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NI FEATURE: THE EDITORIAL DEBATE I-- PROS AND CONS
Year : 2018  |  Volume : 66  |  Issue : 5  |  Page : 1290-1292

Guillain–Barré syndrome caused by Zika virus: A wake-up call for India


1 Department of Neurology, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Microbiology, King George's Medical University, Lucknow, Uttar Pradesh, India

Date of Web Publication17-Sep-2018

Correspondence Address:
Dr. Ravindra Kumar Garg
Department of Neurology, King George's Medical University, Lucknow - - 226 003, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.241356

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How to cite this article:
Garg RK, Jain A, Rizvi I. Guillain–Barré syndrome caused by Zika virus: A wake-up call for India. Neurol India 2018;66:1290-2

How to cite this URL:
Garg RK, Jain A, Rizvi I. Guillain–Barré syndrome caused by Zika virus: A wake-up call for India. Neurol India [serial online] 2018 [cited 2018 Oct 23];66:1290-2. Available from: http://www.neurologyindia.com/text.asp?2018/66/5/1290/241356




Baskar et al., from South India, presented a surprise finding in a cohort of 90 patients with Guillain–Barré syndrome. They demonstrated anti-Zika antibodies in 14 (15.5%) patients with Guillain–Barré syndrome.[1] This is an alarming finding as well. In India, so far, only three serologically confirmed cases of Zika virus disease have been reported. All these cases were found in the state of Gujarat. Subsequently, the Indian Council of Medical Research has tested 34,233 human samples and 12,647 mosquito samples for the presence of Zika virus in the same area of Gujarat but all were tested negative for Zika virus.[2]

Zika virus is a mosquito-borne flavivirus that is associated with a variety of neurological complications. Other flaviviruses, causing neurological complications are yellow fever virus, dengue virus, Japanese encephalitis, and West Nile virus. All flaviviruses, barring yellow fever and Zika viruses, are known to cause recurrent outbreaks in India. Zika virus infection recently surfaced as a major outbreak in many parts of Central and South America and in the Caribbean countries. Consequently, the World Health Organization declared Zika virus epidemic a global public health emergency.

Generally, Zika virus infections do not produce any symptom or manifest with non-specific symptoms such as fever, rash, conjunctivitis, and arthralgia. Severe thrombocytopenia is rare. Zika-virus-associated neurological complications include Guillain–Barré syndrome, myelitis, and meningoencephalitis.[3],[4] In Brazil, among 40 consecutive patients of new-onset acute parainfectious or neuroinflammatory disease admitted to a tertiary referral center, 35 (88%) patients had evidence of recent Zika virus in the serum and/or cerebrospinal fluid.[5]

In countries with active Zika virus circulation, an increased incidence of Guillain–Barré syndrome has been noted. During a recent outbreak in Colombia, among 68 patients with Guillain–Barré syndrome, 66 (97%) patients had symptoms suggestive of Zika virus infection (before the onset of Guillain–Barré syndrome). Half of these patients had bilateral facial paralysis.[6] Cranial nerve involvement, autonomic dysfunction, and the need for mechanical ventilation indicated a severe course of Zika-associated Guillain–Barré syndrome.[7] Electrophysiologically, the acute inflammatory demyelinating polyneuropathy variant is much more frequent than the acute motor axonal neuropathy variant.[8] The exact pathogenesis of Guillain–Barré syndrome, following Zika infection, is not precisely known. A molecular mimicry between glycolipids and surface molecules of infectious agents is postulated to cause Guillain–Barré syndrome in Zika-infected persons. Many workers believe that this virus has neurotropic properties that lead to neuronal cell loss.[9] Typical anti-ganglioside antibodies, in motor variants of Zika-associated Guillain–Barré syndrome, are rarely noted. Preexisting antibodies against other circulating flaviviruses, such as dengue virus, have been associated with a severe clinical course in patients with Zika-associated neurological diseases. Zika-associated Guillain–Barré syndrome may be treated with either plasmapheresis or intravenous immunoglobulins. Many patients need assisted ventilation. Death was reported in 15% of patients.[10]

