There is no evidence for persistent enterovirus infections in chronic medical conditions in humans

Melchers, Willem J. G.; Zoll, Jan; Kuppeveld, Frank J. M. van; Swanink, C.M.A.; Galama, J.M.D.

doi:10.1002/rmv.1980040402

Cited by 17 publications

(9 citation statements)

References 69 publications

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“…productive and`latent'. There has been an implicit assumption that they are the same but this may not be the case and the opposing views have been ably debated recently (Melchers et al, 1994;Muir and Archard, 1994). It has been suggested that abnormal transcription is fundamental to the establishment of persistence but we have shown that transcription was normal in our in vitro model, indicating that mutations which result in reduced viral multiplication and cytopathogenicity, are not necessarily associated with abnormal transcription.…”

Section: Viral Genomic/templatementioning

confidence: 66%

Genomic and template RNA transcription in a model of persistent enteroviral infection

Jw¹,

Wm²,

Cash³

et al. 1997

J Neurovirol

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Enteroviruses have been implicated in persistent infections of the nervous system and in certain paralytic motor neurone syndromes. Enteroviral persistence may depend on defective transcription, resulting in the abnormal production of equal amounts of genomic and template RNA strands rather than the normal ratio of 60 ± 100 : 1. An in vitro model of a persistent coxsackie virus in human skeletal muscle cells was investigated using in situ hybridisation and a semiquantitative parallel, complementary, reverse transcriptase polymerase chain reaction. The ratio of genomic to template RNA was found to be approximately 60 : 1. We conclude that enteroviral persistence in this in vitro model is not dependent on altered transcription. In vivo, other viral and host factors should be considered.

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Section: Viral Genomic/templatementioning

confidence: 66%

Genomic and template RNA transcription in a model of persistent enteroviral infection

Jw¹,

Wm²,

Cash³

et al. 1997

J Neurovirol

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“…In humans there is little evidence that infectious virus persists, and although enteroviral RNA sequences have been reported in various tissues long after the apparent primary infection, 40 even this issue is controversial. 41 But many studies of human heart used myocardial biopsy material which is, for obvious reasons, limited in quantity. As we show in Figure 7, CVB distribution is very focal even at a titer of 10 8 pfu/gram of heart tissue, so perhaps it is not surprising that CVB materials sometimes cannot be identified in biopsies of hearts in which infectious virus is undetectable.…”

Section: Discussionmentioning

confidence: 99%

The Role of B Lymphocytes in Coxsackievirus B3 Infection

Mena

Perry

Harkins

et al. 1999

The American Journal of Pathology

125

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Coxsackieviruses are important human pathogens, frequently causing myocarditis , pancreatitis , and a variety of less severe diseases. B lymphocytes appear central to the interaction between these viruses and their mammalian hosts , because agammaglobulinemic humans , genetically incapable of antibody production , are susceptible to chronic infections by coxsackieviruses and related enteroviruses , such as poliovirus and echovirus. However , recent studies show that Type B coxsackievirus (CVB) infects B lymphocytes soon after infection , suggesting the possibility that these cells may play some role in virus dissemination and/or that the virus may be able to modulate the host immune response. We analyzed the role of B lymphocytes in CVB infection and confirmed that CVB infects B lymphocytes , and extended these findings to show that this is a productive infection involving approximately 1 to 10% of the cells; however , infectious center assays show that other splenocytes are infected at approximately the same frequency. Virus is readily detectable by in situ hybridization in the spleen of immunocompetent mice but is difficult to detect in mice deficient in B cells (BcKO mice) , consistent with much of the splenic signal being the result of B cell infection. Surprisingly , given the extent of their infection, B cells express barely detectable levels of the murine coxsackievirus-adenovirus receptor (mCAR) , suggesting that another means of cell entry may be used. We found no evidence of B cell depletion following CVB infection , indicating that this is not the explanation for the transient immunosuppression previously reported. Virus replication and dissemination are slightly delayed in BcKO mice , consistent with B cells' playing a role as an important early target of infection and/or a means to distribute the virus to many tissues. In addition , we show that BcKO mice recapitulate a central feature of human agammaglobulinemia: CVB establishes chronic infection in a variety of organs (heart , liver , brain , kidney , lung , pancreas , spleen). In most of these tissues the viral titers remain high Coxsackieviruses are members of the family Picornaviridae and lie in the enterovirus genus along with polioviruses, echoviruses, and unclassified enteroviruses. There are two types of coxsackievirus, A and B, classified by their pathogenicity in newborn mice, 1 and within each type are several strains. Type B coxsackieviruses (CVB) are common causes of human disease. As the genus name suggests, they replicate in the gastro-intestinal tract, but they are not restricted to this site; they also infect, for example, skeletal muscle (causing intercostal myalgia (Bornholm disease) and polymyositis), cardiac muscle (with resulting myocarditis), and acinar cells in the exocrine pancreas (causing fulminant pancreatitis), as well as various cells of the immune system. Foci of infection can also be found in the liver, kidney, central nervous system, spleen, and elsewhere. Enteroviruses infect humans with epidemic frequency, reflect...

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“…Research has not been able to verify a persistent polio virus infection or relation to PPS, and it seems unlikely that persistent poliovirus infection plays a role in the pathogenesis of PPS 35–37…”

Section: Pathogenesismentioning

confidence: 99%

Update on current and emerging treatment options for post-polio syndrome

Farbu

2010

TCRM

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Post-polio syndrome (PPS) refers to the clinical deterioration experienced by many polio survivors several decades after their acute illness. The symptoms are new muscle weakness, decreased muscle endurance, fatigue, muscle pain, joint pain, cold intolerance, and this typical clinical entity is reported from different parts of the world. The pathophysiology behind PPS is not fully understood, but a combination of distal degeneration of enlarged motor units caused by increased metabolic demands and the normal aging process, in addition to inflammatory mechanisms, are thought to be involved. There is no diagnostic test for PPS, and the diagnosis is based on a proper clinical workup where all other possible explanations for the new symptoms are ruled out. The basic principle of management of PPS lies in physical activity, individually tailored training programs, and lifestyle modification. Muscle weakness and muscle pain may be helped with specific training programs, in which training in warm water seems to be particularly helpful. Properly fitted orthoses can improve the biomechanical movement pattern and be energy-saving. Fatigue can be relieved with lifestyle changes, assistive devices, and training programs. Respiratory insufficiency can be controlled with noninvasive respiratory aids including biphasic positive pressure ventilators. Pharmacologic agents like prednisone, amantadine, pyridostigmine, and coenzyme Q10 are of no benefit in PPS. Intravenous immunoglobulin (IVIG) has been tried in three studies, all having positive results. IVIG could probably be a therapeutic alternative, but the potential benefit is modest, and some important questions are still unanswered, in particular to which patients this treatment is useful, the dose, and the therapeutic interval.

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There is no evidence for persistent enterovirus infections in chronic medical conditions in humans

Cited by 17 publications

References 69 publications

Genomic and template RNA transcription in a model of persistent enteroviral infection

Genomic and template RNA transcription in a model of persistent enteroviral infection

The Role of B Lymphocytes in Coxsackievirus B3 Infection

Update on current and emerging treatment options for post-polio syndrome

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