New evidence supports Zika, Guillain-Barré link

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A new study in South America has unearthed the strongest biological evidence to date linking the Zika virus to the debilitating and potentially paralyzing Guillain-Barré syndrome, researchers say.

Immunologic and viral evidence of Zika in a substantial number of adults with Guillain-Barré supports epidemiology data that had suggested a close relationship between the two, researchers report.

Their results appear in the New England Journal of Medicine.

“At the beginning of the Zika outbreak in South America, my colleagues in Colombia contacted me with concern about the increasing number of patients with neurological complications in their hospitals,” says Carlos A. Pardo, associate professor of neurology and pathology at the Johns Hopkins School of Medicine. Pardo, who earned his medical degree in Colombia, is an expert in neuroimmune and infectious diseases, including Guillain-Barré.

Pardo’s team provided the Colombian doctors with tools for viral tests of blood, cerebrospinal fluid, and urine samples from patients with symptoms of Guillain-Barré.

Microcephaly and now Guillain-Barré

Guillain-Barré is a very rare but serious disorder of the nervous system that appears days to weeks after infection with viruses or bacteria. It occurs when a person’s own immune system attacks the myelin sheaths that protect nerve cells. That often results in muscle weakness, pain, sensory problems, and, in very acute cases, potentially life-threatening paralysis.

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A Zika outbreak began in South America in mid-2015; recent research has confirmed early suspicions that the disease has caused a rash of microcephaly, causing infants of Zika-infected mothers to be born with severely underdeveloped brains. Doctors have also harbored strong suspicions of a link to Guillain-Barré.

Zika infections occur through mosquito bites or, in some cases, sexual contact. Cases transmitted locally by mosquito have occurred in Puerto Rico and Florida, and travel-related cases have been identified elsewhere in the United States. Most patients develop relatively mild symptoms or none at all, but the connection to microcephaly and, now, Guillain-Barré has made the outbreak an international health emergency.

Guillain-Barré affects an estimated one or two of 100,000 people after infections. Scientists do not know why it strikes some people and not others.

Zika and neurologic symptoms

Of the 68 patients initially evaluated in Colombia, virus and immunology studies were conducted using body fluids from 42. The researchers eventually found urine to be the most reliable fluid to diagnose Zika infection in patients with Guillain-Barré.

Seventeen patients tested positive for Zika virus in their urine. Another 18 had no evidence of Zika in urine but showed immunologic footprints of infection through the presence of virus-specific antibodies in blood or spinal fluid. Most of the patients were adults; 38 were males and 30 females. The average age was 47. Almost all had two or more clinical symptoms of Zika infection, including fever, headache, rash, and conjunctivitis.

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The researchers say that almost one-half of the study participants complained of neurologic symptoms within four days of the onset of Zika symptoms—an unusually fast response, they say, compared with what is found in people who develop Guillain-Barré symptoms after other viral infections, such as influenza and herpes.

Pardo says the study is believed to be the largest of its kind so far to document the role of Zika infection in increased rates of Guillain-Barré. Although the study demonstrates a biological and viral association, it does not reveal the biological mechanisms through which Zika might attack the nerves, he says.

The research team continues to collect clinical data and samples from Colombian hospital patients, but the work is constrained by limited resources and the severe ongoing Zika outbreak.

Colombian researchers working on the study were from Cali, Cucuta, Medellin, Neiva, Barranquilla, and Bogota. The Bart McLean Fund for Neuroimmunology Research, Johns Hopkins Project Restore, VIREM, the Virology Laboratory Fund and the Universidad de Valle supported the work.

Source: Johns Hopkins University