Zika virus disease should be considered in patients presenting with some neurological manifestation and who have recently traveled to or resided in areas with Zika virus transmission. A person who had sex with someone who traveled to those areas is also at risk of Zika-associated neurological complications.[11] In addition to the dengue virus infection, many other flaviviruses are circulating in India such as Japanese encephalitis, chikungunya, and West Nile virus. These flaviviruses can also manifest with an acute lower motor neuron disorder. Prior Zika infection in these patients can be differentiated from chikungunya and dengue infection on the basis that chikungunya- and dengue-infected patients experience a higher grade of fever. Conjunctivitis is characteristically seen in Zika infection.[12] In areas where multiple arboviruses circulate, the presence of rash with pruritus or conjunctivitis without any other general clinical manifestations such as fever, petechia, or anorexia indicate the presence of Zika virus infection [Table 1].[13]
Table 1: Differential diagnosis between Guillain-Barré syndrome caused by Zika virus and dengue virus

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The results of the study by Baskar et al., may be interpreted in many other ways. They demonstrated that 4 (of 14 patients) with Zika positivity also had anti-dengue antibody (IgM) positivity. The first implication of this study is that Zika virus is circulating in some part of India and we need to be cautious to prevent a bigger epidemic from becoming a reality. The second, but more important, implication is that as dengue and Zika viruses have a high degree of structural similarities, this can result in false-positive serological test results.[14] In the United States, the false positivity rate was found to be as high as 27%, and in Puerto Rico it was 6%. In such a situation, the plaque reduction neutralization test is capable of providing a virus-specific diagnosis of Zika virus infection or in ruling out Zika virus infection in the majority of IgM Zika-positive samples.[15] Unfortunately, this test is not widely available in India.

A cross-reactivity with dengue and Zika virus has pathogenical implications as well. Usually, Zika virus is not associated with a severe disease in humans, but if prior infection by other flaviviruses is present, it may be associated with severe Zika-associated complications and may adversely affect the outcome. Dengue virus cross-reactivity induces antibody-dependent aggravation of Zika virus infection.[16],[17]

Why is India protected from a large outbreak of Zika virus infection? Possibly, a subset of antibodies targeting an antigen isolated from patients with dengue virus also potently neutralize Zika virus. So, possibly, antibodies against dengue, in fact, has protected us from Zika epidemics. Still, experts express the need for developing a universal vaccine capable of producing effective cross-neutralizing antibodies against both Zika and dengue virus infections.[18]



 
  References Top

1.
Baskar D, Amarnath D, Mandal J, Dhodapkar R, Vanathi K. Antibodies to Zika virus, Campylobacter jejuni, gangliosides in Guillain–Barre syndrome: A prospective single-center study from southern India. Neurol India 2018;66:1324-31.  Back to cited text no. 1
  [Full text]  
2.
World Health Organization. Zika virus infection—India. Disease Outbreak News 26 May 2017. Available from: http://www.who.int/csr/don/26-may-2017-zika-ind/en/. [Last accessed on 2018 Apr 06].  Back to cited text no. 2
    
3.
Hall V, Walker WL, Lindsey NP, Lehman JA, Kolsin J, Landry K, et al. Update: Noncongenital Zika virus disease cases—50 U.S. States and the District of Columbia, 2016. MMWR Morb Mortal Wkly Rep 2018;67:265-9.  Back to cited text no. 3
    
4.
Grill MF. Infectious myelopathies. Continuum (Minneap Minn) 2018;24:441-73.  Back to cited text no. 4
    
5.
da Silva IRF, Frontera JA, Bispo de Filippis AM, Nascimento OJM do, RIO-GBS-ZIKV Research Group. Neurologic complications associated with the Zika virus in Brazilian adults. JAMA Neurol 2017;74:1190-8.  Back to cited text no. 5
    
