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Innate immune response in patients with acute Zika virus infection.

Abstract

Innate immunity receptors (Toll-like receptors/TLRs and RIG-like receptors/RLRs) are important for the initial recognition of Zika virus (ZIKV), modulation of protective immune response, and IFN-α and IFN-β production. Immunological mechanisms involved in protection or pathology during ZIKV infection have not yet been determined. In this study, we evaluated the mRNA expression of innate immune receptors (TLR3, TLR7, TLR8, TLR9, melanoma differentiation-associated protein 5/MDA-5, and retinoic acid inducible gene/RIG-1), its adapter molecules (Myeloid Differentiation Primary Response Gene 88/Myd88, Toll/IL-1 Receptor Domain-Containing Adaptor-Inducing IFN-β/TRIF), and cytokines (IL-6, IL-12, TNF-α, IFN-α, IFN-β, and IFN-γ) in the acute phase of patients infected by ZIKV using real-time PCR in peripheral blood. Patients with acute ZIKV infection had high expression of TLR3, IFN-α, IFN-β, and IFN-γ when compared to healthy controls. In addition, there was a positive correlation between TLR3 expression compared to IFN-α and IFN-β. Moreover, viral load is positively correlated with TLR8, RIG-1, MDA-5, IFN-α, and IFN-β. On the other hand, patients infected by ZIKV showed reduced expression of RIG-1, TLR8, Myd88, and TNF-α molecules, which are also involved in antiviral immunity. Similar expressions of TLR7, TLR9, MDA-5, TRIF, IL-6, and IL-12 were observed between the group of patients infected with ZIKV and control subjects. Our results indicate that acute infection (up to 5 days after the onset of symptoms) by ZIKV in patients induces the high mRNA expression of TLR3 correlated to high expression of IFN-γ, IFN-α, and IFN-β, even though the high viral load is correlated to high expression of TLR8, RIG-1, MDA-5, IFN-α, and IFN-β in ZIKV patients.

Authors+Show Affiliations

Graduate Program in Parasitary Biology, Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil.Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil.Graduate Program in Parasitary Biology, Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Laboratory of Virology, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal, Brazil.Graduate Program in Parasitary Biology, Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Laboratory of Virology, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal, Brazil.Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Laboratory of Virology, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal, Brazil.Laboratory of Virology, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal, Brazil.Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Laboratory of Virology, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal, Brazil.Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Laboratory of Virology, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal, Brazil.Graduate Program in Parasitary Biology, Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil.Edmond and Lily Safra International Institute of Neuroscience (ELS-IIN), Santos Dumont Institute, Macaíba, RN, Brazil.Graduate Program in Parasitary Biology, Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. Laboratory of Virology, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal, Brazil.Graduate Program in Parasitary Biology, Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. pauloguedes@cb.ufrn.br. Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. pauloguedes@cb.ufrn.br.Graduate Program in Parasitary Biology, Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. veris@cb.ufrn.br. Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, Rio Grande Do Norte, Brazil. veris@cb.ufrn.br.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30879197

Citation

da Silva, Marcelo Henrique Matias, et al. "Innate Immune Response in Patients With Acute Zika Virus Infection." Medical Microbiology and Immunology, 2019.
da Silva MHM, Moises RNC, Alves BEB, et al. Innate immune response in patients with acute Zika virus infection. Med Microbiol Immunol. 2019.
da Silva, M. H. M., Moises, R. N. C., Alves, B. E. B., Pereira, H. W. B., de Paiva, A. A. P., Morais, I. C., ... Fernandes, J. V. (2019). Innate immune response in patients with acute Zika virus infection. Medical Microbiology and Immunology, doi:10.1007/s00430-019-00588-8.
da Silva MHM, et al. Innate Immune Response in Patients With Acute Zika Virus Infection. Med Microbiol Immunol. 2019 Mar 16; PubMed PMID: 30879197.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Innate immune response in patients with acute Zika virus infection. AU - da Silva,Marcelo Henrique Matias, AU - Moises,Raiza Nara Cunha, AU - Alves,Brenda Elen Bizerra, AU - Pereira,Hannaly Wana Bezerra, AU - de Paiva,Anne Aline Pereira, AU - Morais,Ingryd Câmara, AU - Nascimento,Yasmim Mesquita, AU - Monteiro,Joelma Dantas, AU - de Souto,Janeusa Trindade, AU - Nascimento,Manuela Sales Lima, AU - de Araújo,Josélio Maria Galvão, AU - da Guedes,Paulo Marcos Matta, AU - Fernandes,José Veríssimo, Y1 - 2019/03/16/ PY - 2018/03/30/received PY - 2019/02/25/accepted PY - 2019/3/18/entrez PY - 2019/3/18/pubmed PY - 2019/3/18/medline KW - Cytokines KW - Innate immune receptors KW - Patient KW - RIG-like receptors (RLRs) KW - Toll-like receptors (TLRs) KW - Zika virus JF - Medical microbiology and immunology JO - Med. Microbiol. Immunol. N2 - Innate immunity receptors (Toll-like receptors/TLRs and RIG-like receptors/RLRs) are important for the initial recognition of Zika virus (ZIKV), modulation of protective immune response, and IFN-α and IFN-β production. Immunological mechanisms involved in protection or pathology during ZIKV infection have not yet been determined. In this study, we evaluated the mRNA expression of innate immune receptors (TLR3, TLR7, TLR8, TLR9, melanoma differentiation-associated protein 5/MDA-5, and retinoic acid inducible gene/RIG-1), its adapter molecules (Myeloid Differentiation Primary Response Gene 88/Myd88, Toll/IL-1 Receptor Domain-Containing Adaptor-Inducing IFN-β/TRIF), and cytokines (IL-6, IL-12, TNF-α, IFN-α, IFN-β, and IFN-γ) in the acute phase of patients infected by ZIKV using real-time PCR in peripheral blood. Patients with acute ZIKV infection had high expression of TLR3, IFN-α, IFN-β, and IFN-γ when compared to healthy controls. In addition, there was a positive correlation between TLR3 expression compared to IFN-α and IFN-β. Moreover, viral load is positively correlated with TLR8, RIG-1, MDA-5, IFN-α, and IFN-β. On the other hand, patients infected by ZIKV showed reduced expression of RIG-1, TLR8, Myd88, and TNF-α molecules, which are also involved in antiviral immunity. Similar expressions of TLR7, TLR9, MDA-5, TRIF, IL-6, and IL-12 were observed between the group of patients infected with ZIKV and control subjects. Our results indicate that acute infection (up to 5 days after the onset of symptoms) by ZIKV in patients induces the high mRNA expression of TLR3 correlated to high expression of IFN-γ, IFN-α, and IFN-β, even though the high viral load is correlated to high expression of TLR8, RIG-1, MDA-5, IFN-α, and IFN-β in ZIKV patients. SN - 1432-1831 UR - https://www.unboundmedicine.com/medline/citation/30879197/Innate_immune_response_in_patients_with_acute_Zika_virus_infection L2 - https://dx.doi.org/10.1007/s00430-019-00588-8 DB - PRIME DP - Unbound Medicine ER -