Victor Forge
Long Covid is a condition that affects people who have recovered from Covid-19 but continue to experience symptoms such as fatigue, shortness of breath, and muscle weakness. A recent study by the University of Malta has discovered a potential cause of these persistent symptoms, identifying a breakdown in communication between nerves and muscles in patients with long Covid. This discovery could lead to the development of new medications to treat individuals suffering from long Covid. Muscle weakness can also be caused by other factors such as vitamin deficiencies, hormonal imbalances, and aging.
| Characteristics | Values |
|---|---|
| Cause | ACE2 (angiotensin-converting enzyme 2) receptor depletion |
| Symptoms | Lingering fatigue, breathlessness, difficulty concentrating ('brain fog'), and muscle weakness |
| Prevalence | Nearly one-third of individuals recovering from COVID-19 |
| Impact | Life-disrupting, affecting everyday functioning |
| Treatment | Development of medications, managing vitamin deficiencies, graded exercise therapy |
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What You'll Learn
ACE2 receptor depletion
In a recent study by the University of Malta, researchers exploited fruit flies to curb down the levels of the ACE2 receptor. In the absence of the virus, this was enough to induce fatigue and diminished mobility. The study, published in the scientific journal BBA Molecular Basis of Disease, has implications for the development of medications to treat individuals who have not completely recovered from Covid-19 infection.
Through their experiments, Maltese scientists discovered a breakdown in communication between nerves and muscles in organisms with downregulated ACE2 levels. Several key molecules required for nerves to send messages to muscles were found to be compromised. Dr Paul Herrera, who performed the experiments, added that in addition to being hijacked by the virus, the ACE2 receptor on the cell's surface can also be targeted by autoantibodies, with the immune system attacking the body as it does in Multiple Sclerosis.
The discovery sheds light on the lasting impact of Covid-19 infection and paves the way for therapeutic approaches to mitigate chronically disabling complications experienced by long Covid patients.
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Breakdown in communication between nerves and muscles
Long Covid is a condition that affects people who have recovered from Covid-19 but continue to experience symptoms such as fatigue, shortness of breath, "brain fog", and muscle weakness. A recent study by researchers at the University of Malta has identified a possible cause for these persistent symptoms, including muscle weakness. The study found that several key molecules required for nerves to send messages to muscles were compromised in individuals with long Covid. This breakdown in communication between the nerves and muscles is believed to be due to a depletion of ACE2 (angiotensin-converting enzyme 2) receptors, which are targeted by the SARS-CoV-2 virus.
The neuromuscular system includes all the muscles in the body and the nerves that connect them. This system is responsible for movement and important functions such as breathing. Neurons carry messages from the brain via the spinal cord to the muscles, instructing them to contract and make the body move. However, in individuals with long Covid, this communication is disrupted, leading to muscle weakness.
The neuromuscular junction (NMJ) is the connection between the end of a motor nerve and a muscle. To communicate with the muscle, the motor nerve releases a molecule called acetylcholine across the synapse. When this communication is disrupted, it can lead to neuromuscular junction disorders such as Lambert-Eaton myasthenic syndrome (LEMS) and myasthenia gravis.
Myopathies are another type of disorder that directly affects skeletal muscles. These diseases attack muscle fibres, making the muscles weak. Muscular dystrophy, for example, is a group of genetic conditions that cause progressive deterioration of the body's muscles, resulting in increasing weakness and disability.
Peripheral neuropathy is a common type of nerve damage that can be caused by underlying conditions such as diabetes or cancer treatment. It involves damage to the peripheral nerves, which are located away from the centre of the body, including sensory nerves, motor nerves, and the autonomic nervous system. Chemotherapy-induced peripheral neuropathy (CIPN) is a known side effect of certain chemotherapy agents.
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Virus persistence long after initial infection
Long COVID is a collection of symptoms that last three months or longer after the first COVID symptoms. It can also be defined as starting four weeks after the initial infection. The symptoms of long COVID include fatigue, memory problems, shortness of breath, sleep disorders, headaches, mental health issues, loss of taste or smell, muscle weakness, fever, and cognitive dysfunction. These symptoms can be similar to autoimmune, lung, heart, neurological, or psychological disorders.
The causes of long COVID are not yet fully understood, but there are several hypotheses that have been put forward. One hypothesis is that long COVID is caused by lasting damage to organs and blood vessels. Another hypothesis is that it is caused by problems with blood clotting and endothelial dysfunction in the blood vessels. A third hypothesis is that it is caused by neurological issues, such as problems with signalling from the brainstem and the vagus nerve.
