Researchers at the molecular biology unit of the Institute of Medical Sciences in Banaras Hindu University (IMS-BHU) have reported an important finding on Zika virus pathogenesis, which they claim, will be helpful in understanding the molecular pathogenesis of the virus and in therapeutic development.
The study has been published in an international peer-reviewed journal ‘Molecular Neurobiology’.
Prof Sunit K. Singh, head of the Molecular Biology Unit and a well-known molecular virologist, said that most people with Zika virus infection do not develop symptoms.
“The incubation period of ZIKV infection lasts for 2- 7 days. In 2015, the major ZIKV outbreak was reported in Brazil, North America, Pacific and South-east Asia, infecting 1.5 million people and with more than 3,500 microcephaly cases reported in infants. In India, 157 ZIKV positive cases were reported in 2018,” he explained.
Currently, there are no definite antivirals against ZIKV and only symptomatic treatment regime is followed. Zika virus infection is also a trigger of Guillain-Barre syndrome, neuropathy and myelitis, particularly in adults and older children. The Zika virus vaccine is at various stages of development at present.
Zika virus can be transmitted from mother to foetus during pregnancy, which may lead to microcephaly (smaller than normal head size) and other congenital malformations in the infant, collectively referred to as congenital Zika syndrome, whereas in adults, the symptoms are mild-fever, headache, conjunctivitis, joint-pain, and body rash.
Microcephaly leads to abnormal brain development. The outcomes of microcephaly may differ according to the extent of the brain damage.
According to him, the brain is surrounded by a barrier known as blood-brain-barrier (BBB), which separates the brain from the peripheral blood circulation of the body. The BBB is formed by brain endothelial cells and these cells are held together by protein named tight-junction proteins (TJs) and adherent junction proteins (AJs).
If the TJs and AJs proteins expression decreases, the BBB is compromised and allows the movement of immune cells into the brain which causes neuronal damage.
The ZIKV infected cells secrete a viral protein, NS1, which has been directly corelated with the disease severity in patients.
His study reported that Zika virus NS1 protein treatment compromises the BBB integrity and this may lead to microcephaly and other brain related disorders in infants.
The research group reported that Zika virus NS1 protein increases the expression of microRNA-101_3p in human brain microvascular endothelial cells, which in turn suppresses the expression of tight-junction proteins and adherent junction proteins and that leads to the compromise in the integrity of BBB.
“This finding will be very helpful in understanding the molecular pathogenesis of Zika virus and in the therapeutic development. A diagnosis of Zika virus infection can be done by laboratory tests of blood, urine and semen,” said Singh.
