WHAT WE KNOW

Research on COVID-19 and Long COVID is evolving faster than research on any disease in history, with almost every academic medical center around the world somehow involved in COVID research, but there is still so much to learn. This site is not meant to be a comprehensive description of everything we know about Long COVID to date, but we will briefly summarize some key points.

Long COVID is common.
Researchers have reported that 30-50% of SARS-CoV-2 patients are developing long-term symptoms, even if they had mild or asymptomatic initial infections, and even if they were young and healthy at the time of infection. Using a conservative estimate of 30% of all COVID-19 cases, as of September 2021, there are an estimated 67 million people worldwide living with Long COVID. This number will continue to rise as SARS-CoV-2 continues to spread around the world.


Dysautonomia is common in Long COVID.
Researchers from Stanford University and Stony Brook University have found that more than half of Long COVID patients develop moderate to severe autonomic nervous system dysfunction, which is also known as dysautonomia. "Dysautonomia" itself is not a specific diagnosis, but is an umbrella term that includes many different autonomic nervous system disorders. Many Long COVID patients are being diagnosed with various forms of dysautonomia including, postural orthostatic tachycardia syndrome, inappropriate sinus tachycardia, orthostatic intolerance, orthostatic hypertension, orthostatic hypotension, neurally mediated hypotension, autoimmune autonomic ganglionitis, gastroparesis, hyperhidrosis, or small fiber neuropathies that impact autonomic small fiber nerves.


Dysautonomia can cause or contribute to many of the symptoms found in Long COVID.
Dysautonomia, or autonomic nervous system dysfunction, can cause profound fatigue, headaches, shortness of breath, exercise intolerance, lightheadedness, abnormal heart rate, and blood pressure findings, temperature and sweating abnormalities, gastrointestinal symptoms, sleep dysfunction, dry eyes, dry mouth, and more. 

Long COVID can be debilitating.
Long COVID can range in severity from mildly disabling for a few months after the initial COVID infection, to a
completely devastating long-term chronic illness that leaves a previously healthy young person bedridden and unable to care for themselves. More research is needed to understand why patients improve or worsen over time, and what we can do to help all patients fully recover.

Long COVID is not one thing.
SARS-CoV-2 can cause long-term symptoms through a number of different mechanisms. Different patients may have more than one, or even all of these mechanisms, occurring at once. The four primary mechanisms, which are seen with many other viruses that can trigger long term symptoms, are:

 

  • Organ or tissue damage during the acute period of infection (for example, damage to the heart, lungs, blood vessels, or nerves);

  • Active infections: this can include ongoing infection with the SARS-CoV-2 virus, re-activation of latent infections (such as shingles), or the development of secondary infections, like bacterial pneumonia;

  • Ongoing inflammation and/or autoimmunity, which can happen even after a virus has been cleared from the body; and/or

  • Bedrest associated deconditioning - anyone who has had a debilitating infection will likely spend a few days or a few weeks in bed, and even very fit people can become deconditioned in just a few days of bed rest; deconditioning can also develop after the initial infection, in response to Long COVID symptoms that make it hard to exercise or engage in normal daily activities.
     

Many other viruses trigger long term chronic illnesses with significant dysautonomia, similar to Long COVID.
SARS-CoV-2 is not the first virus to trigger a debilitating chronic illness in a subset of individuals infected, and it won't be the last. Other global pandemics, such as the Russian flu of 1889-1890 (believed to be an earlier coronavirus, not influenza), the Spanish flu of 1918, the original severe acute respiratory syndrome (SARS) coronavirus outbreak in 2003, and Middle Eastern Respiratory Syndrome (MERS) in 2012, all resulted in a subset of individuals developing prolonged neurological and cardiovascular symptoms, along with profound fatigue. More common viral infections can also trigger chronic illness, such as Epstein Bar virus (the cause of mononucleosis), H1N1 (a common cause of the season flu), "stomach bugs" and other "common cold" viruses.

Millions of people with infection-triggered dysautonomia were living in the shadows before SARS-CoV-2 existed. These patients were often diagnosed with postural orthostatic tachycardia syndrome (POTS) or orthostatic intolerance (OI). Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is often triggered by an infection and also involves autonomic dysfunction in many patients.

The autonomic nervous system regulates immune function.
While most people understand that viruses and antibodies can damage nerve fibers, what we don't often talk about is that the autonomic nervous system itself is a major regulator of the immune system. Increases in sympathetic nervous system activity ("fight or flight") and decreases in parasympathetic nervous system activity ("rest and digest" or "vagal tone") are found in almost every autoimmune and inflammatory disease, and are known to drive the progression of inflammatory and autoimmune diseases.

Patient voices matter.
From the very start, patient-initiated research and advocacy has laid the groundwork for what we know about Long COVID. Our goal as an organization is to make sure patient voices are being heard when it comes to research planning and decision making. While we may know the facts listed above, there is so much we still need to study, to deliver more effective treatments to millions of people living with Long COVID.