Portable device can detect viruses in minutes Tuesday, 06.16.2009, 06:05pm (GMT+3)
Portable device can detect viruses in minutes
Imagine being
able to detect in just a few minutes whether someone is infected with a virus.
This has now become a reality, thanks to a new ultra-sensitive detector that
has been developed by Ostendum, a spin-off company of the University of Twente.
The company has just completed the first prototype and expects to be able to
introduce the first version of the detector onto the market in late 2010. Not
only does the detector carry out measurements many times faster than do
standard techniques, it is also portable, so it can be used anywhere.
Ostendum’s Aurel Ymeti (R&D director), Alma Dudia (Senior Researcher) and
Paul Nederkoorn (CEO) claim that if they had the right antibodies to the swine
flu at their disposal, they would be able to highlight the presence of the
virus within five minutes. In addition to viruses, the device is also able to
pick up bacteria, proteins and DNA molecules.
Following the outbreak of swine flu, the issue of finding a means of detecting
quickly and simply whether someone is infected with a virus is again very much
on the agenda. It is important to be able to do so as soon as possible in order
to prevent the virus from spreading further. However, the techniques that are
currently available do not yield results for several hours or even days.
Moreover, the tests cannot be carried out without a laboratory or trained
personnel. Researchers at Ostendum, a spin-off company of the University of
Twente, have developed a portable device that can show in five minutes whether
or not a person is infected with a particular virus. The system is able to
detect not only viruses, but also specific bacteria, proteins and DNA
molecules, an increased or reduced concentration of which in a person’s saliva
may be an indication that they have one illness or another. The only thing
needed by the Ostendum detection method is a sample of saliva, blood or another
body fluid from the person being tested and the availability of a specific
receptor (i.e. a substance that binds with a specific micro-organism or
biological substance). For example, in the case of a virus, a specific antibody
served as a receptor on the chip and such antibody to that virus has to be
available in order to be able to apply the underlying detection method.
Ymeti demonstrated during his doctoral research in 2007 that the principle
behind the detector worked. At the time, he used a fairly sizeable laboratory
set-up. The Ostendum company was subsequently founded, in 2008, in order to
develop the principle into a marketable product. The company has just completed
the first prototype of the device, and it is presently working on two others.
The three prototypes are undergoing practical tests, in a collaboration
involving the Laboratorium Microbiologie Twente Achterhoek and the Zwanenberg
Food Group. Ostendum will then make further improvements to the design of the
device on the basis of the test results, and expects to have the first device
ready for introduction to the marketplace in late 2010. The device consists of
two parts: a lab-on-a-chip-system and a portable detector. A lab-on-a-chip is a
miniature laboratory the size of a chip. The chip contains tiny channels that
are coated with receptors. The blood or saliva sample is transported to the
channels with the help of a fluid system. Substances from the saliva or blood
can then bind with the receptors on the chip. Light from a laser is guided
through the channels. If any of the substances binds with the receptors in any
of the channels, this will alter the phase of the light. Such a change will
manifest itself in the interference pattern, and is a fingerprint of any
viruses present, for example, or biomarkers. The method is highly sensitive: it
is possible to measure the binding of a single virus particle.
Poultry carcasses infected with bird flu can remain
infectious in municipal landfills for almost two years
Amid concerns
about a pandemic of swine flu, researchers from Nebraska report for the first
time that poultry carcasses infected with another threat — the 'bird flu' virus
— can remain infectious in municipal landfills for almost 2 years. Their report
is scheduled for the June 15 issue of ACS’ semi-monthly journal Environmental
Science & Technology. Shannon L. Bartelt-Hunt and colleagues note that
avian influenza, specifically the H5N1 strain, is an ongoing public health
concern. Hundreds of millions of chickens and ducks infected with the virus
have died or been culled from flocks worldwide in efforts to control the
disease. More than 4 million poultry died or were culled in a 2002 outbreak in
Virginia, and the carcasses were disposed of in municipal landfills. Until now,
few studies have directly assessed the safety of landfill disposal.
