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The dengue virus and its equally infamous cousin, the Zika virus, together infect up to around 400 million people every year. The Zika virus and genomic studies of it have opened fascinating windows into our knowledge of the infectious disease and its relevance in the context of emerging outbreaks.
The Zika virus is a mosquito-borne flavivirus. Most infections in humans are asymptomatic or with mild symptoms, including fever, rash, and joint pain. The Zika virus became notorious during the 2015-2018 outbreak that swept through the Americas. The outbreak was characterised by an alarming increase in the number of microcephaly cases in newborns, prompting the World Health Organisation to declare it a public health emergency of international concern in early 2016.
Genome Structure: The Zika virus’s genome comprises more than 10,000 bases of single-stranded RNA, with a unique feature of encoding a large polyprotein further cleaved into capsid, membrane precursor (prM), envelope, and seven non-structural proteins.
Diagnosis: Genetic testing is the primary method for diagnosing Zika virus infections due to potential antibody cross-reactivity with dengue, yellow fever, and West Nile viruses.
Epidemiology and Surveillance: The RNA genome’s high mutation potential allows the tracking of virus evolution and genetic epidemiology, offering insights into transmission and pathogenesis.
Genomic studies have identified two main lineages of the Zika virus: African and Asian. The sub-lineage responsible for the devastating 2015-2018 outbreak in the Americas shared genomic similarities with the 2013-2014 outbreak in French Polynesia.
Active surveillance using genetic sequencing revealed a hidden Zika outbreak in Cuba, demonstrating the practical utility of genetic surveillance.
Microcephaly, characterized by abnormally small heads in newborns, has been a major concern in Zika virus infections.
Initial research indicated a mutation in the prM protein was linked to microcephaly, believed to have originated during the French Polynesia outbreak. However, not all Zika-affected pregnancies resulted in microcephaly.
Recent studies on primates have shown that heavy viral loads during pregnancy significantly influence fetal growth.
Preexisting antibodies against dengue (DENV) can exacerbate congenital Zika. These findings emphasize the role of viral load and DENV infections in microcephaly.
Researchers from Tsinghua University demonstrated that Zika and DENV infections in primates suppressed an antimicrobial peptide, encouraging specific microbes to grow on the skin.
These microbes produce acetophenones, volatile molecules that attract mosquitoes, facilitating virus transmission.
Administering isotretinoin can reverse this phenomenon by upregulating the antimicrobial peptide.
Evidence suggests that Zika virus infections can increase the risk of severe dengue.
Exposure to both Zika and DENV in a Nicaraguan cohort revealed that intermediate levels of anti-DENV antibodies due to prior Zika or DENV infections could enhance dengue severity.
These findings are crucial for public health strategies and may inform Zika vaccine designs.
Genomic studies have illuminated our understanding of the Zika virus and its interactions with dengue, microcephaly, and mosquito vectors. As climate change drives the spread of vector-borne diseases, these insights provide guidance for public health measures and vaccine development. Genomic technologies are becoming essential tools in the battle against emerging outbreaks in our ever-changing world.