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3. The systemic pathogenesis of enterovirus

Author

Sooksawasdi Na Ayudhya, Syriam and Sooksawasdi Na Ayudhya, Syriam

Abstract

In recent years, EV-D68 outbreaks have been associated with severe respiratory illness and extra-respiratory complications, of which neurological complications occurred most frequently. However, how EV-D68 infection results in the development of severe disease and the underlying mechanism are largely unknown. This thesis aims to expand our knowledge on the systemic pathogenesis of EV-D68-associated disease focusing on the systemic dissemination and neurotropism of EV-D68 as well as to improve diagnostics for of EV-D68 associated CNS diseases. In Chapter 1, I discussed the different stages in the pathogenesis of EV-D68 infection – infection of the respiratory tract, systemic dissemination and infection of the CNS – based on observations in humans as well as experimental in vitro and in vivo studies. As the systemic dissemination of EV-D68 via the homogenous route is essential for the systemic spread, I explored in Chapter 2 the potential role of immune cells in the systemic disseminations in EV-D68 infection. During the 2014 outbreak, multiple clades were circulating of which subclade B1 was the most prevalent, and therefore associated with the development of neurological complications. In Chapter 3, I investigated whether the ability of EV-D68 viruses to replicate in cells of the CNS is a clade specific feature, and which viral factors are important for virus replication in vitro. Acute flaccid myelitis is the most common CNS complications associated with EV-D68 infections, while encephalitis and meningoencephalitis are infrequently reported. In Chapter 4, I investigated the cell tropism and replication efficiency of different EV-D68 isolates from before-and after-2014 in spinal motor neurons and cortical neurons derived from human pluripotent stem cells as well as the associated effect of virus infection on motor neurons. Diagnostics of EV-D68-associated CNS diseases are challenging because virus antigen or viral RNA are rarely detected in CSF. In Chapter

Published
2023

4. Detection of intrathecal antibodies to diagnose enterovirus infections of the central nervous system

Author

Sooksawasdi Na Ayudhya, Syriam, primary, Sips, Gregorius J., additional, Bogers, Susanne, additional, Leijten, Lonneke M.E., additional, Laksono, Brigitta M., additional, Smeets, Leonard C., additional, Bruning, Andrea, additional, Benschop, Kimberley, additional, Wolthers, Katja, additional, van Riel, Debby, additional, and GeurtsvanKessel, Corine H., additional

Published
2022
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6. The pathogenesis and virulence of enterovirus-D68 infection

Author

Sooksawasdi Na Ayudhya, Syriam, Laksono, Brigitta M., van Riel, Debby, Sooksawasdi Na Ayudhya, Syriam, Laksono, Brigitta M., and van Riel, Debby

Abstract

In 2014, enterovirus D68 (EV-D68) emerged causing outbreaks of severe respiratory disease in children worldwide. In a subset of patients, EV-D68 infection was associated with the development of central nervous system (CNS) complications, including acute flaccid myelitis (AFM). Since then, the number of reported outbreaks has risen biennially, which emphasizes the need to unravel the systemic pathogenesis in humans. We present here a comprehensive review on the different stages of the pathogenesis of EV-D68 infection–infection in the respiratory tract, systemic dissemination and infection of the CNS–based on observations in humans as well as experimental in vitro and in vivo studies. This review highlights the knowledge gaps on the mechanisms of systemic dissemination, routes of entry into the CNS and mechanisms to induce AFM or other CNS complications, as well as the role of virus and host factors in the pathogenesis of EV-D68.

Published
2021

7. Erratum for Sooksawasdi Na Ayudhya et al., 'Enhanced Enterovirus D68 Replication in Neuroblastoma Cells Is Associated with a Cell Culture-Adaptive Amino Acid Substitution in VP1'

Author

Sooksawasdi Na Ayudhya, Syriam, Meijer, Adam, Bauer, Lisa, Oude Munnink, Bas, Embregts, Carmen, Leijten, Lonneke, Siegers, Jurre Y, Laksono, Brigitta M, van Kuppeveld, Frank, Kuiken, Thijs, GeurtsvanKessel, Corine, van Riel, Debby, dI&I I&I-1, Virologie, dI&I I&I-1, and Virologie

