A team of biologists from the Icahn School of Medicine at Mount Sinai in New York City have now found that mice with antibodies from dengue or West Nile virus have a greater risk of developing Zika.
Read more: Zika: how can it be stopped?
Zika surface proteins are of the same flavivirus family as dengue and the close similarities between the two mean that their antibodies can respond to each other in complex and dangerous ways. In 2016, a team from Imperial College London found that the Zika virus is far more likely to infect human cells if they had already been exposed to dengue antibodies. The new results in mice add to the mounting evidence that suggests the close inter-relation of the two pathogens causes dangerous complications.
Zika, spread by the mosquito Aedes aegypti, usually results in a very mild infection and isn't harmful to most people. However, it is more serious for pregnant women, due to evidence that it causes birth defects – in particular, a condition known as microcephaly, which results in babies with abnormally small heads. High-risk areas for the virus include the Pacific region, with cases exploding across South and Central America, the Caribbean and South East Asia.
The speed of Zika's spread through Latin America in February 2016 caused the World Health Organisation to declare the virus a public health emergency. A report published by Neil M. Ferguson et al in 2016 found that "the current epidemic is not containable; at best, interventions can mitigate its health impacts." But the question of intervention is one of mixed effectiveness - advising women to delay pregnancy in affected areas is unrealistic, considering the long-term projections for the virus. Moreover, there are still concerns over Zika's interactions with other flaviviruses.
The team at Mount Sinai used mice in order to explore the effects of this cross-reactivity. Mice are normally resistant to the Zika virus, however, the animals were engineered with a damaged version of the immune gene that would usually afford them protection. They began to develop severe symptoms of the illness, such as weight loss, listlessness, fever, paralysis and even death. The worst cases were recorded when the mice were exposed to plasma from humans who had developed antibodies from dengue or West Nile.
This process, known as 'antibody-dependent enhancement' (ADE) also takes place in people. It could be to blame for Zika’s boom in Brazil, an area in which estimates suggest close to 90 per cent of the population have at one time been infected by dengue. The Aedes aegypti is common in urban areas across Brazil and is the main vector for several viruses closely related to Zika, including chikungunya and yellow fever. With growing concerns around ADE, there are fears that Zika transmissions will rise in the continental United States this spring.
These results from testing on mice are not a precisely transferrable to humans. However, ADE has already been known to worsen Zika infections in some people. There are four strains associated with dengue, and upon initial sickness, the presence of one in the body can result in only a minor infection. However, when antibodies from one type are leftover and another strain takes hold, the matching antibodies can actually feed the spread of the illness through the human body, with the potential to create a fatal hemorrhagic disease.
These complications raise new concerns about the effectiveness of vaccination against certain flavivirus strands. If antibodies in the blood hinder the body's efforts to fight off the Zika virus, how then are healthcare systems meant to protect those at greatest risk? Currently, there is no vaccine to prevent Zika transmission and the most effective preventative measures involve reducing the risk of mosquito bites. These range from wearing long-sleeved clothing, insect repellant with one of four ingredients, such as Picaridin or DEET, or avoiding affected areas.
Research into the relationship between Zika, dengue and West Nile is still underway, but the preliminary findings suggest that greater care needs to be taken when considering the interaction between different flavivirus strands.
This article was originally published by WIRED UK
