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Overview of viral myositis

Overview of viral myositis
Literature review current through: Jan 2024.
This topic last updated: Dec 21, 2022.

INTRODUCTION — Issues related to clinical, pathologic, and diagnostic features of viral myositis will be reviewed here. The management of specific viruses are discussed in separate topic reviews. Issues related to muscle weakness and rhabdomyolysis are discussed separately. (See "Approach to the patient with muscle weakness" and "Etiology and evaluation of the child with weakness" and "Rhabdomyolysis: Epidemiology and etiology" and "Rhabdomyolysis: Clinical manifestations and diagnosis" and "Approach to the patient with myalgia".)

ETIOLOGY — Influenza A and B viruses and enteroviruses are the most commonly reported viruses associated with myositis in the United States [1]. Although a specific virus may not be identified in every patient presenting with a viral syndrome, viral myositis can rarely be complicated by rhabdomyolysis and has been reported with the following viruses:

Influenza A and B [2-7]

Coxsackievirus [8]

Epstein-Barr virus (EBV) [9,10]

Herpes simplex virus (HSV) [11]

Parainfluenza virus [12]

Adenovirus [13,14]

Echovirus [15]

Cytomegalovirus (CMV) [16]

Measles virus [17]

Varicella-zoster virus (VZV) [18]

Human immunodeficiency virus (HIV) [19,20]

Hepatitis B virus (HBV) [21]

Hepatitis C virus (HCV) [22,23]

Human T-lymphotropic virus (HTLV) [24]

Dengue virus [25]

Chikungunya virus [26-28]

Coronavirus disease 2019 (COVID-19) [29-34]

PATHOGENESIS — Little is known regarding the underlying disease mechanisms by which viruses cause muscle complications. However, based on the findings on muscle biopsy, the main histopathologic feature is that of muscle fiber injury, rather than invasion of muscle tissue by inflammatory cells. Hence, myopathologically supported viral myositis is an extremely rare condition that should be carefully considered after excluding more common causes of myositis. Muscle biopsy may be entirely normal [35] or may demonstrate varying degrees of necrosis ranging from scattered necrotic muscle fibers to widespread diffuse necrosis as seen in rhabdomyolysis [8,10]. Depending on the timing of the biopsy, regenerating fibers may also be observed. As previously mentioned, there is usually scant or no inflammation.

Several mechanisms have been proposed to explain the muscle complications of viral infections:

Direct invasion of muscle tissue by the viral agent [22,36]. However, in most cases, no viral particles have been seen on biopsy.

Systemic, excessive, and uncontrolled inflammation associated with a cytokine storm [37]. For instance, patients with COVID-19 infection who have higher inflammatory markers are more likely to have more severe clinical manifestations [38].

Disuse, malnutrition, dehydration, and critical illness in some remain common risk factors for muscle complications.

EPIDEMIOLOGY — While data on specific epidemiologic details about viral myositis related to individual viruses are sparse, demographic features typically follow patterns of each individual viral infection. For example, most of the viruses listed above, including coxsackievirus, Epstein-Barr virus (EBV), herpes simplex virus (HSV), parainfluenza, cytomegalovirus (CMV), measles, and varicella-zoster virus (VZV), are contracted during childhood, whereas Dengue, Chikungunya, adenovirus, and echovirus equally affect children and adults (see 'Etiology' above). Risk factors for developing a myopathy during an acute viral infection remain unclear but are probably related to factors inherent to both the virus and the host. For instance, benign acute childhood myositis (BACM) occurs most commonly with influenza viruses, B more than A, and predominantly affects males [39] (see 'Benign acute childhood myositis' below). Conversely, females are more likely to develop rhabdomyolysis (female to male ratio of four to one), usually following influenza A infection [40].

CLINICAL MANIFESTATIONS — The clinical spectrum of muscle involvement associated with acute viral myositis ranges from the more commonly experienced benign myalgias to rhabdomyolysis (associated with myoglobinuric renal failure in some cases). (See "Rhabdomyolysis: Clinical manifestations and diagnosis".)

Symptoms related to viral infection — Patients may present with systemic symptoms such as fever, anorexia, and arthralgias, in addition to symptoms related to involved organs such as the lungs or the gastrointestinal tract.

For patients who go on to develop rhabdomyolysis, viral symptoms may precede the onset by 1 to 14 days. (See 'Rhabdomyolysis' below.)

