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COMMENTARY
Year : 2016  |  Volume : 144  |  Issue : 1  |  Page : 9-10

The genetics of post-polio syndrome - much to be unravelled!


Department of Biomedical Sciences, School of Biosciences & Technology, VIT University, Vellore 632 014, Tamil Nadu, India

Date of Web Publication3-Nov-2016

Correspondence Address:
Radha Saraswathy
Department of Biomedical Sciences, School of Biosciences & Technology, VIT University, Vellore 632 014, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-5916.193277

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How to cite this article:
Saraswathy R. The genetics of post-polio syndrome - much to be unravelled!. Indian J Med Res 2016;144:9-10

How to cite this URL:
Saraswathy R. The genetics of post-polio syndrome - much to be unravelled!. Indian J Med Res [serial online] 2016 [cited 2020 Feb 19];144:9-10. Available from: http://www.ijmr.org.in/text.asp?2016/144/1/9/193277

Post-polio syndrome (PPS) affects 20-40 per cent of polio survivors and manifests as neuromuscular complications. The incidence, symptoms and severity of PPS vary and some patients are known to develop weakness, atrophy, fatigue, muscle and joint pain and other complications; however, the absence of its incidence or severity has also been reported in some polio survivors [1] .There have been reports that even non-paralytic polio patients succumb to PPS [2] .

The exact cause for PPS and reasons for the differences in its span are still unclear. The treatment generally focuses on reducing the symptoms and improving the quality of life [3] . An early diagnosis of PPS would be helpful in reducing the severity of PPS. There are no diagnostic tests for PPS available. It is difficult to identify who is more susceptible and or at a higher risk.

There has been an interest in analysing the genetic basis of infectious diseases recently [4],[5] . Poliovirus has a common receptor known as poliovirus receptor (PVR) that belongs to immunoglobulin superfamily CD155, a poliovirus cell surface receptor which is located on chromosome 19q13.2 [6],[7] . PVR gene polymorphism in patients with progressive muscular atrophy was reported by Saunderson et al in 2004 [8] . Later, Ala67Thr polymorphism in the PVR gene was reported to be a possible risk factor for the aetiology of poliomyelitis [9] .The heterozygous single nucleotide polymorphism (SNP) (Ala67Thr) in CD155 gene has been reported in healthy population (6.8 to 8.5%) and the incidence has been shown to be significantly higher in polio paresis (13.3%) and progressive muscular atrophy (20%) patients [8],[9] . Nandi and colleagues [10] in this issues have reported development of an SNP assay to detect the single nucleotide substitution (GCGaACG) in CD155/PVR gene. The assay seems to be suitable for large scale screening of PPS samples for identification of heterozygous SNP in the CD155/PVR gene [10] . However, the screening for PVR gene polymorphism (Ala67Thr) should be further confirmed on a large sample of PPS patients in different population groups in India. SNPs used are the most powerful tools for human genetic studies [11] . SNPs as genetic markers can be used to identify the inheritance patterns of chromosomal regions from generation to generation in human genetic diseases [12] .

It has been reported [13] that a number of viruses produce chromosomal abnormalities in circulating lymphocytes during infections in humans (such as, measles virus, chicken pox and mumps viruses and hepatitis virus) with the first report being the chromosome breakage due to herpes simplex virus in culture [14] . However, these chromosomal abnormalities due to direct or indirect effects, as well as the immediate or delayed effects of viruses have not been completely understood. Bhattacharya et al[15] reported a significant increase in chromosome aberrations in PPS patients than in controls showing a delayed effect of the poliovirus in humans. However, many questions still remain unanswered.

Centers for Disease Control and Prevention [16] reported a drop in the incidence of polio myelitis worldwide from an estimated 350,000 in 1988 to 407 in 2013, that is, more than 99 per cent decline in the reported cases. According to the global polio surveillance data (March 9, 2016) [17] , five wild poliovirus cases from Pakistan and one from Afghanistan were reported.

Although India has efficiently eradicated polio and 80 per cent of the world's people now live in polio-free areas, the increase in the prevalence of a polio-like condition known as acute flaccid paralysis (AFP) has been recorded [18] . Many cases of non-polio enteroviruses have also become common in infants and children [19] . It has been reported that Enterovirus 71 (EV 71) causes AFP and is linked to meningitis, encephalitis, hand, foot and mouth diseases [19] . Hence, the research needs to address whether the single nucleotide polymorphism (Ala67Thr) in CD155/PVR gene known to be utilized for screening PPS will also pick up AFP individuals or any motor neuron diseases or will it be specific for PPS alone? Further research analysis will provide characterization of human diversity at the nucleotide level and demonstrate the feasibility of large-scale screening of human SNPs.

Though the cytogenetic studies have shown a significant increase in the frequency of various chromosomal anomalies, the specific chromosome regions where rearrangements occurred have to be analysed in depth. This chromosome specific rearrangement could result in disease specific marker/probe for screening PPS. Ala67Thr polymorphism in PVR gene is known to occur in many motor neurons related diseases [8] . Therefore, a well designed study with a large sample size in other population groups is recommended using this SNP assay and the DNA sequencing method for validation. Further, a study related to the pattern of inheritance of the Ala67Thr polymorphism in the PPS families and a correlation between genotype-phenotype could be addressed at the cytogenetic and molecular levels.