“The objectives of this study were to assess the survival of avian influenza in
landfill leachate and the influence of environmental factors,” says the report.
The data showed that the virus survived in landfill leachate — liquid that
drains or “leaches” from a landfill — for at least 30 days and up to 600 days.
The two factors that most reduced influenza survival times were elevated
temperature and acidic or alkaline pH. “Data obtained from this study indicate
that landfilling is an appropriate method for disposal of carcasses infected
with avian influenza,” says the study, noting that landfills are designed to
hold material for much longer periods of time.
West Nile virus as cause of fatal neurologic
disease in horses, South Africa
Serologic evidence
suggests that West Nile virus (WNV) is widely distributed in horses in southern
Africa. However, because few neurologic cases have been reported, endemic lineage
2 strains were postulated to be nonpathogenic in horses. Recent evidence
suggests that highly neuroinvasive lineage 2 strains exist in humans and mice.
To determine whether neurologic cases are being missed in South Africa, we
tested 80 serum or brain specimens from horses with unexplained fever (n = 48)
and/or neurologic signs (n = 32) for WNV. From March 2007 through June 2008,
using reverse transcription–PCR (RT-PCR) and immunoglobulin (Ig) M ELISA, we
found WNV RNA or IgM in 7/32 horses with acute neurologic disease; 5 horses
died or were euthanized. In 5/7 horses, no other pathogen was detected. DNA
sequencing for all 5 RT-PCR–positive cases showed the virus belonged to lineage
2. WNV lineage 2 may cause neurologic disease in horses in South Africa. West
Nile virus (WNV), a mosquito-born flavivirus of the family Flaviviridae, is
widely distributed throughout Africa, the Middle East, Asia, parts of Europe,
Australia, North and South America, and the Caribbean. The WNV transmission
cycle involves birds as vertebrate hosts and ornithophilic mosquitoes as
maintenance vectors. Isolates of WNV fall into 2 major genetic lineages:
lineage 1 is found in North America, North Africa, Europe, and Australia;
lineage 2 strains are endemic to southern Africa and Madagascar. Recently,
additional lineages in central and eastern Europe (lineages 3 and 4) and India
(lineage 5) have been reported.
Humans and horses are incidental hosts for WNV. Although most infections are
benign, ≈20% of infected persons have fever, rash, arthralgia, and myalgia, and
for ≈1% of these, severe disease, including meningoencephalitis, encephalitis,
and polio-like flaccid paralysis, may develop. Rare cases result in hepatitis,
myocarditis, pancreatitis, and death. Signs in horses are ataxia, weakness,
recumbency, and muscle fasciculation. Seroepidemiologic studies suggest that
asymptomatic infections frequently occur in horses, but neurologic infections
result in a high case-fatality rate (30%–40%). In 2002 the largest outbreak of
WNV encephalomyelitis in horses was recorded in the United States; 15,257 cases
were reported from 40 states. This outbreak was followed in 2003 by the largest
outbreak in humans in the Northern Hemisphere (9,832 cases). The number of
cases among horses was greatly reduced after the introduction of an inactivated
vaccine for animals.
In the Karoo, a semidesert region in South Africa, in 1974, WNV caused one of
the largest outbreaks ever recorded in humans, affecting tens of thousands of
people. During this outbreak thousands of persons visited their local
clinicians; however, no cases of neurologic disease were reported. In the
1980s, an epizootic involving WNV and Sindbis virus occurred in the
Witwatersrand area of the Gauteng Province in South Africa; this epizootic
affected hundreds of persons. Since then, the number of confirmed human cases
has been ≈5–15 per year, although only a proportion of cases are subjected to
laboratory investigation. In South Africa, severe disease has been recognized,
including fatal hepatitis and several nonfatal encephalitis cases in humans as
well as deaths in ostrich chicks, a foal, and a dog. Recently, a lineage 2
strain was isolated from encephalitic birds in central Europe, which suggests
that lineage 2 strains can spread outside their known geographic range and may
cause severe disease in birds in non–WNV-endemic countries. A recent serologic
survey of thoroughbred horses has confirmed that WNV is widely distributed
throughout South Africa; 11% of yearlings seroconverted over 1 year and up to
75% of their dams had been exposed. This study led to the postulation that
endemic lineage 2 WNV strains were not a cause of neuroinvasive disease in
horses because none of these horses had shown any clinical signs. Three
seronegative horses inoculated with a recent WNV lineage 2 strain (SPU381/00)
isolated from a person with benign disease did not develop clinical signs.