Muscle-related symptoms — Muscle-related symptoms can occur simultaneously or right after the symptoms related to the viral infection. Occasionally, muscle symptoms may be the presenting feature of a viral illness.

Myalgias – Mild to moderate myalgias and muscle tenderness occur frequently during the early phase of many acute viral infections and do not necessarily signify the development of a myopathy. The back and legs are most commonly affected. These symptoms are often self-limited [41]. Some patients, such as those with rhabdomyolysis, may develop myalgias that are more severe and diffuse, involving limb, truncal, and/or abdominal muscles.

Weakness – When present, weakness can range in severity from mild to severe quadriparesis requiring ventilatory support if respiratory muscles are involved. Some patients do not develop frank muscle weakness and may only present with myalgia and elevated creatine kinase (CK) level.

Muscle swelling – Muscles are tender and, in children, may be boggy or edematous. In severe cases, a compartment syndrome may develop as a result of muscle edema [42].

Pigmenturia – Dark urine may be reported in patients who develop rhabdomyolysis. (See "Rhabdomyolysis: Clinical manifestations and diagnosis", section on 'Urine findings and myoglobinuria'.)

Rhabdomyolysis — Rhabdomyolysis triggered by a viral infection is relatively uncommon yet can be a life-threatening complication. In a retrospective series from a pediatric emergency department, 38 percent of rhabdomyolysis cases were associated with a viral infection [43]. Risk factors for predicting rhabdomyolysis as a complication of viral infections are not well understood.

Based on limited data from case series and clinical experience, the prognosis of rhabdomyolysis is typically good [39]. However, complications may arise, such as renal failure, fluid and electrolyte abnormalities, compartment syndrome, and, rarely, cardiac arrhythmias [44,45]. The diagnosis and management of rhabdomyolysis are discussed in detail separately. (See "Rhabdomyolysis: Clinical manifestations and diagnosis" and "Clinical features and diagnosis of heme pigment-induced acute kidney injury" and "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

EVALUATION

History and physical examination — Patients with suspected viral myositis should be asked about the distribution of the myalgias and whether the symptom onset was during the prodrome of, or coincident with, the clinical onset of a viral infection. Patients should be asked about whether weakness is present. Inquiring about the presence of dark tea-colored urine may be an indication of rhabdomyolysis. Other historical points should include sick contacts and insect bites. Social history may provide further insights, such as recent travel and risk factors for HIV, hepatitis B virus (HBV), hepatitis C virus (HCV), and COVID-19 infection [46].

A general physical examination should be performed and include a neuromuscular examination to determine whether there is weakness in any muscle group. Proximal muscles are more often involved than distal muscles. Muscles may be edematous in cases of rhabdomyolysis. Examination should also seek to identify complications such as compartment syndrome or compressive neuropathies.

Laboratory and other testing — Laboratory testing is aimed at confirming muscle involvement; ruling out alternative etiologies; assessing for complications such as rhabdomyolysis; and testing for specific viral infections, although the yield of identifying the underlying virus is low. In the acute setting with the appropriate clinical history, further testing for alternative causes of myopathies associated with rhabdomyolysis, such as idiopathic inflammatory, endocrine, metabolic, mitochondrial, and inherited myopathies, is not generally necessary. However, such entities may be considered if the patient continues to experience progressive symptoms despite resolution of their acute viral illness, or recurrence of the rhabdomyolysis. It is noteworthy that some metabolic disorders, such as inborn errors of lipid metabolism, may be triggered by fever.

In mild cases, myalgias and muscle tenderness are present without laboratory abnormalities suggestive of muscle involvement, as such symptoms are not specific for a myopathy and are relatively common during infections. However, creatine kinase (CK) levels may range from mildly to, in rare cases, markedly elevated (>10,000 international units), as can be seen in patients who develop rhabdomyolysis [8,47].

Other laboratory abnormalities consistent with rhabdomyolysis can also be observed, including transaminase elevations and myoglobinuria, as well as varying degrees of renal dysfunction. (See "Rhabdomyolysis: Clinical manifestations and diagnosis".)

Electromyography (EMG) and nerve conduction studies (NCS) may be performed for patients in whom there is diagnostic uncertainty. The presence of prominent myopathic motor unit potential in several muscle groups might raise concern for an underlying myopathy as a predisposing factor to rhabdomyolysis. (See "Overview of and approach to the idiopathic inflammatory myopathies", section on 'Electromyography'.)

