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The influenza virus, or flu, is a respiratory tract infection that affects the nose, throat, and lungs. It is well-known that muscle aches and weakness are prominent symptoms of influenza infection. This is due to inflammation caused by the body's immune response to the virus, and not the virus itself. Specifically, muscle inflammation and weakness, called myositis, and joint and muscle pain, called myalgia, are triggered by the body's production of antibodies and proteins to fight the virus.
| Characteristics | Values |
|---|---|
| Cause of muscle damage | Inflammation caused by the immune system's response to the flu |
| Symptoms | Muscle pain, weakness, soreness, and tenderness |
| Treatment | Rest, hydration, warm showers, fever-reducing medicine, NSAIDs (e.g., ibuprofen), heating pads/blankets |
| Prevention | Flu vaccination, hand hygiene, avoiding close contact with infected individuals |
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What You'll Learn
Inflammation caused by the immune response
When a person is infected with the influenza virus, the body's immune system fights the infection. This immune response can lead to inflammation in the muscles and joints, causing muscle pain and weakness, known as myositis, and joint pain, called myalgia. The inflammation is caused by cytokines, small proteins produced by white blood cells, which are used for cell signalling. Cytokines are essential for intercellular communication and viral clearance in the immune system. However, excessive cytokines can lead to a cytokine storm or hypercytokinemia, resulting in severe immune pathology and serious health consequences, such as acute respiratory distress syndrome (ARDS).
The initial immune response to the influenza virus involves cells of the body's innate immune system, such as macrophages and neutrophils. These cells express receptors that can detect the presence of the virus. Once the virus is detected, these cells produce cytokines and chemokines, small hormone-like molecules, which alert the body to the infection and orchestrate other components of the immune system to fight the virus. Chemokines direct these components to the location of the infection. One of the cell types called into action is T lymphocytes, a type of white blood cell that fights infection.
During an influenza infection, the cytokines and chemokines produced by the innate immune cells in the lungs enter the bloodstream, contributing to systemic symptoms. This process triggers a cascade of biological events, including the activation of Interleukin-1, an inflammatory cytokine. Interleukin-1 is crucial for developing a killer T cell response against the virus, but it also affects the hypothalamus, the part of the brain that regulates body temperature, resulting in fever and headaches. Another important cytokine is tumour necrosis factor alpha, which has direct antiviral effects in the lungs but can also cause fever, appetite loss, fatigue, and weakness.
The inflammatory response triggered by the influenza virus is a double-edged sword. While it is necessary to control infection, it can also cause disease and lung damage. This response is associated with morbidity and mortality from influenza, particularly in the case of Influenza A virus (IAV), a respiratory tract pathogen. The robust inflammatory response following IAV infection can lead to lung damage, secondary bacterial infections, and severe pulmonary disease. Therefore, immunomodulatory strategies that can improve disease outcomes without affecting the host's ability to deal with the infection are an active area of research.
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Muscle-degrading genes are upregulated
Muscle aches and weakness are well-known symptoms of influenza infection. Research has found that influenza infection leads to an increase in the expression of muscle-degrading genes and a decrease in the expression of muscle-building genes in skeletal muscles in the legs. This results in functional hindrances to walking and leg strength.
The FoxO (forkhead box O) class of transcription factors has been found to play a role in muscle degradation. Specifically, FoxO1 and FoxO3 upregulate the muscle-specific ubiquitin ligases: MAFbx/atrogin-1 (muscle atrophy F-box protein) and MuRF1 (muscle RING finger-1). These ligases target muscle proteins for degradation by the ubiquitin proteasome system.
The pro-inflammatory cytokine IL-6 has been reported to regulate atrogin-1 and thus promote muscle atrophy. In animal models and humans infected with influenza A, IL-6 and TNF-α are rapidly detected in bronchoalveolar lavage fluid and nasal washings. IL-6 promotes muscle degradation via JAK/STAT, FOXO3a, and atrogin-1 upregulation.
In a mouse model of severe influenza A pneumonia, researchers found that IL-6 was necessary for the development of muscle dysfunction. Treatment with an antibody antagonist to the IL-6 receptor (tocilizumab) reduced the severity of influenza A-induced muscle dysfunction. Similarly, in cultured myotubes, it was observed that IL-6 promoted muscle degradation via the same pathway.
In summary, influenza infection leads to an increase in muscle-degrading genes, specifically through the upregulation of atrogin-1 by IL-6, resulting in muscle atrophy and dysfunction.
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Muscle-building genes are downregulated
The influenza virus causes infection in the respiratory tract, nose, throat, and lungs. It is transmitted to the mucous membranes of the mouth, nose, or eyes, usually via the fingers. Once inside the body, the virus hijacks the protein manufacturing machinery of the cell to create more viral particles. This process causes some lung injury, but most flu symptoms are caused by the immune response.
The flu is known to cause muscle aches and weakness. Research has found that influenza infection leads to an increase in the expression of muscle-degrading genes and a decrease in the expression of muscle-building genes in the skeletal muscles of the legs. This results in functional hindrances to walking and leg strength. While these effects are transient in young individuals, they can cause long-term disability in older folks, especially if they are hospitalized.
