Journal
VIROLOGY
Volume 560, Issue -, Pages 86-95Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2021.04.008
Keywords
Zika virus; Virus transmission; Host receptors; Virus transmigration; Host-virus immune response; Diagnostics; Therapeutics
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Zika virus is a mosquito-borne neurotropic flavivirus that can cause microcephaly in developing fetus and GBS-like symptoms in adults. The virus was first reported in humans in 1952 and has caused major outbreaks in various regions since then. Understanding the molecular mechanism of Zika virus pathogenesis is crucial for developing potential diagnostic and therapeutic interventions.
Zika virus (ZIKV) is a mosquito-borne neurotropic flavivirus. ZIKV infection may lead to microcephaly in developing fetus and Guillain-Barre ' Syndrome (GBS) like symptoms in adults. ZIKV was first reported in humans in 1952 from Uganda and the United Republic of Tanzania. Later, ZIKV outbreak was reported in 2007 from the Yap Island. ZIKV re-emerged as major outbreak in the year 2013 from French Polynesia followed by second outbreak in the year 2015 from Brazil. ZIKV crosses the blood-tissue barriers to enter immune-privileged organs. Clinical manifestations in ZIKV disease includes rash, fever, conjunctivitis, muscle and joint pain, headache, transverse myelitis, meningoencephalitis, Acute Disseminated Encephalomyelitis (ADEM). The understanding of the molecular mechanism of ZIKV pathogenesis is very important to develop potential diagnostic and therapeutic interventions for ZIKV infected patients.
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