For the moment no one knows the answer to this question. Maybe in few months we will get some information about the mechanism if the link between Zika and microcephaly is confirmed.

Bovine Viral Diarrhea Virus, another Flaviviridae, causes microcephaly in bovine foetuses; maybe there's a homologous pathogeny when it comes to Zika.

I also looking for same answer. However so far, there are case reports and speculations, Couldn't reach the best answer yet (maybe this part is homework for researchers). I found one piece of puzzle that one group shares the real-time data of Zika infection experiment in non-human primate, this might helpful for your curiosity.

https://dholk.primate.wisc.edu/project/dho/public/Zika/public/ZIKV-001-public/begin.view

Thank you I will take a look of it.

Guess this article could give you some ideas: http://trstmh.oxfordjournals.org/content/46/5/521.full.pdf+html?sid=7e623118-9570-44c7-938b-b30894df4ad9

We have identified two areas of pathogenesis and are looking for a lab partner for validation. Please contact me for further details. Here is one article that has been published, "The Zika Virus sfRNA Secondary Structure Reveals a miR-147a Homologue that Targets Neurofascin as a Potential Cause of its Neurologic Syndromes" (Link here: http://www.webmedcentral.com/article_view/5076).  We have just submitted another entitled, "Zika-Virus Induced Neurotropic Brain Injury: Lessons for the Study of Disease Etiology and Vaccine Development Against Pathogens" that details what we consider to be the contribution of two viral proteins in the pathogenesis of the neurotropism. 

 CDC announced today that Zika is more dangerous than previously thought, in addition to microcephaly in newborns and Guillain-Barre, the American Academy of Neurology announced late yesterday that it is the cause of Acute Disseminated Encephalomyelitis.

Possible Immunopathogenesis of the Guillain–Barré Syndrome : It seems that Zika virus has a kind of lipooligosaccharide (or other substances) which is similar to one expressed on human motor nerves. This Zika lipooligosaccharide induces autoantibodies against normal lipooligosaccharide on human motor nerves and causes Guillain-barré syndrome as you can see in the captured file. Ref:Nobuhiro Yuki, Hans-Peter Hartung. N Engl J Med 2012;366:2294-304.

 Dear Azadeh Safaei,

re: : It seems that Zika virus has a kind of lipooligosaccharide (or other substances)

my apologies but I do not have access to the complete article  but I noticed it is a 2002 one, before the Zika epidemy.

Does the article  cite Zika ?

May you please share a copy?

APOLOGIES: Knowing my post is not connected to the initial question but:

Information added with regard to actuality (has been reported today in Austrian Newspaper for the first time):

MEYER SAUTEUR PM et al:

Research Article

Mycoplasma pneumoniae triggering the Guillain-Barré syndrome: A case-control study

Annals of Neurology, Volume 80, Issue 4 October 2016

Pages 566–580

First published: 26 August 2016   

DOI: 10.1002/ana.24755

http://onlinelibrary.wiley.com/doi/10.1002/ana.24755/abstract

For (your) convenience only:

Abstract

Objective

Guillain-Barré syndrome (GBS) is an acute postinfectious immune-mediated polyneuropathy. Although preceding respiratory tract infections with Mycoplasma pneumoniae have been reported in some cases, the role of M. pneumoniae in the pathogenesis of GBS remains unclear. We here cultured, for the first time, M. pneumoniae from a GBS patient with antibodies against galactocerebroside (GalC), which cross-reacted with the isolate. This case prompted us to unravel the role of M. pneumoniae in GBS in a case-control study.

Methods

We included 189 adults and 24 children with GBS and compared them to control cohorts for analysis of serum antibodies against M. pneumoniae (n = 479) and GalC (n = 198).

Results

Anti–M. pneumoniae immunoglobulin (Ig) M antibodies were detected in GBS patients and healthy controls in 3% and 0% of adults (p = 0.16) and 21% and 7% of children (p = 0.03), respectively. Anti-GalC antibodies (IgM and/or IgG) were found in 4% of adults and 25% of children with GBS (p = 0.001). Anti-GalC-positive patients showed more-frequent preceding respiratory symptoms, cranial nerve involvement, and a better outcome. Anti-GalC antibodies correlated with anti–M. pneumoniae antibodies (p < 0.001) and cross-reacted with different M. pneumoniae strains. Anti-GalC IgM antibodies were not only found in GBS patients with M. pneumoniae infection, but also in patients without neurological disease (8% vs 9%; p = 0.87), whereas anti-GalC IgG was exclusively found in patients with GBS (9% vs 0%; p = 0.006).

Interpretation

M. pneumoniae infection is associated with GBS, more frequently in children than adults, and elicits anti-GalC antibodies, of which specifically anti-GalC IgG may contribute to the pathogenesis of GBS. Ann Neurol 2016;80:566–580

Thank you.