Testing for specific viral infections — In patients suspected of a particular infection based upon the clinical presentation or epidemiologic features (eg, residence in or travel to an endemic area or other potential exposure to a pathogenic agent, such as influenza A or B), we perform serologic, antigen, or polymerase chain reaction testing (specific to the suspected virus) and limit initial testing to the virus(es) of interest.

Laboratory testing may also demonstrate leukocytosis, with or without atypical lymphocytes. In some cases, additional testing of clinical specimens collected based on symptoms (nasopharyngeal swab, serology, stool specimen, and/or cerebrospinal fluid) may implicate a viral pathogen [11,13,47,48]. It is not always possible to establish a definitive viral etiology; the likelihood of detection is greatest early in the course of the infection.

The approaches to the diagnosis of specific viral infections are described separately:

Influenza A and B – (See "Seasonal influenza in adults: Clinical manifestations and diagnosis", section on 'Diagnosis of influenza' and "Seasonal influenza in children: Clinical features and diagnosis", section on 'Diagnosis'.)

Coxsackie – (See "Enterovirus and parechovirus infections: Clinical features, laboratory diagnosis, treatment, and prevention".)

Epstein-Barr virus (EBV) – (See "Infectious mononucleosis", section on 'Diagnosis'.)

Herpes viruses – (See "Diagnosis of varicella-zoster virus infection" and "Infectious mononucleosis", section on 'Diagnosis' and "Epidemiology, clinical manifestations, and diagnosis of herpes simplex virus type 1 infection" and "Approach to the diagnosis of cytomegalovirus infection".)

Parainfluenza virus – (See "Parainfluenza viruses in adults", section on 'Diagnosis' and "Parainfluenza viruses in children", section on 'Diagnosis'.)

Adenovirus – (See "Diagnosis, treatment, and prevention of adenovirus infection".)

Echovirus – Establishing the specific diagnosis of echovirus is generally difficult because of the endemic nature of these viruses in most populations, and confirmation of such a diagnosis is generally not required in clinical practice. (See "Enterovirus and parechovirus infections: Clinical features, laboratory diagnosis, treatment, and prevention".)

Measles virus – (See "Measles: Clinical manifestations, diagnosis, treatment, and prevention", section on 'Diagnosis'.)

HIV – (See "Acute and early HIV infection: Clinical manifestations and diagnosis", section on 'Diagnosis' and "Screening and diagnostic testing for HIV infection".)

Hepatitis B and C viruses – (See "Hepatitis B virus: Screening and diagnosis in adults" and "Clinical manifestations and diagnosis of hepatitis B virus infection in children and adolescents" and "Screening and diagnosis of chronic hepatitis C virus infection" and "Clinical manifestations, diagnosis, and treatment of acute hepatitis C virus infection in adults".)

Human T-lymphotropic virus (HTLV) – (See "Human T-lymphotropic virus type I: Disease associations, diagnosis, and treatment".)

Dengue virus – (See "Dengue virus infection: Clinical manifestations and diagnosis".)

Chikungunya virus – (See "Chikungunya fever: Epidemiology, clinical manifestations, and diagnosis".)

COVID-19 – (See "COVID-19: Diagnosis", section on 'Diagnostic approach'.)

DIAGNOSIS — In most cases, the diagnosis of acute viral myositis is made on clinical grounds and is based upon the reported history, examination features, and confirmatory laboratory findings. Nerve conduction studies/electromyography (NCS/EMG) may be performed to confirm disease localization in the muscles rather than joints and ligaments. Muscle imaging and muscle biopsy are reserved to those cases with true weakness unrelated to acute pain, markedly elevated creatine kinase (CK), or needle EMG abnormalities suggestive of true myositis.

DIFFERENTIAL DIAGNOSIS — The overwhelming majority of patients suspected of acute viral myositis do not present with rhabdomyolysis but rather present with nonspecific acute myalgias of varying severity. The differential diagnosis for diffuse myalgias is broad and includes rheumatic diseases such as polymyalgia rheumatica (PMR), early rheumatoid arthritis (RA), inflammatory myopathies, drug reactions (eg, secondary to statins), other rare infectious myopathies (bacterial, fungal, parasitic), and endocrine disorders such as thyroid disease.

The differential diagnosis and distinguishing features of diffuse myalgias are summarized in a table (table 1). (See "Approach to the patient with myalgia".)