Subjects
Enterovirus D, Human, Chemistry, Cell Culture Techniques, Amino acid substitution, Virus Internalization, Virus Replication, Microbiology, Molecular biology, QR1-502, Neuroblastoma cell, Kinetics, Neuroblastoma, Amino Acid Substitution, Neural Stem Cells, Cell culture, Cell Line, Tumor, Replication (statistics), Enterovirus Infections, Humans, Capsid Proteins, Erratum, Molecular Biology, Enterovirus D68
Abstract

Volume 5, no. 6, e00941-20, 2020, [https://doi.org/10.1128/mSphere.00941-20][1]. Page 1: Corine GeurtsvanKessel’s surname was misspelled as “Geurts-van Kessel” in the byline and was corrected on 6 November 2020. [1]: /lookup/doi/10.1128/mSphere.00941-20

Published
2020

8. Enhanced Enterovirus D68 Replication in Neuroblastoma Cells Is Associated with a Cell Culture-Adaptive Amino Acid Substitution in VP1

Author

Sooksawasdi Na Ayudhya, Syriam, Meijer, Adam, Bauer, Lisa, Oude Munnink, Bas, Embregts, Carmen, Leijten, Lonneke, Siegers, Jurre Y, Laksono, Brigitta M, van Kuppeveld, Frank, Kuiken, Thijs, Geurts-van Kessel, Corine, van Riel, Debby, Lakdawala, Seema, dI&I I&I-1, Virologie, dI&I I&I-1, Virologie, and Virology

Subjects
0301 basic medicine, replication, viruses, 030106 microbiology, Cell, Biology, neuroblastoma cells, Microbiology, Virus, Host-Microbe Biology, 03 medical and health sciences, chemistry.chemical_compound, medicine, Molecular Biology, pathogenesis, neurotropism, enterovirus D68, in vitro, Heparan sulfate, VP1, cell culture adaptation, Virology, Phenotype, QR1-502, Acute flaccid myelitis, In vitro, 030104 developmental biology, medicine.anatomical_structure, Viral replication, chemistry, Cell culture, heparan sulfate, Research Article
Abstract

Enterovirus D68 (EV-D68) causes mild to severe respiratory disease and is associated with acute flaccid myelitis since 2014. Currently, the understanding of the ability of EV-D68 to replicate in the central nervous system (CNS), and whether it is associated with a specific clade of EV-D68 viruses or specific viral factors, is lacking. Comparing different EV-D68 clades did not reveal clade-specific phenotypic characteristics. However, we did show that viruses which acquired a cell culture-adapted amino acid substitution in VP1 (E271K) recognized heparan sulfate as an additional receptor. Recognition of heparan sulfate resulted in an increase in attachment, infection, and replication in neuroblastoma cells compared with viruses without this specific amino acid substitution. The ability of EV-D68 viruses to acquire cell culture-adaptive substitutions which have a large effect in experimental settings emphasizes the need to sequence virus stocks., Since its emergence in the United States in 2014, enterovirus D68 (EV-D68) has been and is associated with severe respiratory diseases and acute flaccid myelitis. Even though EV-D68 has been shown to replicate in different neuronal cells in vitro, it is currently poorly understood which viral factors contribute to the ability to replicate efficiently in cells of the central nervous system and whether this feature is a clade-specific feature. Here, we determined the replication kinetics of clinical EV-D68 isolates from (sub)clades A, B1, B2, B3, and D1 in human neuroblastoma cells (SK-N-SH). Subsequently, we compared sequences to identify viral factors associated with increased viral replication. All clinical isolates replicated in SK-N-SH cells, although there was a large difference in efficiency. Efficient replication of clinical isolates was associated with an amino acid substitution at position 271 of VP1 (E271K), which was acquired during virus propagation in vitro. Recognition of heparan sulfate in addition to sialic acids was associated with increased attachment, infection, and replication. Removal of heparan sulfate resulted in a decrease in attachment, internalization, and replication of viruses with E271K. Taken together, our study suggests that the replication kinetics of EV-D68 isolates in SK-N-SH cells is not a clade-specific feature. However, recognition of heparan sulfate as an additional receptor had a large effect on phenotypic characteristics in vitro. These observations emphasize the need to compare sequences from virus stocks with clinical isolates in order to retrieve phenotypic characteristics from original virus isolates. IMPORTANCE Enterovirus D68 (EV-D68) causes mild to severe respiratory disease and is associated with acute flaccid myelitis since 2014. Currently, the understanding of the ability of EV-D68 to replicate in the central nervous system (CNS), and whether it is associated with a specific clade of EV-D68 viruses or specific viral factors, is lacking. Comparing different EV-D68 clades did not reveal clade-specific phenotypic characteristics. However, we did show that viruses which acquired a cell culture-adapted amino acid substitution in VP1 (E271K) recognized heparan sulfate as an additional receptor. Recognition of heparan sulfate resulted in an increase in attachment, infection, and replication in neuroblastoma cells compared with viruses without this specific amino acid substitution. The ability of EV-D68 viruses to acquire cell culture-adaptive substitutions which have a large effect in experimental settings emphasizes the need to sequence virus stocks.