6.
Parra B, Lizarazo J, Jiménez-Arango JA, Zea-Vera AF, González-Manrique G, Vargas J, et al. Guillain-Barré syndrome associated with Zika virus infection in Colombia. N Engl J Med 2016;375:1513-23.  Back to cited text no. 6
    
7.
Uncini A, González-Bravo DC, Acosta-Ampudia YY, Ojeda EC, Rodríguez Y, Monsalve DM, et al. Clinical and nerve conduction features in Guillain-Barré syndrome associated with Zika virus infection in Cúcuta, Colombia. Eur J Neurol 2018;25:644-50.  Back to cited text no. 7
    
8.
Leonhard SE, Lant S, Jacobs BC, Wilder-Smith A, Ferreira MLB, Solomon T, et al. Zika virus infection in the returning traveler: What every neurologist should know. Pract Neurol 2018;pii: practneurol-2017-001789.  Back to cited text no. 8
    
9.
Anaya J-M, Ramirez-Santana C, Salgado-Castaneda I, Chang C, Ansari A, Gershwin ME. Zika virus and neurologic autoimmunity: The putative role of gangliosides. BMC Med 2016;14:49.  Back to cited text no. 9
    
10.
Mahecha MP, Ojeda E, Vega DA, Sarmiento-Monroy JC, Anaya JM. Guillain-Barré syndrome in Colombia: Where do we stand now? Immunol Res 2017;65:72-81.  Back to cited text no. 10
    
11.
Walker WL, Lindsey NP, Lehman JA, Krow-Lucal ER, Rabe IB, Hills SL, et al. Zika virus disease cases—50 States and the District of Columbia, January 1-July 31, 2016. MMWR Morb Mortal Wkly Rep 2016;65:983-6.  Back to cited text no. 11
    
12.
Long D, Long B, Koyfman A. Zika virus: What do emergency physicians need to know? J Emerg Med 2016;50:832-8.  Back to cited text no. 12
    
13.
Braga JU, Bressan C, Dalvi APR, Calvet GA, Daumas RP, Rodrigues N, et al. Accuracy of Zikavirusdisease case definition during simultaneous Dengue and Chikungunya epidemics. PloS One 2017;12:e0179725.  Back to cited text no. 13
    
14.
Rockstroh A, Moges B, Barzon L, Sinigaglia A, Palù G, Kumbukgolla W, et al. Specific detection of dengue and Zika virus antibodies using envelope proteins with mutations in the conserved fusion loop. Emerg Microbes Infect 2017;6:e99.  Back to cited text no. 14
    
15.
Lindsey NP, Staples JE, Powell K, Rabe IB, Fischer M, Powers AM, et al. Ability to serologically confirm recent Zika virus infection in areas with varying past incidence of Dengue virus infection in the United States and U.S. territories in 2016. J Clin Microbiol 2018;56:e01115-17.  Back to cited text no. 15
    
16.
Raboni SM, Bonfim C, Almeida BM, Zanluca C, Koishi AC, Rodrigues PRVP, et al. Flavivirus cross-reactivity in serological tests and Guillain-Barré syndrome in a hematopoietic stem cell transplant patient: A case report. Transpl Infect Dis Off J Transplant Soc 2017:19.  Back to cited text no. 16
    
17.
Dejnirattisai W, Supasa P, Wongwiwat W, Rouvinski A, Barba-Spaeth G, Duangchinda T, et al. Dengue virus sero-cross-reactivity drives antibody-dependent enhancement of infection with zika virus. Nat Immunol 2016;17:1102-8.  Back to cited text no. 17
    
18.
Barba-Spaeth G, Dejnirattisai W, Rouvinski A, Vaney MC, Medits I, Sharma A, et al. Structural basis of potent Zika-dengue virus antibody cross-neutralization. Nature 2016;536:48-53.  Back to cited text no. 18
    



 
 
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