Researchers have sequenced the full-length genome of a Zika virus taken from a patient in Brazil and identified a virus-derived molecule that inhibits part of the infected person’s immune system.

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The researchers also sequenced the non-coding regions of the Zika virus genome.

We have known about the existence of Zika virus for decades; it was first found in monkeys and then humans in Africa just after World War II.

However, it is only recently we have learned Zika infections can lead to birth defects, such as microcephaly and Guillain-Barré syndrome, in humans.

In February 2016, the World Health Organization (WHO) declared the recent cluster of microcephaly cases and other neurological disorders associated with Zika virus infections in the Americas a global public health emergency.

The current escalating epidemic started in Brazil in 2015 and has so far given rise to over 1.5 million suspected cases. According to the WHO, a total of 67 countries have reported evidence of Zika virus transmission since 2015.

Yet, while much research has been done on the virus, there remain some huge gaps – such as why has it spread so fast in the current epidemic, and what has given rise to new disease symptoms?

The new study, led by the University of Glasgow in the United Kingdom and published in the journal PLOS Neglected Tropical Diseases, reveals some valuable insights to these questions.

The international team of researchers sequenced the whole genome of a Zika virus isolated from a patient in Recife in Brazil. They also compared the results with other available Zika sequences.

Fast facts about Zika
  • Outbreaks of Zika virus disease have been recorded in Africa, the Americas, Asia, and the Pacific
  • The mosquito that carries Zika is the same one that carries dengue and chikungunya
  • People can also become infected through sexual intercourse.

Learn more about Zika

One reason the study is significant is because it sequences not only the coding regions of the viral genome – which hold instructions for making proteins – but also the noncoding regions, which are often missing from many currently available sequences, say the authors.

During their work, the researchers identified a molecule in Zika virus-infected cells that appears to block an important part of the host’s immune system.

The authors note that the molecule – called subgenomic flavivirus RNA (sfRNA) – has “antagonist activity against RIG-I induced type I interferon induction, with a lesser effect on MDA-5 mediated action.”

The molecule sfRNA is also known to be present in infections by other relatives of Zika – such as dengue – where it interacts in a similar way with the host immune system.

The researchers say the findings show why it is important not only to study lab-cultured viruses but also samples from patients. The lab-cultured ones could mutate and lose significant features.

This information is important for understanding the pathogenesis of Zika virus infection but may also be useful for the design of attenuated viruses for vaccine studies in the future.”

Corresponding author Dr. Alain Kohl, MRC-University of Glasgow Centre for Virus Research

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