The Zika virus may cause severe neurological disorder Guillain-Barré syndrome (GBS), according to research published last night (29 February, 2016).
The findings confirm suspicions of a link between the virus and the disorder.
Some 42 patients in French Polynesia were diagnosed with GBS during the Zika virus outbreak between October 2013 and April 2014.
Based on the analysis of data, if 100,000 people were infected with Zika virus, 24 would develop GBS, says researchers.
Professor Arnaud Fontanet from the Institut Pasteur, Paris, France, who led the study, which is published in The Lancet, said: “This is the first study to look at a large number of patients who developed Guillain-Barré syndrome following Zika virus infection and provide evidence that Zika virus can cause GBS.”
During the Zika outbreak, an estimated 32,000 patients consulted a doctor about possible Zika virus infection. A total of 42 patients were diagnosed with GBS – disorder which affects the immune and nervous systems, and is the leading cause of non-trauma related paralysis – between November 2013 and February 2014.
Researchers wanted to determine the link between Zika virus infection and GBS and because the region is also prone to outbreaks of dengue virus, they also wanted to establish if dengue virus was an additional risk factor for GBS.
The 42 patients were put into two control groups, the first of which was matched for age, gender and island of residence and comprised a total of 98 patients who attended the same hospital but did not have a fever.
The second control group comprised 70 patients who tested positive for Zika virus infection, but did not develop any of the neurological symptoms associated with GBS. Blood samples were collected from all patients.
Researchers found that 88% of the patients with GBS had reported symptoms of Zika virus infection about six days before any neurological symptoms were reported. None tested positive for a Zika virus infection once in hospital and blood tests showed that 98% were carrying Zika virus antibodies. All had neutralising antibodies against Zika virus.
However, only 56% of the patients without a fever in the first control group carried Zika virus neutralising antibodies. Researchers also found that 95.2% of patients with GBS showed signs of previous dengue virus infection. In the first control group, this number was 88.8% and in the second it was 82.9%.
All 42 patients were diagnosed with a type of GBS called ‘acute-motor axonal neuropathy’ (AMAN), but few carried the biological markers typically associated with AMAN, suggesting a previously unknown disease mechanism. The patients in the study generally recovered faster than is usually expected with GBS.
Professor Fontanet said: “Although it is unknown whether attack rates of Zika virus epidemics will be as high in affected regions in Latin America than in the Pacific Islands, high numbers of cases of Guillain-Barré syndrome might be expected in the coming months as the result of this association. The results of our study support that Zika virus should be added to the list of infectious pathogens susceptible to cause Guillain-Barré syndrome.”
Cao-Lormeau VM, Blake A et al. Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study. The Lancet 29 February 2016 [abstract]
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