Zika virus as a causative agent for primary microencephaly: the evidence so far

Arch Microbiol (2016) 198:595601 DOI 10.1007/s00203-016-1268-7

MINI-REVIEW

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Web End = Zika virus as a causative agent for primary microencephaly: the evidence so far

Bor Luen Tang1,2http://orcid.org/0000-0002-1925-636X

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http://orcid.org/0000-0002-1925-636X

Web End = Received: 9 June 2016 / Revised: 30 June 2016 / Accepted: 8 July 2016 / Published online: 13 July 2016 Springer-Verlag Berlin Heidelberg 2016

Introduction

The recent global emergence of Zika virus (ZIKV) (Musso and Gubler 2016; Bharucha and Breuer 2016; Ramos da Silva and Gao 2016) has received unprecedented attention from the health and biomedical sciences community. First isolated and identied in 1948 (Dick 1952), infections by this (+)strand RNA virus of the family Flaviviridae and

genus Flavivirus may be asymptomatic, or non-febrile, and in the case of a febrile disease result in relatively mild symptoms which include fever, headache, conjunctivitis, arthralgia and a maculopapular rash (Hamel et al. 2016; Ramos da Silva and Gao 2016). The reason why it was declared a public health emergency of international concern by the World Health Organization (WHO) in February 2016 (Heymann et al. 2016) is largely down to its association with congenital defects in the form of primary or congenital microcephaly (Vargas et al. 2001), as well as paralytic neuropathy symptoms of GuillainBarr syndrome (GBS) (Willison et al. 2016).

Primary microencephaly is presented with a signi-cant degree of reduction in the head circumference of the newborn and is associated with varying degrees of impairment in motor, sensory and cognitive functions (Woods et al. 2005). Microcephaly is manifested by reduced production of neurons during brain development in utero, resulting from the demise, or diminished proliferation of cortical progenitor cells, or a reduction in its number of cell divisions. The primary etiological cause for micro-cephaly ranges from mutations in a number of recognized microcephaly genes, many of which encode centrosomal proteins (Tang 2006; Chae and Walsh 2007), to various in utero insults, including microbial infection. For the latter, fetal exposure to Toxoplasma, Rubella virus, Cytomegalo-virus, Herpes virus and the Syphilis bacteria (termed the

Abstract Zika virus (ZIKV) infection has been associated with congenital microcephaly and peripheral neuropathy. The ongoing epidemic has triggered swift responses in the scientic community, and a number of recent reports have now conrmed a causal relationship...