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J Gen Virol. 2017 Aug;98(8):2061-2068. doi: 10.1099/jgv.0.000886. Epub 2017 Aug 8.

Axl is not an indispensable factor for Zika virus infection in mice.

Author information

1
1​Department of Microbiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
2
2​Institute of Clinical Medicine, China-Japan Friendship Hospital, Beijing 100029, PR China.
3
3​Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100730, PR China.
4
4​Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing 100093, PR China 1​Department of Microbiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.

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.

PMID:
28786784
PMCID:
PMC5656784
DOI:
10.1099/jgv.0.000886
[Indexed for MEDLINE]
Free PMC Article

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