Two separate studies have proven in the lab for the first time that the Zika virus does cause birth defects in animals, including reduced head growth.
The new research has established that the virus can cross the placenta and cause growth restriction, or microcephaly, in mice.
The findings will add to the increasing body of knowledge around the virus, and could help in vaccine and treatment development.
The first study, by scientists in the US and Brazil, has also found that the Brazilian strain of Zika can infect artificial mini human brains grown in the lab.
Once inside the organoids, the virus has been found to cause cells to die and lead to the disruption of the development of layers of brain tissue.
It is the first time that direct evidence has been found linking birth defects with Zika, which is thought to be behind the births of thousands of babies with smaller than normal head growth in Brazil.
The team of researchers from the University of California San Diego and the University of Sao Paulo infected two types of pregnant mice with Zika isolated from a case in Brazil.
The mouse pups, whose mothers were of one particular variety, were born with clearly smaller than normal bodies, including signs of microcephaly.
The offspring of the other type of Zika infected mouse showed no obvious malformations, which the scientists say may be because that particular variety of mouse has a robust anti-viral immune response mechanism.
The scientists’ work, published in the journal Nature, also suggests that the virus crosses the placenta and causes microcephaly by targeting cells which have a tendency to develop into cortical cells.
The research has been welcomed by scientists involved in the battle to understand Zika and find a vaccine.
However, some have also cautioned that more research is needed in animal models more closely connected to humans, and to try to establish why the Brazilian strains behave differently to those seen in other parts of the world.
"This opens the door to mechanistic studies to understand the mode of its attack on nerve cells of this virus and molecular pathways of this mode of pathogenesis," said Prof Daniel Altmann, British Society for Immunology spokesperson and Professor of Immunology at Imperial College London.
In the second study published in the journal Cell, researchers at Washington University in St Louis developed two mouse models.
In one, the females were genetically wired to have a defective immune system, in order to mimic a severe infection with Zika.
The other saw genetically normal female mice receive injections of an antibody that partially prevented their immune systems from functioning.
Once infected with Zika, the researchers were able to see the virus being transmitted to the foetus in the immunocompromised mice.
They also observed that virus levels in the placenta were 1,000 times higher than in the mother's serum - a clear indication that Zika preferentially invades the placenta.
The foetal blood capillaries were also clearly damaged once the virus had entered the placenta and the foetus, leading to the type of damage that has been seen in humans infected by the virus.
Meanwhile, another study by scientists in China has found that mouse foetuses injected with the Asian Zika virus strain and carried to term within their pregnant mothers display the characteristic features of microcephaly.
The study, published in the journal Cell Stem Cell, found that the virus infected the early stage neural cells.
The infected brains also showed evidence of the expression of genes related to viral entry, altered immune response, and cell death.
The authors at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences and the Beijing Institute of Microbiology and Epidemiology claim this is direct evidence that Zika infection causes microcephaly in a mammalian animal model.
