Microcephaly, male fertility and beyond: A long-term perspective on Zika virus


I was watching the news the other day and was surprised to learn that Zika virus was declared to no longer be a public health emergency by the World Health Organization (WHO). That sounds like good news, right? Wrong! According to WHO representatives, this is not a downgrading of the threat of this virus, but in fact, an upgrade. Why is that? Zika virus was declared an emergency when we knew very little about it. Today, we know that Zika causes brain damage in fetuses and newborns. We know that it is still spreading. What is now required is a long-term strategy to tackle this virus, to prevent its spread, and to limit and ultimately eliminate its impact across the globe. This is essentially an acknowledgement of the fact that the fight against Zika is not over. It has, in fact, escalated into a long-term program that will require continued funding for research, diagnostics and treatment projects.

What do we really know?

What is the actual number of people infected with Zika virus and how many subsequent cases of Zika-linked microcephaly in babies are there worldwide? We still don’t have concrete figures. Why is that? Approximately 80% of people infected with the virus are asymptomatic. So far, around 2100 cases of microcephaly in babies have been linked to Zika but 3000 more are currently being investigated. Worryingly, babies that appear healthy at birth can develop microcephaly later on, and subsequently experience brain development problems.

Could Zika infection reduce male fertility?

Most studies on Zika virus have predominantly focused on the consequences of Zika infection on pregnant women and its effect on the developing fetus. But what impact does Zika infection have on the male reproductive system?

A recent study published in Nature evaluated the consequences of infection by a mouse-adapted African Zika virus strain (Dakar 41519), in the reproductive tract of male mice (1). The research found that this particular strain preferentially infected spermatogonia, primary spermatocytes and Sertoli cells in the testes, resulting in cell death and the destruction of the seminiferous tubules. Zika virus infection resulted in a decrease in the levels of testosterone and other sex hormones, reduced sperm count, and, in some cases, shrinkage of the testicles to 1/10th of their normal size, possibly irreversibly. Consequently, Zika virus infected male mice were found to be significantly less fertile than their healthy counterparts, fathering fewer viable offspring when mated with healthy female mice.

Could these findings also apply to humans? If so, how serious is the impact? One way of finding out would be to compare the sperm counts of men infected with Zika and the numbers of children they have against a social and age matched Zika-negative group. What is clear is that the global impact of Zika virus is far more insidious than anticipated and further research is required to determine its long-term consequences.

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  1. 1. Govero, J. et al. (2016) Zika virus infection damages the testes in mice. Nature. (Link)
Devika Mathur

Devika Mathur is a Senior Technical & Marketing Writer at QIAGEN. Devika joined QIAGEN in 2008 and has been responsible for creating literature for numerous QIAGEN products, including the REPLI-g and QIAseq product lines, and has written extensively on various scientific topics ranging from next-generation sequencing and single cell analysis to PCR and sample preparation. Devika is a graduate from University College Cork, Ireland, and has a microbiology research background, focusing primarily on the molecular characterization of the replication module of the lactococcal bacteriophage Tuc2009.

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