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Table of Contents    
Year : 2018  |  Volume : 66  |  Issue : 5  |  Page : 1286-1287

Zika virus: A wake up call

Department of Neurology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Date of Web Publication17-Sep-2018

Correspondence Address:
Dr. Vivek Lal
Department of Neurology, Post Graduate Institute of Medical Education and Research, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.241374

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How to cite this article:
Balaini N, Lal V. Zika virus: A wake up call. Neurol India 2018;66:1286-7

How to cite this URL:
Balaini N, Lal V. Zika virus: A wake up call. Neurol India [serial online] 2018 [cited 2019 Feb 16];66:1286-7. Available from:

Zika virus (ZIKV) belongs to the family Flaviviridae and was first isolated in 1947 from a monkey in Uganda. It is a RNA virus having only one ZIKV serotype and two lineages, Asian and African. ZIKV infection was declared as a public health emergency of global importance by the World Health Organisation (WHO) in February 2016. India saw its first patient with ZIKV infection in May, 2017.[1] Being a neurotropic virus, it is implicated in various neurological complications like Guillain Barre syndrome (GBS), transverse myelitis, meningoencephalitis, and more importantly, microcephaly as well as congenital zika virus syndrome. No vaccine is available against the ZIKV at present.

Environmental conditions in India are favourable for the ZIKV spread, as a vector that helps in spreading ZIKV (the Aedes aegypti mosquito) is already in abundance. Although there may be a low level of viral transmission presently, it may increase with time and can cause an epidemic, as was seen in Brazil. A good proportion of infected patients are asymptomatic (29-82%) and missed clinically, and those patient who are having symptoms cannot be differentiated clinically from other flavivirus infections.[2] It has been shown that ZIKV can be transmitted sexually as well as vertically from the mother to the foetus causing multiple complications like foetal loss, hearing loss, seizures, cardiac conduction defects and microcephaly [Figure 1].[3] Mechanisms causing microcephaly are not fully known but ZIKV preferentially infects human neural progenitor cells causing apoptosis. ZIKV can cause symptoms due to direct infection or by triggering the autoimmune mechanism in the body, as tabulated in [Table 1].
Figure 1: Zika virus: modes of transmission

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Table 1: Manifestations of zika virus

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The diagnosis of ZIKV is challenging, especially when other flaviviruses are prevalent in India. The laboratory diagnosis of the ZIKV can be performed by identification of the virus by real time reverse transcription polymerase chain reaction (rRT-PCR) in the blood in first week of symptom onset. Immunoglobulin M (IgM) antibodies against the ZIKV are positive after 3-5 days of the symptom onset. These antibodies are useful for establishing the diagnosis especially when the patient presents with complications like GBS, which appears when the fever subsides. At this time, it is difficult to get the rRT-PCR test positivity. The plaque reduction neutralization test can differentiate between false and true positive IgM ZIKV antibodies.[4]

The prevalence of ZIKV-associated GBS is around 1.23%.[5] It is difficult clinically to differentiate between GBS due to ZIKV and other etiology. Rash and arthralgias are reported to be more with ZIKV as compared to non-zika virus etiologies causing GBS. The patients with ZIKV associated GBS require ventilation more frequently, and the GBS subtype that has a greater association with ZIKV is acute inflammatory demyelinating polyneuropathy (AIDP). The cerebrospinal fluid findings and the mortality remains the same in ZIKV-associated and non-ZIKV associated GBS. The pathogenesis responsible for GBS has not been characterised. The diagnosis of ZIKV infection prior to the development of GBS is again challenging, as viral antigens disappear when symptoms of GBS appear after around 1 week of presentation; and, using immunoglobulin M (IgM) antibodies against the ZIKV is again not definitive because of its cross reactivity with other diseases caused by flaviviruses like dengue and chikungunya, already prevalent in our country. The treatment of ZIKV associated GBS is as for non- ZIKV associated GBS.

ZIKV antibodies were present in 15.5% (14/90) patients with GBS in the present study. This finding can be interpreted in two ways: either we can discard the finding stating that the presence of these antibodies was due to the cross reactivity with other flaviviruses; or, the finding can be considered as a wake-up call. In the latter case, the finding demonstrates that ZIKV might have been present in India for a much longer time than anticipated, and that we are just looking at the tip of the iceberg.[5],[6],[7],[8] General measures like storing water in closed containers, avoiding mosquito bites using mosquito nets or mosquito repellents will go a long way in ameliorating the spread of this infection. Simultaneous research on developing vaccination against ZIKV may be undertaken. It is high time that necessary measures to prevent this infection from turning into a wide-spread epidemic are undertaken with the concerned public health authorities at the local and national level.

  References Top

Mourya DT, Shil P, Sapkal GN, Yadav PD. Zika virus: Indian perspectives. Indian J Med Res 2016;143:553-64.  Back to cited text no. 1
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Haby MM, Pinart M, Elias V, Reveiz L. Prevalence of asymptomatic Zika virus infection: A systematic review. Bull World Health Organ [Internet]. 2018;96:402–13D. Available from: [Last accessed on 2018 Aug 12].  Back to cited text no. 2
Carod-Artal FJ. Neurological complications of Zika virus infection. Vol. 16, Expert Review of Anti-Infective Therapy. Taylor & Francis; 2018. 399-410 p. Available from: [Last accessed on 2018 Aug 12].  Back to cited text no. 3
Keane Í, Dias R, Luciana C, Maria R, Martins G, Fernanda K, et al. Zika virus : A review of the main aspects of this type of arbovirosis. 2018;51:261-9.  Back to cited text no. 4
Hajra A, Bandyopadhyay D, Hajra SK. Zika virus: New interest in neurology. Neurol India 2016;64:1102-4.  Back to cited text no. 5
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Joob B, Wiwanitkit V. Neurological problem due to Zika virus infection: What should be discussed?. Neurol India 2017;65:439-40.  Back to cited text no. 6
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Baskar D, Amalnath 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. 7
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Barbi L, Coelho AVC, Alencar LCA de, Crovella S. Prevalence of Guillain-Barré syndrome among Zika virus infected cases: a systematic review and meta-analysis. Brazilian J Infect Dis [Internet]. 2018;22(2):137-41. Available from: [Last accessed on 2018 Aug 12].  Back to cited text no. 8


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