For patients with muscle weakness and limited or no pain, it is important to rule out other acute motor disorders, such as Guillain-Barré syndrome with a pure motor form (acute motor axonal neuropathy [AMAN]), botulism, anterior horn cell disorder (poliomyelitis), or acute presentation of myasthenia gravis. Other causes of myopathies, presenting during a viral illness, need to be ruled out in the proper clinical context. (See "Approach to the patient with muscle weakness" and "Guillain-Barré syndrome in children: Epidemiology, clinical features, and diagnosis", section on 'Differential diagnosis'.)

Rhabdomyolysis secondary to acute viral myositis must be distinguished from other causes of nontraumatic rhabdomyolysis and is discussed in detail elsewhere. (See "Rhabdomyolysis: Epidemiology and etiology", section on 'Nontraumatic exertional' and "Rhabdomyolysis: Epidemiology and etiology", section on 'Nonexertional and nontraumatic'.)

MANAGEMENT — The treatment of viral myositis should be individualized based on symptom type, severity, and, if present, degree of creatine kinase (CK) elevation. The majority of cases are self-limited and do not have pathologic evidence of inflammation. Hence, there is no evidence to support the use of any form of immunosuppression or immunomodulation (intravenous immunoglobulins). Therefore, management is generally directed at relief of symptoms and managing complications if they occur. Patients may be treated with analgesic agents (eg, acetaminophen) and nonsteroidal antiinflammatory drugs (NSAIDs) for relief of other virus-associated symptoms.

Patients with acute viral myositis complicated by rhabdomyolysis typically require additional therapy to prevent acute kidney injury. The treatment of rhabdomyolysis is discussed in detail separately. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

SPECIFIC CLINICAL SYNDROMES — Two specific clinical syndromes worth highlighting are benign acute childhood myositis (BACM) and echovirus-related myopathy. In addition, we discuss other viruses that have been linked to the development of prolonged muscle symptoms.

Benign acute childhood myositis — BACM is a self-limited illness accompanying acute viral infections that is primarily observed in children during influenza epidemics [39,49-51]. It consists of marked pain and tenderness, usually localized to the calves. This presentation has been reported most commonly with influenza A or B infections. It is often seen during influenza epidemics including an outbreak of influenza B in Germany in 2007 to 2008 [52] and the 2009 to 2010 pandemic influenza A (H1N1) virus [53]. It occurs as the acute illness is subsiding, usually 24 to 48 hours after the resolution of the presenting symptoms of fever, cough, and coryza.

The child will often refuse to walk or will have difficulty walking due to pain or true muscle weakness. The ankles are held in a plantar-flexed position, and the patient will resist attempts to dorsiflex the ankle because of pain [54,55]. BACM should be included in the differential diagnosis of children with sudden difficulty walking [56]. (See "Overview of the causes of limp in children".)

Muscle enzymes are elevated up to 20 to 30 times normal [57]. Rhabdomyolysis is rare, occurring in only 3 percent of 316 cases of childhood myositis in a retrospective literature review [40].

Muscle biopsy during the symptomatic phase reveals evidence of muscle necrosis and muscle fiber regeneration, with mild infiltration of polymorphonuclear or mononuclear leukocytes [58]. Full clinical recovery is typically seen in 3 to 10 days, with resolution of the elevated muscle enzymes within 3 weeks.

Echovirus-related myopathy — Echovirus (an enterovirus) has been associated with a chronic myopathy in patients with hypogammaglobulinemia that clinically can resemble polymyositis (PM) or dermatomyositis (DM). Most of the reported cases have occurred in males with X-linked recessive agammaglobulinemia [59]. The muscle disease is usually preceded by viral meningoencephalitis. (See "Agammaglobulinemia", section on 'Viral, fungal, and parasitic infections'.)

Echovirus has been cultured from the cerebrospinal fluid, muscle, blood, and urine of these patients. Serum creatine kinase (CK) levels may be normal or elevated. Muscle biopsy may be consistent with an inflammatory myopathy. (See "Enterovirus and parechovirus infections: Clinical features, laboratory diagnosis, treatment, and prevention".)

Other viruses associated with prolonged muscle symptoms — Most commonly, patients present with their muscle symptoms as part of an acute viral illness. As previously mentioned, symptoms are typically self-limited; however, some patients may not recover immediately, and post-viral syndromes, such as those seen with COVID-19 (long COVID) and Epstein-Barr virus (EBV) infections, have been associated with more long-lasting symptoms, namely muscle fatigue and exercise intolerance. Rare cases of immune-mediated myopathies, such as DM, have been also observed soon after COVID-19 infection, although a causal relationship has not been established [60,61]. These specific conditions are discussed in detail in separate topics. (See "Clinical manifestations and treatment of Epstein-Barr virus infection", section on 'Other manifestations' and "COVID-19: Evaluation and management of adults with persistent symptoms following acute illness ("Long COVID")", section on 'Persistent symptoms' and "COVID-19: Care of adult patients with systemic rheumatic disease", section on 'COVID-19 as a risk factor for rheumatologic disease'.)

