We thank Gerardin et al. for the comments on our Zika virus (ZIKV) clinical/scientific note [1]. Our patient was of particular interest because he suffered an illness clinically and electrophysiologically indistinguishable from Guillain-Barré syndrome (GBS) which developed within a few days of acute ZIKV infection, in the context of contemporaneous Zika vireamia. [1] Concurrently obtained CSF was negative for ZIKV. Brain and spine MRI were also normal. Importantly, there was no serologic evidence of priming by previous dengue or other flaviviruses.
These clinical data suggested a direct ZIKV neural-injury mechanism, without a requirement for priming. We postulated that although molecular mimicry between ZIKV and peripheral nerve components might be relevant to antibody-induced GBS, such a rapidly developing polyradiculoneuritis mimicking GBS might also have been mediated by a direct pathogenic ZIKV effect on peripheral nerves. [2,3] This observation and ZIKV neurotropsim may also account for delayed CNS ZIKV effects in some patients. The fact that our patient was ZIKV negative in CSF suggests efficacy of the blood-brain barrier to ZIKV at that time point and strengthens the suggestion that ZIKV CNS invasion may be via neuronal transmission rather than directly across the blood brain barrier.
1. Siu R, Bukhari W, Todd A, et al. Acute Zika infection with concurrent onset of Guillain-Barré Syndrome. Neurology 2016;87:1623-1624.
2. Neal JW. Flaviviruses are neurotropic, but how do they invade the CNS? J Infect 2014;69:203-215.
3. Velandia ML, Castellanos JE. Flavivirus Neurotropism, Neuroinvasion, Neurovirulence and Neurosusceptibility: Clues to Understanding Flavivirus- and Dengue-Induced Encephalitis. In: Garcia ML, Romanowski V, editors. Viral Genomes - Molecular Structure, Diversity, Gene Expression Mechanisms and Host-Virus Interactions. Rijeka, Croatia: InTech; 2012:219-240.
For disclosures, please contact the editorial office at [email protected].
We thank Gerardin et al. for the comments on our Zika virus (ZIKV) clinical/scientific note [1]. Our patient was of particular interest because he suffered an illness clinically and electrophysiologically indistinguishable from Guillain-Barré syndrome (GBS) which developed within a few days of acute ZIKV infection, in the context of contemporaneous Zika vireamia. [1] Concurrently obtained CSF was negative for ZIKV. Brain and spine MRI were also normal. Importantly, there was no serologic evidence of priming by previous dengue or other flaviviruses.
These clinical data suggested a direct ZIKV neural-injury mechanism, without a requirement for priming. We postulated that although molecular mimicry between ZIKV and peripheral nerve components might be relevant to antibody-induced GBS, such a rapidly developing polyradiculoneuritis mimicking GBS might also have been mediated by a direct pathogenic ZIKV effect on peripheral nerves. [2,3] This observation and ZIKV neurotropsim may also account for delayed CNS ZIKV effects in some patients. The fact that our patient was ZIKV negative in CSF suggests efficacy of the blood-brain barrier to ZIKV at that time point and strengthens the suggestion that ZIKV CNS invasion may be via neuronal transmission rather than directly across the blood brain barrier.
1. Siu R, Bukhari W, Todd A, et al. Acute Zika infection with concurrent onset of Guillain-Barré Syndrome. Neurology 2016;87:1623-1624.
2. Neal JW. Flaviviruses are neurotropic, but how do they invade the CNS? J Infect 2014;69:203-215.
3. Velandia ML, Castellanos JE. Flavivirus Neurotropism, Neuroinvasion, Neurovirulence and Neurosusceptibility: Clues to Understanding Flavivirus- and Dengue-Induced Encephalitis. In: Garcia ML, Romanowski V, editors. Viral Genomes - Molecular Structure, Diversity, Gene Expression Mechanisms and Host-Virus Interactions. Rijeka, Croatia: InTech; 2012:219-240.
For disclosures, please contact the editorial office at [email protected].