A newly emergent, deadly virus
Throughout
the last fifteen years, a highly fatal virus has emerged. Since its first discovery in 1998, Nipah
virus has infected nearly 500 people throughout Asia, and produced a mortality rate greater than 50% (1). Nipah virus can
be spread from either human-animal or human-human contact. During the first outbreak of Nipah,
transmission occurred primarily via respiratory droplets from infected pigs in
Malaysia (2). On the other hand, some of
the outbreaks in India and Bangladesh were most likely due to contact with
fruit bat saliva or urine (1). In
addition, some of the more recent cases of Nipah were transmitted directly from
person to person, with many of the infections occurring in a hospital setting
(1). At first, Nipah virus symptoms
resemble those of the flu, as many patients report headaches, muscle pains,
vomiting, and a sore throat (1).
However, as the disease progresses, people experience encephalitis, and
possible respiratory illness (1). In
serious cases, Nipah can lead to coma and death (1). There currently are no
vaccines or treatment options for Nipah.
Nipah virus
is a member of the Paramyxoviridae
family (2). It is closely related to the
Hendra virus, which causes similar respiratory and neurological symptoms
(3). Nipah virus is a (-) sense,
single-stranded RNA virus that contains a nonsegmented genome (2). Because Nipah is such a fatal virus, and
there are no vaccines or treatment options available, there is little known
about it. All research involving Nipah
must be completed at BSL-4 facilities containing the highest possible levels of
security and safety. Recently,
researchers at the Institute of Virology, Philipps University of Marburg, Germany
investigated how Nipah virus enters and exits an infected epithelial cell. Although
researchers have clinically proven that Nipah infects epithelial cells in the
respiratory and urinal tracts, the mechanisms behind this are largely unknown.
Researching the unknown Nipah virus
The first
major objective of this study was to observe the mechanisms of Nipah virus
(NiV) entry into a polarized epithelial cell.
To start, the researchers observed the distribution of the NiV entry
receptors on the cells. Specifically,
they looked at the ephrin receptor expressions on polarized kidney epithelial
cells (MDCK). The researchers found an
even distribution of ephrin throughout the apical and basolateral surfaces of
the cell. Then, MDCK cells were
selectively infected to either the apical or basal filter chamber; and
immunostained for presence of NiV in the cell.
As expected, NiV was able to infect the MDCK cells regardless of the
surface domain. Thus, NiV entry was
found to be bipolar.
