Abstract
Following the recent outbreak of Zika virus (ZIKV) infections in Latin America, ZIKV has emerged as a global health threat due to its ability to induce neurological disease in both adults and the developing fetus. ZIKV is largely mosquito-borne and is now endemic in many parts of Africa, Asia, and South America. However, several reports have demonstrated persistent ZIKV infection of the male reproductive tract and evidence of male-to-female sexual transmission of ZIKV. Sexual transmission may broaden the reach of ZIKV infections beyond its current geographical limits, presenting a significant threat worldwide. Several mouse models of ZIKV infection have been developed to investigate ZIKV pathogenesis and develop effective vaccines and therapeutics. However, the majority of these models focus on mosquito-borne infection, while few have considered the impact of sexual transmission on immunity and pathogenesis. This review will examine the advantages and disadvantages of current models of mosquito-borne and sexually transmitted ZIKV and provide recommendations for the effective use of ZIKV mouse models.
Highlights
The majority of these models focus on mosquito-borne infection, while few have considered the impact of sexual transmission on immunity and pathogenesis
Several local outbreaks of Zika virus (ZIKV) infections have been reported in India, with concerns that a future ZIKV outbreak could be devastating in densely populated areas of India and other countries [5]
Significant research focus has been channeled towards understanding mosquito-borne ZIKV and establishing mouse models of ZIKV infection, our understanding of sexually transmitted ZIKV infections remains limited
Summary
Ifnar−/− mice on both backgrounds have been shown to develop sufficient adaptive immunity, including memory T cells and neutralizing antibodies in response to infection or vaccination, and can be employed to investigate potential vaccines [18,36,37,38,39,40]. Smith et al established a partially immunocompetent model of ZIKV infection that demonstrated severe ZIKV-induced disease, neuroinflammation, and mortality following administration of anti-IFNAR in C57BL/6 WT mice 1 day before ZIKV inoculation [31]. Both subcutaneous and intraperitoneal inoculations led to weight loss, viremia, and neuropathologic changes [31]. Several studies have demonstrated strong efficacy of candidate vaccine-induced adaptive immunity in the absence of IFNAR signaling for both HSV-2 and ZIKV, suggesting that use of an IFNAR-deficient mouse model may be sufficient to evaluate vaccine strategies against ZIKV [36,37,38,40,45]
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