While it would be atypical for a viral infection to have a long-lasting or chronic course, viruses have been invoked in the pathogenesis of certain chronic immune conditions, as conceivably, an acute infection may trigger an ongoing, self-sustained, or chronic immune response. Nevertheless, there is no strong evidence to support such association with any of the chronic inflammatory myopathies. Hepatitis C seropositivity was reported in 28 percent of Japanese patients with inclusion body myositis (IBM); however, these findings were not reproduced in other populations [62-64]. Similarly, case reports and series of patients with idiopathic inflammatory myopathies, IBM, and concurrent HIV and human T-lymphotropic virus (HTLV) 1 infections have been reported [22,24,62,65-70]. However, these patients present similarly to PM and IBM patients without these viruses. (See "Overview of and approach to the idiopathic inflammatory myopathies".)

SUMMARY AND RECOMMENDATIONS

Etiology – Influenza A and B viruses and enteroviruses are the most commonly reported viruses associated with myositis in the United States. Viral myositis can rarely be complicated by rhabdomyolysis, and few cases has been reported in association with a variety of different viruses. (See 'Etiology' above.)

Epidemiology – While data on specific epidemiologic details about viral myositis related to individual viruses are sparse, demographic features typically follow patterns of each individual viral infection. As an example, coxsackievirus, Epstein-Barr virus (EBV), herpes simplex virus (HSV), parainfluenza, cytomegalovirus (CMV), measles, and varicella-zoster virus (VZV) are typically contracted during childhood, whereas Dengue, Chikungunya, adenovirus, and echovirus equally affect children and adults.

Clinical manifestations – The clinical spectrum of muscle involvement associated with acute viral myositis ranges from the more commonly experienced benign myalgias to rhabdomyolysis (associated with myoglobinuric renal failure in some cases).

Symptoms related to viral infection – Patients may present with systemic symptoms such as fever, anorexia, and arthralgias, in addition to symptoms related to involved organs such as the lungs or gastrointestinal tract. (See 'Symptoms related to viral infection' above.)

Muscle-related symptoms – Muscle-related symptoms can occur simultaneously or right after the symptoms related to the viral infection. Occasionally, muscle symptoms may be the presenting feature of a viral illness. Such symptoms include myalgias, weakness, muscle swelling, and pigmenturia. (See 'Muscle-related symptoms' above.)

Rhabdomyolysis – Rhabdomyolysis triggered by a viral infection is relatively uncommon yet can be a life-threatening complication. (See 'Rhabdomyolysis' above.)

Evaluation

History and physical examination – Patients with suspected viral myositis should be asked about the distribution of the myalgias and whether the symptom onset was during the prodrome of, or coincident with, the clinical onset of a viral infection. A general physical examination should include a neuromuscular examination to evaluate for weakness in any muscle group. Proximal muscles are more often involved than distal muscles. (See 'History and physical examination' above.)

Laboratory and other testing – Laboratory testing is aimed at confirming muscle involvement, ruling out alternative etiologies, assessing for complications such as rhabdomyolysis, and testing for specific viral infections. Electromyography (EMG) and nerve conduction studies (NCS) may be performed for patients in whom there is diagnostic uncertainty. (See 'Laboratory and other testing' above and 'Testing for specific viral infections' above.)

Diagnosis – In most cases, the diagnosis of acute viral myositis can be made on clinical grounds and is based on reported history, physical examination features, and confirmatory laboratory findings. (See 'Diagnosis' above.)

Management – The treatment of viral myositis should be individualized based on symptom type, severity, and, if present, degree of creatine kinase (CK) elevation. The majority of cases are self-limited and do not have pathologic evidence of inflammation. Management is directed at relief of symptoms and managing complications if they occur. Patients may be treated with analgesic agents (eg, acetaminophen) and nonsteroidal antiinflammatory drugs (NSAIDs) for relief of other virus-associated symptoms. (See 'Management' above.)

Patients with acute viral myositis complicated by rhabdomyolysis typically require additional therapy to prevent acute kidney injury. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

Specific clinical syndromes – Benign acute childhood myositis (BACM) is a self-limited illness accompanying acute viral infections that is primary observed in children during influenza epidemics. (See 'Benign acute childhood myositis' above.)