 
   References Top

1.
Falconer M, Bollenbach E. Survey results in process. Lincolnshire, 2006. Available from: http://www.poliosurvivorsnetwork.org.uk/archive/lincolnshire/library/bollenbach/bioloyg12.html, accessed on May 2, 2016.   Back to cited text no. 1
    
2.
Falconer M, Bollenbach E. Late functional loss in non-paralytic polio. Am J Phys Med Rehabil 2000; 79 : 19-23.  Back to cited text no. 2
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3.
Post-Polio Syndrome Fact Sheet. National Institute of Neurological Disorders and Stroke (NINDS). April 16, 2014. Bethesda. Available from: http://www.ninds.nih.gov/disorders/post_polio/detail_post_polio.htm, accessed on May 2, 2016.  Back to cited text no. 3
    
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Chapman SJ, Hill AV. Human genetic susceptibility to infectious disease. Nat Rev Genet 2012; 13 : 175-88.  Back to cited text no. 4
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5.
Zhang X, Xu H, Chen X, Li X, Wang X, Ding S, et al. Association of functional polymorphisms in the MxA gene with susceptibility to enterovirus 71 infection. Hum Genet 2014; 133 : 187-97.  Back to cited text no. 5
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6.
Mendelsohn CL, Wimmer E, Racaniello VR. Cellular receptor for poliovirus: molecular cloning, nucleotide sequence, and expression of a new member of the immunoglobulin superfamily. Cell 1989; 56 : 855-65.  Back to cited text no. 6
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7.
Koike S, Horie H, Ise I, Okitsu A, Yoshida M, Iizuka N, et al. The polio virus receptor protein is produced both as membrane-bound and secreted forms. EMBO J 1990; 10 : 3217-24.  Back to cited text no. 7
    
8.
Saunderson R, Yu B, Trent RJ, Pamphlett R. A polymorphism in the poliovirus receptor gene differs in motor neuron disease. Neuroreport 2004; 15 : 383-6.  Back to cited text no. 8
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9.
Kindberg E, Ax C, Fiore L, Svensson L. Ala67Thr mutation in the poliovirus receptor CD155 is a potential risk factor for vaccine and wild-type paralytic poliomyelitis. J Med Virol 2009; 81 : 933-6.  Back to cited text no. 9
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10.
Nandi SS, Sharma DK, Deshpande JM. Assay for identification of heterozygous single-nucleotide polymorphism (Ala67Thr) in human poliovirus receptor gene. Indian J Med Res 2016; 144 : 38-45.  Back to cited text no. 10
    
11.
Wang DG, Fan JB, Siao C-J, Berno A, Young P, Sapolsky R, et al. Large-scale identification, mapping, and genotyping of single-nucleotide polymorphisms in the human genome. Science 1998; 280 : 1077-82.  Back to cited text no. 11
    
12.
Kwok P-Y, Chen X. Detection of single nucleotide polymorphisms. Curr Issues Mol Biol 2003; 5 : 43-60.   Back to cited text no. 12
    
13.
Bhattacharya SK, Sengupta S, Austin JC. Chromosome abnormalities in peripheral blood cells of post-polio patients in south Indian population. J Ecobiotechnol 2010; 2 : 1-5.  Back to cited text no. 13
    
14.
Hampar B, Ellison SA. Chromosomal aberrations induced by an animal virus. Nature 1961; 192 : 145-7.  Back to cited text no. 14
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15.
Bhattacharya SK, Saraswathy R, Sivakumar E. Genotoxic assessment in peripheral blood lymphocytes of post-polio individuals using sister chromatid exchange analysis & micronucleus assay. Hum Exp Toxicol 2011; 30 : 636-48.   Back to cited text no. 15
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16.
Edna KM, Kimberly AP, Steven GFW, Rudolf HT, Ousmane MD, Cara CB, et al. CDC. Progress Toward Polio Eradication-Worldwide, 2013-2014. MMWR Morb Mortal Wkly Rep 2014; 63 : 468-72.  Back to cited text no. 16
    
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Snider CJ, Diop OM, Burns CC, Tangermann RH, Wassilak SG. Surveillance Systems to Track Progress Toward Polio Eradication-Worldwide, 2014-2015. MMWR Morb Mortal Wkly Rep 2016; 65 : 346-51  Back to cited text no. 17
    
18.
John TJ, Vashishtha VM. Eradicating poliomyelitis: India′s journey from hyperendemic to polio-free status. Indian J Med Res 2013; 137 : 881-94.  Back to cited text no. 18
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19.
Rao CD. Non-polio enteroviruses, the neglected and emerging human pathogens: Are we waiting for the sizzling enterovirus volcano to erupt? Proc Indian Natn Sci Acad 2015; 81 : 447-62.  Back to cited text no. 19
    



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