Immune Recognition versus Immune Evasion Systems in Zika Virus Infection
Yee Teng Chan,
Yi Ying Cheok,
Heng Choon Cheong,
Ting Fang Tang,
Sofiah Sulaiman,
Jamiyah Hassan,
Chung Yeng Looi,
Kim-Kee Tan,
Sazaly AbuBakar,
Won Fen Wong
Affiliations
Yee Teng Chan
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia
Yi Ying Cheok
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia
Heng Choon Cheong
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia
Ting Fang Tang
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia
Sofiah Sulaiman
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia
Jamiyah Hassan
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia
Chung Yeng Looi
School of Biosciences, Faculty of Health & Medical Sciences, Taylor’s University, 1, Jalan Taylors, Subang Jaya 47500, Malaysia
Kim-Kee Tan
Tropical Infectious Diseases Research and Education Centre (TIDREC), Higher Education Center of Excellence (HICoE), University of Malaya, Kuala Lumpur 50603, Malaysia
Sazaly AbuBakar
Tropical Infectious Diseases Research and Education Centre (TIDREC), Higher Education Center of Excellence (HICoE), University of Malaya, Kuala Lumpur 50603, Malaysia
Won Fen Wong
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia
The reemergence of the Zika virus (ZIKV) infection in recent years has posed a serious threat to global health. Despite being asymptomatic or mildly symptomatic in a majority of infected individuals, ZIKV infection can result in severe manifestations including neurological complications in adults and congenital abnormalities in newborns. In a human host, ZIKV is primarily recognized by RIG-like receptors and Toll-like receptors that elicit anti-viral immunity through the secretion of type I interferon (IFN) to limit viral survival, replication, and pathogenesis. Intriguingly, ZIKV evades its host immune system through various immune evasion strategies, including suppressing the innate immune receptors and signaling pathways, mutation of viral structural and non-structural proteins, RNA modulation, or alteration of cellular pathways. Here, we present an overview of ZIKV recognition by the host immune system and the evasion strategies employed by ZIKV. Characterization of the host–viral interaction and viral disease mechanism provide a platform for the rational design of novel prophylactic and therapeutic strategies against ZIKV infection.
