Tests in mice reveal other flaviviruses can cause deadly harm
Zika relatives can also damage a fetus
B Y AIMEE CUNNINGHAM
Zika virus may not be the black sheep
of the family. Two related viruses also
cause defects in the fetuses of infected
mice, researchers find.
Some scientists have speculated that
Zika’s capacity to harm a fetus might be
unique among its kind, perhaps due to a
recent change in the virus’s genetics (SN:
10/28/17, p. 9). Others have argued that
this dangerous ability might have always
been there. It just wasn’t until the 2015–
2016 epidemic in the Western Hemisphere that enough pregnant women
were affected for public health researchers to identify the association with fetal
defects (SN: 12/24/16, p. 19).
But new work suggests this capacity is
not Zika’s alone. Pregnant mice infected
with West Nile or Powassan virus — both
flaviviruses, like Zika— showed fetal
harm. Over 40 percent of infected fetuses
died. Among pregnant mice infected with
one of two other mosquito-borne viruses
unrelated to Zika, all of the fetuses survived, scientists report online January 31
in Science Translational Medicine.
The research suggests that “many
viruses, including some similar to Zika,
can infect the placenta and the cells of
the baby,” says George Saade, an obste-
trician-gynecologist and cell biologist at
the University of Texas Medical Branch
at Galveston. “This list keeps growing
and highlights the risks from viruses
that we are not very familiar with.”
Like Zika, West Nile and Powassan are
neurotropic, meaning they target nerve
cells. Both viruses can cause inflam-
mation of the brain or the membranes
surrounding it. West Nile is transmitted
to humans by mosquitoes that have bitten
infected birds. From 1999 to 2016, there
were more than 46,000 cases reported to
the U. S. Centers for Disease Control and
Prevention. Powassan, spread by ticks
that have fed on infected rodents (SN:
8/19/17, p. 16 ), is less widespread; 98 cases
were reported from 2007 to 2016.
West Nile virus (green in this micrograph)
grows in a sample of human placental tissue. In
tests in mice, West Nile harmed fetuses.
Jonathan Miner, a virologist at
the Washington University School of
Medicine in St. Louis, and colleagues
conducted early work in mice demonstrating that Zika could harm fetuses
(SN: 6/11/16, p. 15). The new study tests
four other viruses: the two flaviviruses
and two alphaviruses, chikungunya and
Mayaro, which also have led to outbreaks
in Zika-affected areas.
The researchers infected 14 mice early
in their pregnancies with one of the
four viruses. By late pregnancy, 12 out
of 30 fetuses from West Nile–infected
mice had died, and half of the 16 fetuses
from Powassan-infected mice had died.
All fetuses from mice with chikungunya
and Mayaro virus survived. The flaviviruses also multiplied more efficiently
than the alphaviruses in lab samples of
human placental tissue.
Zika, West Nile and Powassan share
genetic similarities, Miner says. “So
there may be certain features of those
virus genes and proteins in that particular
family that confers this ability to infect
certain cell types,” he says. Scientists
don’t yet fully understand those features.
Past studies have raised the possibility of fetal damage from infections with
flaviviruses other than Zika, Miner says.
A 2006 study of 77 pregnant women
infected with West Nile virus reported
that two had infants with microcephaly,
the birth defect lately associated with
Zika that results in unusually small and
damaged brains. s
involved with the study. “Just sitting in
your office and breathing could fill the
air with infectious influenza.”
The CATCH study aims to find out
if what’s in the air is catching. In two
University of Maryland dorms, carbon
dioxide sensors measure how much of
the air comes from people’s exhalations.
In addition, laboratory tests measure
how much virus sick students are shed-
ding into the air. To get those samples,
students sit in a ticket booth–sized con-
traption called the Gesundheit-II and
breathe into a giant cone. These data can
help researchers estimate students’ air-
borne exposure to viruses, Milton says.
Another key dataset comes from DNA
testing of the viruses infecting the students. “The virus mutates reasonably
fast,” Milton says, and the more people
it has moved through, the more changes
it will have. By combining this molecular chain of transmission with the social
chain of transmission, the researchers
will try to “establish who infected whom,
and where, and how,” Milton says.
The goal is to enroll 130 students in
CATCH. It’s doubtful they’ll all get sick,
but not that many students from this
initial group are needed to start the ball
rolling, says Jennifer German, a virolo-
gist and CATCH student engagement
coordinator. “For every index case that
has an infection we’re interested in,
we’re following four additional con-
tacts,” she says. “And then if any of those
contacts becomes sick, we’ll get their
contacts and so on.”
The study began in November. As
of the end of January, German says,
researchers have collected samples
from five sick students, but only one was
infected with a target virus, influenza.
The researchers now are following three
contacts from that case.
Timing and the size of the current flu
outbreak may be on the researchers’ side.
Kleb says that students are still waiting
for this season’s flu to sweep through the
dorms. “Once one person gets sick, it goes
around to everyone on the floor,” he says.
“I’m very interested to see what happens
in the next few weeks, and how the study
will hopefully benefit.” s