Abstract
Zika virus (ZIKV) causes mostly asymptomatic infection or mild febrile illness. However, with an increasing number of patients, various clinical features such as microcephaly, Guillain-Barré syndrome and thrombocytopenia have also been reported. To determine which host factors are related to pathogenesis, the E protein of ZIKV was analyzed with the Informational Spectrum Method, which identifies common information encoded by primary structures of the virus and the respective host protein. The data showed that the ZIKV E protein and the complement component C1q cross-spectra are characterized by a single dominant peak at the frequency F = 0.338, suggesting similar biological properties. Indeed, C1q-specific antibodies were detected in sera obtained from mice and monkeys infected with ZIKV. As C1q has been known to be involved not only in immunity, but also in synaptic organization and different autoimmune diseases, a ZIKV-induced anti-C1q antibody response may contribute to the neurological complications. These findings might also be exploited for the design of safe and efficacious vaccines in the future.
Highlights
Zika virus (ZIKV), a member of the family Flaviviridae, is the causative agent of Zika fever
We demonstrate that ZIKV infection elicited antibodies specific to C1q in mice and non-human primates (NHP), which may contribute to the observed neurological complications
This indicates that ZIKV E protein may modulate the function of the human complement system via induction of E protein-specific antibodies that cross-react with C1q
Summary
Zika virus (ZIKV), a member of the family Flaviviridae, is the causative agent of Zika fever. Due to the rapid increase of ZIKV infections causing fetal deaths and more than 4,000 microcephaly cases and neurological disorders in affected areas, the World Health Organization (WHO) declared a public health emergency of international concern on February 1, 20162. ZIKV was discovered nearly 70 years ago, data on the interaction of this virus with host targets is lacking and viral pathogenesis is still poorly understood. To determine if there are host proteins with a pattern similar to the ZIKV envelope (E) glycoprotein, we analyzed this protein with informational spectrum method (ISM). Our analysis identified C1q, a member of the complement complex, as a host protein with common informational features, suggesting some similarity in biological properties. We demonstrate that ZIKV infection elicited antibodies specific to C1q in mice and non-human primates (NHP), which may contribute to the observed neurological complications
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