Immune Recognition versus Immune Evasion Systems in Zika Virus Infection

Abstract

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.

Investigation of the impact of AXL, TLR3, and STAT2 in congenital Zika syndrome through genetic polymorphisms and protein–protein interaction network analyses

“…For genetic susceptibility studies in teratogenesis, it is important to select genes that are expressed and play a role during the development of the affected organs/structures. AXL , TLR3 , and STAT2 are expressed in different neural cells (Chan et al, 2023; Chen et al, 2018; Grant et al, 2016; Hastings et al, 2019; Liu et al, 2019; Meertens et al, 2017; Nowakowski et al, 2016; Ojha et al, 2019) and play roles on neurodevelopment during both embryonic and fetal periods (Ackerman, 1992). These characteristics make them good candidates of investigation on its participation on the occurrence of CZS regardless of the moment of infection.…”

“…STAT2 activation triggers the expression of several IFN‐stimulated genes (ISGs) to suppress the infection (MacMicking, 2012). Additionally, studies have also shown that the NS5 protein of ZIKV binds and degrades the human STAT2, via the proteasome, inhibiting the IFN signaling and allowing ZIKV infection and viral dissemination to the central nervous system (Chan et al, 2023; Grant et al, 2016; Hertzog et al, 2018; A. Kumar et al, 2016).…”

Viral RNA capping: Mechanisms and antiviral therapy

“…112,113 These assessments go into certain viral details in greater detail. 114 process (Table 1). However, only a small part of them have access to clinical research and applications.…”

Analysis of highly frequent point mutations in glycoprotein C, glycoprotein N, and nucleoprotein of CCHFV

“…24 A study has witnessed an elevation in Zika virus replication due to I39T mutation in the NS2B protein and A188V mutation in NS1 gene has augmented virulence by escalating the antigenicity of the NS1 protein. 25 Chen et al have reported E92Q and N155H mutations in HIV-1 integrase, which has altered its binding with elvitegravir drug. 26 Another study has reported that Q148H/R and G140S/A caused resistance to ratlegravir drug, and molecular dynamic (MD) simulation has shown that mutant models are less flexible than wild-type, as a result the susceptibility to drug in patients have been reduced.…”

“…A single‐point mutation (R292K) in neuraminidase protein of H7N9 virus led to oseltamivir drug resistance often used for treating influenza 24 . A study has witnessed an elevation in Zika virus replication due to I39T mutation in the NS2B protein and A188V mutation in NS1 gene has augmented virulence by escalating the antigenicity of the NS1 protein 25 . Chen et al.…”