Echovirus (an enterovirus) has been associated with a chronic myopathy in patients with hypogammaglobulinemia that clinically can resemble polymyositis (PM) or dermatomyositis (DM). (See 'Echovirus-related myopathy' above.)

Some patients may not recover immediately after an acute viral infection, and post-viral syndromes, such as those seen with COVID-19 (long COVID) and EBV infections, have been associated with more long-lasting symptoms, namely muscle fatigue and exercise intolerance. (See 'Other viruses associated with prolonged muscle symptoms' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Marc L Miller, MD, who contributed to an earlier version of this topic review.

  1. Crum-Cianflone NF. Bacterial, fungal, parasitic, and viral myositis. Clin Microbiol Rev 2008; 21:473.
  2. Singh U, Scheld WM. Infectious etiologies of rhabdomyolysis: three case reports and review. Clin Infect Dis 1996; 22:642.
  3. Shenouda A, Hatch FE. Influenza A viral infection associated with acute renal failure. Am J Med 1976; 61:697.
  4. Cunningham E, Kohli R, Venuto RC. Influenza-associated myoglobinuric renal failure. JAMA 1979; 242:2428.
  5. Gamboa ET, Eastwood AB, Hays AP, et al. Isolation of influenza virus from muscle in myoglobinuric polymyositis. Neurology 1979; 29:1323.
  6. Abe M, Higuchi T, Okada K, et al. Clinical study of influenza-associated rhabdomyolysis with acute renal failure. Clin Nephrol 2006; 66:166.
  7. D'Silva D, Hewagama S, Doherty R, et al. Melting muscles: novel H1N1 influenza A associated rhabdomyolysis. Pediatr Infect Dis J 2009; 28:1138.
  8. Fodili F, van Bommel EF. Severe rhabdomyolysis and acute renal failure following recent Coxsackie B virus infection. Neth J Med 2003; 61:177.
  9. Friedman BI, Libby R. Epstein-Barr virus infection associated with rhabdomyolysis and acute renal failure. Clin Pediatr (Phila) 1986; 25:228.
  10. McCabe JL, Duckett S, Kaplan P. Epstein-Barr virus infection complicated by acute rhabdomyolysis. Am J Emerg Med 1988; 6:453.
  11. Schlesinger JJ, Gandara D, Bensch KG. Myoglobinuria associated with herpes-group viral infections. Arch Intern Med 1978; 138:422.
  12. O'Connor JV, Iyer SK. Myoglobinuria associated with parainfluenza type 2 infection. N Y State J Med 1982; 82:1469.
  13. Wright J, Couchonnal G, Hodges GR. Adenovirus type 21 infection. Occurrence with pneumonia, rhabdomyolysis, and myoglobinuria in an adult. JAMA 1979; 241:2420.
  14. Meshkinpour H, Vaziri ND. Association of myoglobinuria with adenovirus infection. West J Med 1982; 137:130.
  15. Josselson J, Pula T, Sadler JH. Acute rhabdomyolysis associated with an echovirus 9 infection. Arch Intern Med 1980; 140:1671.
  16. Hughes GS Jr, Hunt R. Cytomegalovirus infection with rhabdomyolysis and myoglobinuria. Ann Intern Med 1984; 101:276.
  17. Seibold S, Merkel F, Weber M, Marx M. Rhabdomyolysis and acute renal failure in an adult with measles virus infection. Nephrol Dial Transplant 1998; 13:1829.
  18. Hollenstein U, Thalhammer F, Burgmann H. Disseminated intravascular coagulation (DIC) and rhabdomyolysis in fulminant varicella infection--case report and review of the literature. Infection 1998; 26:306.
  19. Mahé A, Bruet A, Chabin E, Fendler JP. Acute rhabdomyolysis coincident with primary HIV-1 infection. Lancet 1989; 2:1454.
  20. Guillaume MP, Van Beers D, Delforge ML, et al. Primary human immunodeficiency virus infection presenting as myopericarditis and rhabdomyolysis. Clin Infect Dis 1995; 21:451.
  21. Nojima T, Hirakata M, Sato S, et al. A case of polymyositis associated with hepatitis B infection. Clin Exp Rheumatol 2000; 18:86.
