Zika virus is associated with microcephaly in newborns and currently has no effective treatment or vaccines against it. A recent study in Science Advances demonstrated that the Zika virus causes testicular atrophy and could impair fertility in men.
The recent Zika virus (ZIKV) outbreak in Brazil and other parts of South and North America was quite alarming, particularly because of rising evidence suggesting that the virus caused birth defects and neurological problems, like microcephaly. Since then, researchers around the world have conducted rigorous experiments on the ZIKV, in an attempt to characterize the disease more completely. Studies have investigated unknown ZIKV-associated complications, the different modes of transmission, and potential novel strategies against the virus, including vaccines and antiviral therapies. Despite such exhaustive efforts, there are still no effective treatments or vaccines that target the disease itself. Recommendations by Centers for Disease Control and Prevention (CDC) are aimed at treating accompanying symptoms, or involve resting and drinking plentiful fluids, none of which target the virus itself. To develop novel therapeutic options, further research must be conducted to understand how the ZIKV works, and identify other unknown aspects of human health that it can affect.
A recent study, published in Science Advances, demonstrated that ZIKV infection contributes to testicular atrophy, and may have significant consequences for fertility in men. The study utilized a mouse model, where mice were infected with the ZIKV and subsequently studied in the following days. Five days after the infection, ZIKV was detected in the brain, testes, and blood of the mice. Specifically, the virus was detected most profoundly in the Leydig cells of the testes, which are responsible for testosterone production, and subsequently sperm development. The expression of genes involved in testosterone production was found to be significantly lower in Leydig cells of infected mice. These findings suggest that the ZIKV infects the Leydig cells, and compromises their ability to produce testosterone-synthesizing proteins. Consequently, the levels of testosterone drop and sperm production is impaired, leading to testicular atrophy in these mice, as noted twenty-one days after infection. Similar associations between ZIKV and testicular atrophy have been suggested in men. Moreover, it was shown that cytokines, which are substances that play a role in immunity and inflammation, were upregulated following ZIKV infection. This immune response to the infection could further enhance or contribute to testicular atrophy in mice, and in men.
In conclusion, the current study showed that ZIKV infection of the Leydig cells contributes to testicular atrophy in mice, and possibly in men. Further studies are warranted to confirm the proposed effects of ZIKV on the testes, and its potential effects on fertility in men. Most importantly, the study highlights the need for appropriate vaccines and antiviral therapies to help combat the virus itself.
Written By: Haisam Shah, BSc