Zika virus-associated Guillain-Barré syndrome: Post-infectious or para-infectious complication?
PatrickGerardin, Clinician Researcher, INSERM CIC 1410, CHU de La Reunion, Saint Pierre, Reunion, France; UMR 134 PIMIT, Universite de La R[email protected]
V.M Cao-Lormeau, P. Tournebize, T. Cerny
Submitted January 24, 2017
Siu et al. reported the concurrent onset of polyradiculoneuritis and acute Zika virus (ZIKV) infection, while the virus was not cleared from the serum. [1] Guillain-Barre syndrome (GBS) is usually described as a post-infectious disease during which progressive flaccid paralysis develops after a phase of latency following infection. In the most common pathogenetic framework, this free interval permits the generation of sufficient levels of antibodies that crossreact by molecular mimicry with specific components of peripheral nerves, causing myelin or axonal injury, as previously documented with ZIKV infection. [2] However, this case report suggested other mechanisms. Given ZIKV cross-reactivity with dengue virus and increasing reports of ZIKV-associated GBS in dengue seropositive patients, [1,3] a hyperacute immune response is possible. [4] Given prolonged ZIKV shedding in bodily fluids, and the overlap between GBS onset and persistent shedding in fomites, a direct viral neuropathic effect may also contribute to ZIKV-associated GBS. [4] Indeed, ZIKV is able to infect cranial neural-crest cells that stem Schwann cell formation. [5] ZIKV-associated GBS could reflect a direct viral neuropathic effect on the blood-nerve barrier, allowing cross-reactive antibodies formed during previous infections to have a deleterious effect on nerve function.
1. Siu R, Bukhari W, Todd A, et al. Acute Zika infection with concurrent onset of Guillain-Barre Syndrome. Neurology 2016;87:1623-1624.
2. Cao-Lormeau VM, Blake A, Mons S, et al. Guillain-Barre syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study. Lancet 2016;387:1531-1539.
3. Parra B, Lizarazo J, Jimenez-Arango JA, et al. Guillain-Barre syndrome associated with Zika virus in Colombia. N Engl J Med 2016;375:1513-1523.
4. Dejnirattisai W, Supasa P, Wongwiwat W, et al. Dengue virus sero-cross-reactivity drives antibody dependent enhancement of infection with Zika virus. Nat Immunol 2016;17:1102-1108.
5. Bayless NL, Greenberg RS, Swigut T, Wysocka J, Blish CA. Zika Virus Infection Induces Cranial Neural Crest Cells to Produce Cytokines at Levels Detrimental for Neurogenesis. Cell Host Microbe 2016;20:423-428.
For disclosures, please contact the editorial office at [email protected].
Siu et al. reported the concurrent onset of polyradiculoneuritis and acute Zika virus (ZIKV) infection, while the virus was not cleared from the serum. [1] Guillain-Barre syndrome (GBS) is usually described as a post-infectious disease during which progressive flaccid paralysis develops after a phase of latency following infection. In the most common pathogenetic framework, this free interval permits the generation of sufficient levels of antibodies that crossreact by molecular mimicry with specific components of peripheral nerves, causing myelin or axonal injury, as previously documented with ZIKV infection. [2] However, this case report suggested other mechanisms. Given ZIKV cross-reactivity with dengue virus and increasing reports of ZIKV-associated GBS in dengue seropositive patients, [1,3] a hyperacute immune response is possible. [4] Given prolonged ZIKV shedding in bodily fluids, and the overlap between GBS onset and persistent shedding in fomites, a direct viral neuropathic effect may also contribute to ZIKV-associated GBS. [4] Indeed, ZIKV is able to infect cranial neural-crest cells that stem Schwann cell formation. [5] ZIKV-associated GBS could reflect a direct viral neuropathic effect on the blood-nerve barrier, allowing cross-reactive antibodies formed during previous infections to have a deleterious effect on nerve function.
1. Siu R, Bukhari W, Todd A, et al. Acute Zika infection with concurrent onset of Guillain-Barre Syndrome. Neurology 2016;87:1623-1624.
2. Cao-Lormeau VM, Blake A, Mons S, et al. Guillain-Barre syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study. Lancet 2016;387:1531-1539.
3. Parra B, Lizarazo J, Jimenez-Arango JA, et al. Guillain-Barre syndrome associated with Zika virus in Colombia. N Engl J Med 2016;375:1513-1523.
4. Dejnirattisai W, Supasa P, Wongwiwat W, et al. Dengue virus sero-cross-reactivity drives antibody dependent enhancement of infection with Zika virus. Nat Immunol 2016;17:1102-1108.
5. Bayless NL, Greenberg RS, Swigut T, Wysocka J, Blish CA. Zika Virus Infection Induces Cranial Neural Crest Cells to Produce Cytokines at Levels Detrimental for Neurogenesis. Cell Host Microbe 2016;20:423-428.
For disclosures, please contact the editorial office at [email protected].