Abstract
Recently, Zika virus (ZIKV) outbreak has been associated with a sharp increase in cases of Guillain–Barré syndrome and severe fetal abnormalities. However, the mechanism underlying the interaction of ZIKV with host cells is not yet clear. Axl, a receptor tyrosine kinase, is postulated as a receptor for ZIKV entry; however, its in vivo role during ZIKV infection and its impact on the outcome of the disease have not been fully characterized and evaluated. Moreover, there are contradictory results on its involvement in ZIKV infection. Here we utilized Axl-deficient mice (Axl−/−) and their littermates (Axl+/−) to study the in vivo role of Axl in ZIKV infection. Our results showed that both Axl+/− and Axl−/− suckling mice supported the replication of ZIKV and presented clinical manifestations. No significant difference has been found between Axl-deficient mice and their littermates in terms of the survival rate, clinical manifestations, viral load, ZIKV distribution and histopathological changes in major organs. These results therefore indicate that Axl is not an indispensable factor for ZIKV infection in mice.
Highlights
Zika virus (ZIKV) belongs to the Flavivirus genus within the Flaviviridae family [1, 2], which includes a number of human pathogens such as dengue virus (DENV), yellow fever virus, West Nile virus and Japanese encephalitis virus and threats to global human health
To investigate whether Axl plays a crucial role in ZIKV infection in mice, newborn AxlÀ/À and Axl+/À mice generated from AxlÀ/À x Axl+/À were characterized by genotyping PCR (Fig. S1, available in the online Supplementary Material) and were injected intracerebrally with 100 pfu ZIKV (CAS-ZK01 strain) within 72 h after birth
By using Axl-deficient suckling mice and their heterozygous littermate controls, we showed that all these mice were able to support the replication of ZIKV and displayed clinical manifestations via intracerebral injection
Summary
Zika virus (ZIKV) belongs to the Flavivirus genus within the Flaviviridae family [1, 2], which includes a number of human pathogens such as dengue virus (DENV), yellow fever virus, West Nile virus and Japanese encephalitis virus and threats to global human health. Since 2007, ZIKV has infected several million people in more than 70 countries and caused thousands of microcephaly in newborns and Guillain–Barre syndrome in adults [3, 4]. Clinical and animal experimental data have shown that the nervous system is the main target for ZIKV infection [5,6,7,8]. ZIKV can be detected in urine for a long time, suggesting that kidneys may be susceptible to ZIKV infection [9]. Testis damage caused by ZIKV infection in mice has recently been reported [10,11,12], but its implication in humans requires a long-term investigation. Great progress was achieved to reveal the pathogenesis of ZIKV. The molecular mechanism underlying the entry process of ZIKV still needs to be elucidated
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