The MMWR update, co-authored by scientists from CDC and Colombia's ministry of health and national institute of health, offers «preliminary information» about 476 cases
of microcephaly identified over the last 11 months.
Not exact matches
Even as the Zika virus becomes more prevalent — the Centers for Disease Control reports that the number
of U.S. infants born with
microcephaly and other birth defects is 20 times over the normal rate — researchers are still trying to fully pin down the
identifying consequences
of the viral infection.
The approach enabled a wide range
of studies
of human brain development, including implicating a new class
of neural stem cell recently discovered by the lab in the evolutionary expansion
of the human brain and
identifying how the mosquito - borne Zika virus may contribute to
microcephaly in infants infected in utero.
Contracted through the bite
of an infected mosquito or through sexual or other modes
of transmission, Zika virus (ZIKV) infection can be prenatally passed from mother to fetus.1 The virus was first
identified in the region
of the Americas in early 2015, when local transmission was reported in Brazil.2 Six months later, a notable increase in the number
of infants with congenital
microcephaly was observed in northeast Brazil.3, 4 Clinical, epidemiologic, and laboratory evidence led investigators to conclude that intrauterine ZIKV infection was a cause
of microcephaly and serious brain anomalies.5 - 7 However, as with other newly recognized teratogens, these features likely represent a portion
of a broader spectrum.
The central nervous system damage seen with prenatal ZIKV infection is likely due to direct cellular injury, as ZIKV RNA15, 17,32 and live virus15 have been
identified in the brain tissue
of infants with
microcephaly.
On Wednesday, U.S. health officials reported that traces
of the Zika virus had been
identified in the tissue
of two babies who died in Brazil from
microcephaly.