  22. Villanova M, Caudai C, Sabatelli P, et al. Hepatitis C virus infection and myositis: a polymerase chain reaction study. Acta Neuropathol 2000; 99:271.
  23. Di Muzio A, Bonetti B, Capasso M, et al. Hepatitis C virus infection and myositis: a virus localization study. Neuromuscul Disord 2003; 13:68.
  24. Morgan OS, Rodgers-Johnson P, Mora C, Char G. HTLV-1 and polymyositis in Jamaica. Lancet 1989; 2:1184.
  25. Acharya S, Shukla S, Mahajan SN, Diwan SK. Acute dengue myositis with rhabdomyolysis and acute renal failure. Ann Indian Acad Neurol 2010; 13:221.
  26. Dev N, Kumar R, Gogna A, Sharma S. Chikungunya-induced inflammatory myositis: a case report in India. Trop Doct 2019; 49:241.
  27. Ozden S, Huerre M, Riviere JP, et al. Human muscle satellite cells as targets of Chikungunya virus infection. PLoS One 2007; 2:e527.
  28. Martins HA, Bernardino SN, Santos CC, Ribas VR. Chikungunya and Myositis: A Case Report in Brazil. J Clin Diagn Res 2016; 10:OD05.
  29. Rivas-García S, Bernal J, Bachiller-Corral J. Rhabdomyolysis as the main manifestation of coronavirus disease 2019. Rheumatology (Oxford) 2020; 59:2174.
  30. Husain R, Corcuera-Solano I, Dayan E, et al. Rhabdomyolysis as a manifestation of a severe case of COVID-19: A case report. Radiol Case Rep 2020; 15:1633.
  31. Jin M, Tong Q. Rhabdomyolysis as Potential Late Complication Associated with COVID-19. Emerg Infect Dis 2020; 26:1618.
  32. Suwanwongse K, Shabarek N. Rhabdomyolysis as a Presentation of 2019 Novel Coronavirus Disease. Cureus 2020; 12:e7561.
  33. Buckholz AP, Kaplan A, Rosenblatt RE, Wan D. Clinical Characteristics, Diagnosis, and Outcomes of 6 Patients With COVID-19 Infection and Rhabdomyolysis. Mayo Clin Proc 2020; 95:2557.
  34. Manzano GS, Woods JK, Amato AA. Covid-19-Associated Myopathy Caused by Type I Interferonopathy. N Engl J Med 2020; 383:2389.
  35. Tanaka T, Takada T, Takagi D, et al. Acute renal failure due to rhabdomyolysis associated with echovirus 9 infection: a case report and review of literature. Jpn J Med 1989; 28:237.
  36. Filippone C, Legros V, Jeannin P, et al. Arboviruses and Muscle Disorders: From Disease to Cell Biology. Viruses 2020; 12.
  37. Soares MN, Eggelbusch M, Naddaf E, et al. Skeletal muscle alterations in patients with acute Covid-19 and post-acute sequelae of Covid-19. J Cachexia Sarcopenia Muscle 2022; 13:11.
  38. Mulchandani R, Lyngdoh T, Kakkar AK. Deciphering the COVID-19 cytokine storm: Systematic review and meta-analysis. Eur J Clin Invest 2021; 51:e13429.
  39. Mackay MT, Kornberg AJ, Shield LK, Dennett X. Benign acute childhood myositis: laboratory and clinical features. Neurology 1999; 53:2127.
  40. Agyeman P, Duppenthaler A, Heininger U, Aebi C. Influenza-associated myositis in children. Infection 2004; 32:199.
  41. Stang H. Acute transient myositis associated with influenza virus infection. Pediatr Infect Dis J 1989; 8:257.
  42. Paletta CE, Lynch R, Knutsen AP. Rhabdomyolysis and lower extremity compartment syndrome due to influenza B virus. Ann Plast Surg 1993; 30:272.
  43. Mannix R, Tan ML, Wright R, Baskin M. Acute pediatric rhabdomyolysis: causes and rates of renal failure. Pediatrics 2006; 118:2119.
  44. Hocking WG, Reza MJ. Letter: Nontraumatic rhabdomyolysis and renal failure. N Engl J Med 1975; 292:979.
  45. Nauss MD, Schmidt EL, Pancioli AM. Viral myositis leading to rhabdomyolysis: a case report and literature review. Am J Emerg Med 2009; 27:372.e5.
  46. Mantilla E, Pasnoor M, Dimachkie M. Rhabdomyolysis and COVID-19 Infection: Is It due to statin use or anti-TIF1-y antibodies? RRNMF Neuromuscular Journal 2020; 1:22.
  47. Dunnet J, Paton JY, Robertson CE. Acute renal failure and Coxsackie viral infection. Clin Nephrol 1981; 16:262.