Another hypothesis for the cause of long COVID is virus persistence long after the initial infection. This hypothesis is supported by a recent study conducted by researchers from the University of Malta, which identified a possible cause for the prolonged and frequently debilitating symptoms faced by individuals with long COVID-19. The study found that there was a breakdown in communication between nerves and muscles in organisms with downregulated ACE2 levels. Several key molecules required for nerves to send messages to muscles were compromised. This breakdown in communication may be caused by the virus hijacking the ACE2 receptor on the cell's surface or by autoantibodies targeting the ACE2 receptor, leading to the immune system attacking the body.
The discovery by the University of Malta sheds light on the lasting impact of COVID-19 infection and paves the way for therapeutic approaches to mitigate chronically disabling complications. The study has implications for the development of medications to treat individuals who have not completely recovered from COVID-19 infection. Nearly one-third of individuals who recover from COVID-19 continue to experience symptoms such as lingering fatigue, breathlessness, brain fog, and muscle weakness.
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Mitochondrial dysfunction
Long Covid is a condition characterised by persistent symptoms following the resolution of the acute phase of SARS-CoV-2 infection. A recent study by the University of Malta has identified a possible cause for the prolonged symptoms of long Covid, including muscle weakness. The study found that the SARS-CoV-2 virus latches onto the ACE2 (angiotensin-converting enzyme 2) receptor, which acts as the doorway through which the virus infects cells. This results in a breakdown of communication between nerves and muscles, compromising several key molecules required for nerves to send messages to muscles.
Elevated levels of circulating biomarkers associated with oxidative stress and mitochondrial damage have been reported in patients with long Covid. These biomarkers indicate that oxidative stress is a contributing factor to mitochondrial dysfunction in long Covid. Genomic studies have also identified expression changes in genes associated with mitochondrial function and the cellular response to viral infections in Covid-19 patients. These changes may be due to direct viral effects on mitochondrial integrity and function or secondary effects related to the immune response to the infection.
The recognition of the role of mitochondrial dysfunction in long Covid opens new avenues for therapeutic intervention aimed at restoring mitochondrial health and function. Effective management of mitochondrial dysfunction and restoration of cellular energetics could potentially alleviate some of the persistent symptoms experienced by long Covid patients, including muscle weakness. Strategies to improve mitochondrial function may involve a combination of pharmacological interventions, lifestyle modifications, and nutritional support.
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Treatable conditions such as myasthenia gravis
Myasthenia gravis is a rare, chronic autoimmune disorder that affects the signals between nerves and muscles, resulting in muscle weakness and fatigue. While there is no cure for this condition, various treatments can help manage symptoms and improve quality of life.
One of the most common medications used to treat myasthenia gravis is pyridostigmine, which helps electrical signals travel between nerves and muscles, reducing muscle weakness. Mestinon® (ICN Pharmaceuticals Inc) is a brand name for pyridostigmine bromide, which comes in fast-acting 60 mg tablets or long-lasting slow-release 180 mg capsules (Timespan®). However, the effects of pyridostigmine are temporary, lasting only a few hours, and it may cause side effects such as stomach cramps, diarrhoea, muscle twitching, and nausea. If pyridostigmine is ineffective or provides only short-term relief, doctors may suggest steroid tablets like prednisolone.
In addition to medication, surgery to remove the thymus gland, known as a thymectomy, may be recommended for some patients with myasthenia gravis. This surgery has been shown to improve symptoms, especially in those with an unusually large thymus gland. However, it is important to note that surgery is not always effective and may not significantly impact symptoms in all cases.
Intravenous immunoglobulin therapy is another treatment option. This therapy, derived from donated blood, works by temporarily altering the immune system's functioning, thereby improving muscle strength. Plasmapheresis is also an option, where the patient's blood is filtered through a machine to remove harmful antibodies that interfere with nerve-muscle communication.
Finally, it is important for patients with myasthenia gravis to avoid triggers that may worsen their symptoms. For example, certain infections, medicines, and surgeries can trigger symptoms, so patients should be cautious and inform their doctors and surgeons about their condition.
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Frequently asked questions
Yes, muscle weakness is a symptom of long Covid. Researchers from the University of Malta have identified a possible cause for the prolonged and frequently debilitating symptoms faced by individuals with long Covid.
Angiotensin-converting enzyme 2 (ACE2) depletion has been identified as a possible cause of muscle weakness in people with long Covid. ACE2 exists in two forms: one anchored to cell membranes (mACE2) in the intestines, kidney, testis, gallbladder, and heart, and the other as a soluble variant (sACE2).
Excluding treatable conditions, managing concomitant problems such as vitamin D deficiency, and explaining that improvement is likely over a period of 2–3 years can support the patient while they heal.
