The first evidence that Zika virus might be causing Guillain-Barré syndrome (GBS), a severe neurological disorder, has emerged from a retrospective study of 42 patients diagnosed with GBS during the Zika virus outbreak in French Polynesia (between October 2013 and April 2014).
According to results published on March 1 in the journal The Lancet , based on the analysis of data from French Polynesia, the incidence of GBS was estimated to be 24 in 100,000 people infected with the virus.
Till now, the link between Zika virus and GBS was less clear. But that has changed with this study showing for the first time an epidemiological link between Zika virus and GBS. However, the researchers have not been able to establish a clear pathophysiological mechanism for GBS.
According to the World Health Organization, during 2015 and 2016, eight countries (including Colombia) and territories have reported an increased incidence of GBS and/or laboratory confirmation of a Zika virus infection among GBS cases.
GBS is a disorder in which a person’s immune system attacks the peripheral nerves, and is the leading cause of non-trauma related paralysis. Symptoms develop rapidly and include weakness in the legs and arms, muscle weakness and pain. In about 20-30 per cent of cases, severe GBS can lead to respiratory failure, and about 5 per cent of patients die.
For the study, all the 42 people who were infected with Zika virus and developed GBS were included. Two more control groups of patients were also included in the study. The first of the two control groups consisted of 98 patients who attended the same hospital but who did not have Zika virus infection. The second group consisted of 70 patients who was infected with Zika virus but did not develop any of the symptoms associated with GBS.
The risk of GBS increases with age and men seem to be more commonly affected. Most patients (88 per cent) had Zika virus infection about six days before symptoms of GBS began manifesting. Patients developed GBS symptoms rapidly — generalised muscle weakness (74 per cent), with incapacity to walk (44 per cent). About 64 per cent had facial palsy.
Just as symptoms developed rapidly, patients also recovered faster than is usually expected with GBS. For instance, three months after discharge, 24 (57 per cent) patients were able to walk without assistance. No patients with GBS died. But deaths have been reported from the current outbreaks in the Americas.
All 42 patients were diagnosed with a type of GBS called “acute-motor axonal neuropathy” (AMAN), but none carried the biological markers typically associated with AMAN. The authors note that a previously unknown mechanism might have caused GBS. The authors did not find any evidence that previous dengue infection enhanced the severity of disease.
Patients with GBS did not have the virus in the blood at the time of admission, which is consistent with already known information that the virus is not present in the blood for more than five days after the onset of the disease.
“The results of our study support that Zika virus should be added to the list of infectious pathogens susceptible to cause GBS,” the authors write. GBS is usually triggered by an infection and can sometimes develop following infections of herpes, influenza or dengue virus.
“A little caution should be taken because the data are still scarce and we do not know whether the current Zika virus is identical to that in previous outbreaks, whether it will behave exactly the same in a different population with a different genetic and immunity background, or whether a cofactor or co-infection is responsible,” cautions an accompanying Comment piece.
