Zika virus: Scientists find direct evidence of link with Guillain-Barré syndrome

The Zika virus can trigger a mysterious neurological disorder that results in temporary paralysis according to the first large-scale study to examine the role the virus plays in Guillain-Barré syndrome.

The findings suggest that in addition to a significant increase in the birth of “small-brain” babies suffering from microcephaly, health authorities in Latin America, where Zika is widespread, can expect a large rise in the number of people suffering from Guillain-Barré, when the body’s immune system attacks the nerves, leading to muscle weakness and paralysis.

Several countries in South America, such as Colombia and Venezuela, where Zika virus has spread rapidly by mosquito transmission, have already reported sharp increases in Guillain-Barré syndrome, which is normally exceedingly rare.

Although scientists have suspected that the Zika virus raises the risk of someone developing Guillain-Barré syndrome, the study is the first time that scientists have found direct evidence of the link by studying individuals in a large outbreak of Zika.

The researchers analysed blood samples from 42 patients with Guillain-Barré syndrome who developed the disorder during the Zika virus outbreak in French Polynesia between 2013 and 2014 – the largest reported outbreak at that time.

They found that infection with the Zika virus can raise the risk of someone developing the Guillain-Barré syndrome by more than 20 fold, from a risk of about 1 or 2 in 100,000 to about 24 in 100,000.

“This is the first study to look at a large number of patients who developed Guillain-Barre syndrome following Zika virus infection and provide evidence that Zika virus can cause GBS,” said Professor Arnaud Fontanet of the Pasteur Institute in Paris, who led the study published in the journal The Lancet.

“Most of the patients with GBS reported they had experienced symptoms of Zika virus infection on average 6 days before any neurological symptoms, and all carried Zika virus antibodies,” Professor Fontanet said.

“The evidence of a link between Zika and GBS was until now known at the population level from epidemiological studies. We’ve shown it at the individual level, but what is still missing is the actual mechanism that would explain how Zika can trigger GBS,” he said.

Professor Fontanet said that Latin American countries where Zika is currently spreading rapidly should expect an increase in cases of Guillain-Barré syndrome in the coming months, which could overwhelm their health services given that many patients need intensive care treatment for a month or more.

“Only at the end of the outbreak can you have any idea of how many people will have been infected with Zika. I think countries have to be ready for a subsequent increase in GBS with might lead to saturation of intensive care beds. This really is a cause for concern,” Professor Fontanet said.

A number of viral infections were already suspected of triggering Guillain-Barré, which is a leading cause of paralysis not resulting from accidents or trauma. In about 20 to 30 per cent of cases of GBS, patients suffer respiratory failure and 5 per cent of patients die.

“The results of our study support that Zika virus should be added to the list of infectious pathogens susceptible to cause Guillain-Barre syndrome,” Professor Fontanet said.

The study of the Zika outbreak in French Polynesia found that 88 per cent of the 42 patients with GBS reported that they had symptoms of Zika infection in the week before the onset of neurological problems – and 41of the 42 patients were carrying Zika antibodies in their bloodstream, indicating they had recently been infected with the virus.

A comparison with other patients who had been infected with the dengue virus, which, like Zika, is also transmitted by mosquitoes, did not show a significantly increased risk of Guillain-Barré, indicating that dengue was unlikely to trigger the condition.