By now, the healthcare community is aware that the Zika virus causes microcephaly—at least among some babies born to mothers infected with the mosquito-borne virus.
It was an aspect of the epidemic in South America and the Caribbean between 2014 and 2016—and its coverage in the media—that was both heartbreaking, and unavoidable.
However, there are other infectious causes of the birth defect, which carries with it significant neurologic complications, and that is just what the authors of a review
, published in The Lancet
in August 2017, want to emphasize. Their hope is that clinicians keep a watchful eye on pregnant women who present with symptoms of these infections, and appropriately manage their treatment with the goal of preventing microcephaly-related complications.
“We think that Zika is very important and [it] has raised the profile of microcephaly; [however], there are many other infectious and noninfectious causes,” Delanjathan Devakumar, MPH, PhD, Lecturer in Public Health, Institute for Global Health, University College-London, told Contagion®
. “A lot of research is being focused on Zika, but globally there will be more cases of microcephaly due to other infectious causes and this is a great opportunity to allow all patients with infectious microcephaly to benefit from research findings.”
In their review, Dr. Devakumar and his colleagues focus on the infections “with the largest disease burden and the strongest evidence for causation” of microcephaly—namely, cytomegalovirus (CMV), herpes simplex virus (HSV), rubella virus, Toxoplasma gondii
, and, of course, Zika virus. Each plays a distinct role in the potential development of the birth complication. Citing earlier research, for example, they note that CMV has been linked with alterations in the “progenitor and neuronal fates” via downregulation of multipotency markers such as Sox2 and Nestin. However, more recently, peroxisome proliferator-activated receptor γ (PPARγ) has been shown to increase following CMV infection of human neural stem cells and fetal brain sections, and that activation alone has proved sufficient to “impair neuronal differentiation.”