  48. Christenson JC, San Joaquin VH. Influenza-associated rhabdomyolysis in a child. Pediatr Infect Dis J 1990; 9:60.
  49. Magee H, Goldman RD. Viral myositis in children. Can Fam Physician 2017; 63:365.
  50. Rosenberg T, Heitner S, Scolnik D, et al. Outcome of Benign Acute Childhood Myositis: The Experience of 2 Large Tertiary Care Pediatric Hospitals. Pediatr Emerg Care 2016.
  51. Costa Azevedo A, Costa E Silva A, Juliana Silva C, et al. Benign acute childhood myositis: A 5-year retrospective study. Arch Pediatr 2022; 29:490.
  52. Mall S, Buchholz U, Tibussek D, et al. A large outbreak of influenza B-associated benign acute childhood myositis in Germany, 2007/2008. Pediatr Infect Dis J 2011; 30:e142.
  53. Koliou M, Hadjiloizou S, Ourani S, et al. A case of benign acute childhood myositis associated with influenza A (H1N1) virus infection. Clin Microbiol Infect 2010; 16:193.
  54. Middleton PJ, Alexander RM, Szymanski MT. Severe myositis during recovery from influenza. Lancet 1970; 2:533.
  55. Farrell MK, Partin JC, Bove KE. Epidemic influenza myopathy in Cincinnati in 1977. J Pediatr 1980; 96:545.
  56. Zafeiriou DI, Katzos G, Gombakis N, et al. Clinical features, laboratory findings and differential diagnosis of benign acute childhood myositis. Acta Paediatr 2000; 89:1493.
  57. Dietzman DE, Schaller JG, Ray CG, Reed ME. Acute myositis associated with influenza B infection. Pediatrics 1976; 57:255.
  58. Ruff RL, Secrist D. Viral studies in benign acute childhood myositis. Arch Neurol 1982; 39:261.
  59. Crennan JM, Van Scoy RE, McKenna CH, Smith TF. Echovirus polymyositis in patients with hypogammaglobulinemia. Failure of high-dose intravenous gammaglobulin therapy and review of the literature. Am J Med 1986; 81:35.
  60. Qian J, Xu H. COVID-19 Disease and Dermatomyositis: A Mini-Review. Front Immunol 2021; 12:747116.
  61. Aschman T, Schneider J, Greuel S, et al. Association Between SARS-CoV-2 Infection and Immune-Mediated Myopathy in Patients Who Have Died. JAMA Neurol 2021; 78:948.
  62. Uruha A, Noguchi S, Hayashi YK, et al. Hepatitis C virus infection in inclusion body myositis: A case-control study. Neurology 2016; 86:211.
  63. Alverne AR, Marie SK, Levy-Neto M, et al. [Inclusion body myositis: series of 30 cases from a Brazilian tertiary center]. Acta Reumatol Port 2013; 38:179.
  64. Naddaf E, Shelly S, Mandrekar J, et al. Survival and associated comorbidities in inclusion body myositis. Rheumatology (Oxford) 2022; 61:2016.
  65. Sola P, Galassi G, Merelli E, et al. Detection of HCV-specific sequences in chronic myopathy with hepatitis C: improvement with interferon-alpha 2A therapy. Eur Neurol 1999; 42:181.
  66. Ueno Y, Kondo K, Kidokoro N, et al. Hepatitis C infection and polymyositis. Lancet 1995; 346:319.
  67. Lloyd TE, Pinal-Fernandez I, Michelle EH, et al. Overlapping features of polymyositis and inclusion body myositis in HIV-infected patients. Neurology 2017; 88:1454.
  68. Johnson RW, Williams FM, Kazi S, et al. Human immunodeficiency virus-associated polymyositis: a longitudinal study of outcome. Arthritis Rheum 2003; 49:172.
  69. Desdouits M, Cassar O, Maisonobe T, et al. HTLV-1-associated inflammatory myopathies: low proviral load and moderate inflammation in 13 patients from West Indies and West Africa. J Clin Virol 2013; 57:70.
  70. Matsuura E, Umehara F, Nose H, et al. Inclusion body myositis associated with human T-lymphotropic virus-type I infection: eleven patients from an endemic area in Japan. J Neuropathol Exp Neurol 2008; 67:41.
Topic 5165 Version 24.0

References

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