Genetics plays a significant role in muscle growth and development. Scientists have discovered numerous genes involved in muscle growth, although the mechanisms are complex and not yet fully understood. For example, testosterone is a hormone that influences muscle growth, with men having higher levels than women, resulting in greater muscle mass and strength. Other genes, such as those involved in muscle hypertrophy, can also impact muscle size and function.
In a study on mice, RNA-Seq analysis revealed several upregulated and downregulated genes in the soleus and EDL muscles following long-term muscle atrophy. Specifically, the genes Adora1, E230016M11Rik, and Gm10718 were upregulated, while Gm20515 and Fzd7 were downregulated. These findings suggest that certain genes may play a role in maintaining atrophied skeletal muscle size.
Understanding the genetic factors influencing muscle growth can help set realistic expectations and inform strength training goals. For instance, individuals with low testosterone levels may struggle with muscle building and may require specific training and lifestyle recommendations to support healthy hormone levels. By considering genetic predispositions, trainers can design more effective workouts and help clients adjust their expectations accordingly.
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Cytokines cause inflammation in muscles
When a person is infected with the influenza virus, their immune system springs into action, using a host of different cells to attack the virus. A type of white blood cell called a macrophage recognises foreign material like viruses and attempts to destroy them. The body mounts an immune response, sending antibodies to seek out and attack the virus, blocking it from spreading further.
Once the antibodies have bonded with the influenza virus, the body produces a type of protein to kill the virus. This protein is what causes the symptoms of the flu. Additionally, white blood cells produce cytokines, which are small proteins used for cell signalling, which cause inflammation in muscles and joints. Cytokines tell the body to produce more immune cells, and in turn, these new cells release even more pro-inflammatory cytokines. A subset of cytokines, known as chemokines, are critical in the recruitment of cells to sites of inflammation and help to fight pathogens. However, this process can have a detrimental overall effect. The positive feedback loop of cytokine creation can lead to a "cytokine storm", a situation in which excessive cytokine production causes an immune response that can damage organs, especially the lungs and kidneys, and even lead to death.
Cytokine release syndrome (CRS), or cytokine storm, happens when your immune system responds to infection or immunotherapy drugs more aggressively than it should. CRS symptoms include fever, nausea, fatigue, body aches, joint pain, muscle pain, shortness of breath, confusion, difficulty swallowing, and swelling. These symptoms can range from mild and flu-like to severe and life-threatening. CRS may affect multiple organ systems at once, which can result in possible organ failure and death.
Acute viral myositis is a rare condition that occurs during the recovery phase of an illness, most commonly influenza. It is characterised by muscle pain and weakness. Myositis refers to muscle inflammation and weakness, while myalgia refers to joint and muscle pain. These aches and pains are temporary and should subside once the body fights the infection.
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Myositis and myalgia cause muscle pain
Myositis and myalgia are conditions that cause muscle pain and weakness. Myositis is a disease that causes the immune system to attack the muscles, leading to chronic inflammation, swelling, and pain. It can affect people of all ages, including children, and there is currently no cure for it. The main muscles affected are those around the shoulders, hips, and thighs. Myositis can also impact other parts of the body, such as the skin, lungs, or heart, and in severe cases, it may cause trouble breathing or swallowing.
Myalgia, on the other hand, refers to joint and muscle pain. It is a common symptom of influenza infection, and it occurs due to the body's immune response to the virus. When infected by a virus, the body mounts an immune response, sending antibodies to seek out and attack the virus. This immune response can lead to inflammation in the muscles and joints, causing pain similar to mild arthritis.
During the 2019-2020 flu season, nearly 56 million cases of influenza were reported, many of which were accompanied by muscle and joint aches. Myositis has also been observed in some patients during the recovery phase of influenza-like illnesses, such as during the 2009 H1N1 pandemic. Influenza infection leads to an increase in muscle-degrading genes and a decrease in muscle-building genes in skeletal muscles, causing muscle weakness and pain.
It is important to note that muscle pain can also be caused by strain injuries or ordinary illnesses like colds and flu, and is not always indicative of myositis or myalgia. However, if you experience any symptoms of myositis, it is recommended to consult a doctor for a proper diagnosis.
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Frequently asked questions
The flu causes inflammation in the body, which leads to muscle aches. White blood cells produce cytokines, small proteins that cause cell signaling, which causes inflammation in muscles and joints.
To relieve muscle aches caused by the flu, it is recommended to get plenty of rest and sleep, stay hydrated, and take warm showers. Over-the-counter anti-inflammatory drugs such as ibuprofen can also help alleviate muscle pain.
Myalgia refers to joint and muscle pain caused by a virus. It is a common symptom of the flu and can be frustrating for people with existing joint or bone health issues.
Acute viral myositis is a rare condition that occurs during the recovery phase of an illness, most commonly influenza. It is characterised by muscle pain, weakness, and elevated serum creatine kinase (CK) levels.