However, the strain used in these experiments was subsequently shown to be of
low neuroinvasiveness in mice, compared with certain other South African
strains. Subclinical cases are also frequently reported in horses in the United
States. Experimental infection of 12 horses with the highly neuroinvasive NY99
strain resulted in neuroinvasive disease in only 1 animal; the remaining
animals all seroconverted, but clinical disease did not develop and virus could
not be isolated from their organs. Comparison of South African and North
American strains of WNV has shown that differences in neuroinvasiveness are
associated with specific genotypes, not with lineage, and that highly
neuroinvasive strains exist in lineages 1 and 2. To determine whether equine
cases of WNV are being missed in South Africa, for 16 months we investigated
horses with pyrexia or unexplained neurologic signs.
Scientists around the
world are accelerating their efforts to develop a vaccine against the H1N1
influenza virus (Swine flu) as rapidly as possible, reports Genetic Engineering
& Biotechnology News (GEN). The need for such a vaccine received a strong
impetus from the World Health Organization, which has issued a Phase 5 pandemic
alert, a strong signal that the WHO believes a pandemic is imminent, according
to the June 1 issue of Genetic Engineering & Biotechnology News. "It
can take five or six months to come up with an entirely novel influenza
vaccine," says John Sterling, Editor in Chief of GEN. "There is a great
deal of hope that biotech and pharma companies might be able to have something
ready sooner." One company, Replikins, actually predicted over a year ago
that significant outbreaks of the H1N1 flu virus would occur within 6-12
months.
The predictions were based on correlations of flu virus specimens and PubMed
documentation of major outbreaks during the past 90 years, focusing on
concentrations of, and spacings between, replikins—the lysine and histidine
residues in the hemagglutinin (HA) unit genetic sequences of the eight major
genes in the influenza virus. Replikins' officials say the company's PanFLu™
vaccine is ready for clinical trials. Novavax plans to create a virus-like
particle-based (VLP) vaccine against the H1N1 strain, which obviates the need
for a live virus seed for manufacturing. The VLPs contain the proteins that
make the virus' outer shell and the surface proteins, without the RNA required
for replication. Other H1N1 vaccine programs covered in the GEN article include
those at Medicago, VaxInnate, NanoBio, Vaxart, Pulmatrix, and Purdue
University.
Old seasonal flu antibodies target swine flu virus
Antibodies against some
seasonal flu strains from prior years may be active against the new H1N1 swine
flu currently circulating the globe, a recent study reports. The findings
suggest an explanation for why swine flu appears to infect the young more often
than the elderly, who are normally more susceptible to seasonal flu viruses.
Only 1% of swine flu cases in the United States are in people over the age of
65. The study, published today in the Morbidity and Mortality Weekly Report,
analyzed blood samples taken from 359 participants in flu vaccine studies
conducted from 2005 to 2009. 33% of the samples from people over 60 years old
had antibodies that reacted with the swine flu virus, as compared to 6%-9% of
the samples from people aged 18–64 years, and none of the samples taken from
children. The results match the apparent current epidemiology of swine flu
infection, says Anne Schuchat, interim deputy director for the Science and
Public Health Program at the Centers for Disease Control and Prevention (CDC)
in Atlanta. Most cases of swine flu have occurred in people who are under 60
years old, and only 1% of confirmed swine flu infections in the United States
were in patients over the age of 65.
