hints at a fork in the road.
Either we lower the bar and call it a new normal,
or this is a hidden population burden that will surface later as comorbidities🧵
A new study on the cytokine IL-32 after COVID-19 points directly at this uncomfortable question.
The authors analyzed nearly 1,000 healthy blood donors sampled before and during the pandemic, plus 212 hospitalized COVID-19 patients.
The result is consistent - plasma collected after 2020 shows systematically higher IL-32 levels compared to pre-pandemic plasma.
A new population-level study from Singapore looked at 1.4 million COVID cases in a setting with >90% booster coverage.
Result - multi-organ Long COVID largely attenuates.
But the brain remains an exception.
The study tracked new medical diagnoses 31–300 days after infection across Delta and multiple Omicron waves (BA.1/2, BA.4/5, XBB).
Across variants, most organ systems normalize.
Neurocognitive diagnoses do not.
This study does not tell us what exactly causes long COVID or ME/CFS, nor does it test clinical symptoms like PEM.
But it may tell us something just as important - what type of biological problem this likely is..🧵
The authors isolated immunoglobulins (IgG) from people with post-infectious ME/CFS, including post-COVID ME/CFS, and tested what these antibodies do to healthy cells.
In a subset of patients, these IgG alter the behavior of endothelial cells and their mitochondria.
Not by killing the cells or shutting down ATP production.
This isn’t a new comparison.
For years, parallels between NeuroHIV and neuro-COVID/Long COVID have been discussed across fields.
What’s new is that they are now formally described as shared CNS mechanisms, not just analogy!🧵
Just a few years ago, parallels like
HIV - SARS-CoV-2
HAND - brain fog/neuro-LC
microglia - chronic inflammation
vasculature - cognition
were treated mainly as interesting analogies. With caution not to overstate them.
This new review formalizes the shift. These parallels are not Twitter pattern recognition, but convergent CNS phenotypes following viral insults.
A new review shows they are biologically grounded similarities.