Published
2020

9. Erratum for Sooksawasdi Na Ayudhya et al., 'Enhanced Enterovirus D68 Replication in Neuroblastoma Cells Is Associated with a Cell Culture-Adaptive Amino Acid Substitution in VP1'

Author

dI&I I&I-1, Virologie, Sooksawasdi Na Ayudhya, Syriam, Meijer, Adam, Bauer, Lisa, Oude Munnink, Bas, Embregts, Carmen, Leijten, Lonneke, Siegers, Jurre Y, Laksono, Brigitta M, van Kuppeveld, Frank, Kuiken, Thijs, GeurtsvanKessel, Corine, van Riel, Debby, dI&I I&I-1, Virologie, Sooksawasdi Na Ayudhya, Syriam, Meijer, Adam, Bauer, Lisa, Oude Munnink, Bas, Embregts, Carmen, Leijten, Lonneke, Siegers, Jurre Y, Laksono, Brigitta M, van Kuppeveld, Frank, Kuiken, Thijs, GeurtsvanKessel, Corine, and van Riel, Debby

Published
2020

10. Enhanced Enterovirus D68 Replication in Neuroblastoma Cells Is Associated with a Cell Culture-Adaptive Amino Acid Substitution in VP1

Author

dI&I I&I-1, Virologie, Sooksawasdi Na Ayudhya, Syriam, Meijer, Adam, Bauer, Lisa, Oude Munnink, Bas, Embregts, Carmen, Leijten, Lonneke, Siegers, Jurre Y, Laksono, Brigitta M, van Kuppeveld, Frank, Kuiken, Thijs, Geurts-van Kessel, Corine, van Riel, Debby, Lakdawala, Seema, dI&I I&I-1, Virologie, Sooksawasdi Na Ayudhya, Syriam, Meijer, Adam, Bauer, Lisa, Oude Munnink, Bas, Embregts, Carmen, Leijten, Lonneke, Siegers, Jurre Y, Laksono, Brigitta M, van Kuppeveld, Frank, Kuiken, Thijs, Geurts-van Kessel, Corine, van Riel, Debby, and Lakdawala, Seema

Published
2020

14. Reverse Zoonosis of COVID-19: Lessons From the 2009 Influenza Pandemic.

Author

Sooksawasdi Na Ayudhya S and Kuiken T

Subjects
Animals, Animals, Domestic, Animals, Wild, Animals, Zoo, Humans, Pets, Risk Factors, COVID-19 epidemiology, COVID-19 transmission, Influenza A Virus, H1N1 Subtype, Influenza, Human epidemiology, Influenza, Human transmission, Zoonoses transmission
Abstract

Over the past decade, pandemics caused by pandemic H1N1 (pH1N1) influenza virus in 2009 and severe acute respiratory syndrome virus type 2 (SARS-CoV-2) in 2019 have emerged. Both are high-impact respiratory pathogens originating from animals. Their wide distribution in the human population subsequently results in an increased risk of human-to-animal transmission: reverse zoonosis. Although there have only been rare reports of reverse zoonosis events associated with the ongoing coronavirus disease 2019 (COVID-19) pandemic from SARS-CoV-2 so far, comparison with the pH1N1 influenza pandemic can provide a better understanding of the possible consequences of such events for public and animal health. The results of our review suggest that similar factors contribute to successful crossing of the host species barriers in both pandemics. Specific risk factors include sufficient interaction between infected humans and recipient animals, suitability of the animal host factors for productive virus infection, and suitability of the animal host population for viral persistence. Of particular concern is virus spread to susceptible animal species, in which group housing and contact network structure could potentially result in an alternative virus reservoir, from which reintroduction into humans can take place. Virus exposure in high-density populations could allow sustained transmission in susceptible animal species. Identification of the risk factors and serological surveillance in SARS-CoV-2-susceptible animal species that are group-housed should help reduce the threat from reverse zoonosis of COVID-19.

Published
2021
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