Nevertheless, the results should be interpreted with caution, Schuchat urged in
a press briefing today. Researchers have shown that the antibodies react with
the virus in test-tube assays, but they have not yet shown that the antibodies
can fend off the virus in animals or people. "Whether this particular
assay will pan out over time as predictive of clinical protection, we can't
say," Schuchat said. For the study, CDC researchers used two tests to
determine whether antibodies in the blood were active against the swine flu.
One test studied the impact of the antibodies on growth of the virus in cell
culture, and the other assayed the ability of the antibodies to inhibit an
important viral protein called hemagglutinin. The results indicated that
vaccination against recent H1N1 seasonal flu viruses did not generate
antibodies that react with the swine flu virus. But exposure to older seasonal
flu viruses or vaccines — perhaps dating back to the 1950s or earlier — may
have yielded cross-reactive antibodies in some older study participants.
Although the results have not yet been confirmed clinically, the researchers
used standard techniques that are often used in preclinical studies of flu
vaccines, says Ralph Tripp, a viral immunologist at the University of Georgia
in Athens. "The reality is, there does appear to be a substantial level of
cross-reactivity in those adults aged 60 years and older," he says.
Genetic analysis of the new swine flu virus has shown that it differs
dramatically from previous seasonal viruses. But Tripp notes that H1N1 viruses
were circulating in swine during the 1940s and 1950s and could have mixed with
seasonal flu viruses during that time. Exposure to these viruses could have
launched an antibody response that continues to protect individuals against
today's swine flu. Meanwhile, Schuchat notes that it is possible for immune
responses to the current swine flu and past seasonal viruses to overlap,
despite the genetic dissimilarity. "We don't have a particular virus that
we're thinking about," she says, "but we're wondering if there might
have been some viruses around in the '30s, '40s and '50s that might be
immunologically similar to the one we're seeing now."
For the first time UK
scientists have shown what the food poisoning bug Salmonella feeds on to
survive as it causes infection: glucose. Their discovery of Salmonella’s
weakness for sugar could provide a new way to vaccinate against it. The
discovery could also lead to vaccine strains to protect against other
disease-causing bacteria, including superbugs. “This is the first time that
anyone has identified the nutrients that sustain Salmonella while it is
infecting a host’s body,” says Dr Arthur Thompson from the Institute of Food
Research. The nutrition of bacteria during infection is an emerging science.
This is one of the first major breakthroughs, achieved in collaboration with
Dr. Gary Rowley at the University of East Anglia. Salmonella food
poisoning causes infection in around 20 million people worldwide each year and
is responsible for about 200,000 human deaths. It also infects farm animals and
attaches to salad vegetables. During infection, Salmonella bacteria are
engulfed by immune cells designed to kill them. But instead the bacteria
multiply.
Salmonella must acquire nutrients to replicate. The scientists focused
on glycolysis, the process by which sugars are broken down to create chemical
energy. They constructed Salmonella mutants unable to transport glucose
into the immune cells they occupy and unable to use glucose as food. These
mutant strains lost their ability to replicate within immune cells, rendering
them harmless. “Our experiments showed that glucose is the major sugar used by Salmonella
during infection,” said Dr Thompson. The mutant strains still stimulate the
immune system, and the scientists have filed patents on them which could be
used to develop vaccines to protect people and animals against poisoning by
fully virulent Salmonella. Glycolysis occurs in most organisms including
other bacteria that occupy host cells. Disrupting how the bacteria metabolise
glucose could therefore be used to create vaccine strains for other pathogenic
bacteria, including superbugs.
The harmless strains could also be used as vaccine vectors. For example, the
flu gene could be expressed within the harmless Salmonella strain and
safely delivered to the immune system. The next stage of the research will be
to test whether the mutants elicit a protective immune response in mice. In
Germany the nutrition of bacteria is the subject of a six-year priority
programme of research to investigate why bacteria are able to multiply inside a
host’s body to cause disease.
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