Viral Myositis

Myositis may also have an infective basis. Viral myositis has been recorded in association with influenza and picomavirus infections, particularly those due to viruses of the Coxsackie group, and HIV infection is an increasingly common cause of myositis seen in routine practice. Fungal, bacterial, and parasitic myositis is seen much more rarely in North America and Europe than in tropical parts of the world, but in these regions these forms of infective myositis constitute a significant problem. In any survey of inflammatory muscle disorders, it is also necessary to consider other inflammatory conditions which affect muscle indirectly, but do not cause myositis in the strict sense of the word. In this group are to be found various forms of arteritis and fascitis and granulomatous conditions such as sarcoidosis. 

Bacterial and viral myositis is well recognized as a clinical entity by muscle pathologists. The viruses most commonly involved appear to be the Coxsackie viruses, the arboviruses, influenza virus, and HIV, but the mechanism whereby the viral infection gives rise to the myositic syndrome is not known. A detailed discussion of such problems is presented later on pages 333-334. 

Complications of influenza may include exacerbation of underlying comorbidities, primary viral pneumonia, secondary bacterial pneumonia or other respiratory illnesses (e.g., sinusitis, bronchitis, otitis), encephalopathy, transverse myelitis, myositis, myocarditis, pericarditis, and Reye s syndrome. 

The alphaviruses are a group of 26 icosahedral, positive-sense RNA viruses primarily transmitted by mosquitoes [64]. These 700-A-diameter viruses are some of the simplest of the membrane-enveloped viruses, and members of this group cause serious tropical diseases with characteristic symptoms such as myositis, fever, rash, encephalitis, and polyarthritis [65]. The structures of two different alphavirus-Fab complexes have been determined by cryo-TEM Ross River virus (RR) and Sindbis virus (SIN) [66]. The amino acid sequences of the RR and SIN virus structural and nonstructural proteins are 49 and 64% identical, respectively [67]. The viral RNA genome and 240 copies of the capsid protein form the nucleocapsid core [68-73], and the El and E2 glycoproteins form heterodimers that associate as 80 trimeric spikes on the viral surface. Native SIN and RR lack the E3 glycoprotein because it disassociates from the spike complex after its display on the plasma membrane surface [74, 75]. El has a putative fusion domain that may facilitate host membrane penetration [76, 77]. E2 contains most of the neutralizing epitopes and is also probably involved in host cell recognition [78-80]. 

Observational studies Yellow fever vaccine can very rarely cause severe adverse reactions, particularly neurotropic and visceral complications. Viral and host factors have been postulated to explain the basis of these reactions. However, the mechanisms underlying their occurrence remain unknown. A detailed immunological analysis of a 23-year-old woman has been published. She developed encephalitis, pancreatitis, and myositis after receiving a 17D-204 yellow fever vaccine and had various immunological abnormalities, which are described in detail in this chapter. The authors considered that the results supported the hypothesis that a strong adaptive response and abnormalities in the innate immune system may be involved in the establishment of severe adverse reactions after yellow fever vaccination [32 ]. 

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