http://www.healthscoutnews.com/printer.cfm?id=513476
Deadly Cold Virus Strikes Disabled in N.Y.
Outbreak blamed for as many as 3 deaths in special home By Adam Marcus
HealthScoutNews Reporter MONDAY, June 2 (HealthScoutNews) -- New York health
officials are investigating a mysterious virus that has attacked a Yonkers
home for the developmentally disabled and left as many as three people there
dead. But health officials say the virus is definitely not SARS. The
organism, which has been identified as an adenovirus, has sickened more than
40 people at the center, Richmond of New York, since it appeared last month,
according to WABC-TV in New York. Adenoviruses typically cause cold-like
symptoms, but they can lead to serious infections in people with weakened
immune systems."With this population, which is very medically involved, what
happens is their immune system doesn't fight it," says Maryann
Arcoleo-Koltun, Richmond's senior vice president. Officials at the facility
first began noticing fevers in residents about two weeks ago. Tests revealed
the presence of adenovirus. Four residents have died since the outbreak
began, though only three, and possibly just two, of those deaths are
probably related to the infection, she says. Seven Richmond residents remain
in the hospital as the facility undergoes decontamination, Arcoleo-Koltun
says. Staff go around in gowns and gloves and hand-washing is rigorous.
Meanwhile, daytime activities that take residents off the Yonkers campus
have been temporarily suspended.Arcoleo-Koltun says that step doesn't
constitute a quarantine because staff members are allowed to leave the
grounds.Health officials stress that the disease is not related to sudden
acute respiratory syndrome, or SARS. New York has had 47 possible cases of
SARS since the outbreak began last winter. The state has reported no recent
cases of the illness.Arcoleo-Koltun says the U.S. Centers for Disease
Control and Prevention is not yet involved in the investigation.
http://www.cdc.gov/ncidod/dvrd/revb/respiratory/eadfeat.htm
Clinical features: Adenoviruses most commonly cause respiratory illness;
however, depending on the infecting serotype, they may also cause various
other illnesses, such as gastroenteritis, conjunctivitis, cystitis, and
rash illness. Symptoms of respiratory illness caused by adenovirus infection
range from the common cold syndrome to pneumonia, croup, and bronchitis.
Patients with compromised immune systems are especially susceptible to
severe complications of adenovirus infection. Acute respiratory disease (ARD),
first recognized among military recruits during World War II, can be caused
by adenovirus infections during conditions of crowding and stress.
The viruses: Adenoviruses are medium-sized (90-100 nm), nonenveloped
icosohedral viruses containing double-stranded DNA. There are 49
immunologically distinct types (6 subgenera: A through F) that can cause
human infections. Adenoviruses are unusually stable to chemical or physical
agents and adverse pH conditions, allowing for prolonged survival outside of
the body.
Epidemiologic features: Although epidemiologic characteristics of the
adenoviruses vary by type, all are transmitted by direct contact, fecal-oral
transmission, and occasionally waterborne transmission. Some types are
capable of establishing persistent asymptomatic infections in tonsils,
adenoids, and intestines of infected hosts, and shedding can occur for
months or years. Some adenoviruses (e.g., serotypes 1, 2, 5, and 6) have
been shown to be endemic in parts of the world where they have been studied,
and infection is usually acquired during childhood. Other types cause
sporadic infection and occasional outbreaks; for example, epidemic
keratoconjunctivitis is associated with adenovirus serotypes 8, 19, and 37.
Epidemics of febrile disease with conjunctivitis are associated with
waterborne transmission of some adenovirus types, often centering around
inadequately chlorinated swimming pools and small lakes. ARD is most often
associated with adenovirus types 4 and 7 in the United States. Enteric
adenoviruses 40 and 41 cause gastroenteritis, usually in children. For some
adenovirus serotypes, the clinical spectrum of disease associated with
infection varies depending on the site of infection; for example, infection
with adenovirus 7 acquired by inhalation is associated with severe lower
respiratory tract disease, whereas oral transmission of the virus typically
causes no or mild disease. Outbreaks of adenovirus-associated respiratory
disease have been more common in the late winter, spring, and early summer;
however, adenovirus infections can occur throughout the year.
Diagnosis: Antigen detection, polymerase chain reaction assay, virus
isolation, and serology can be used to identify adenovirus infections.
Adenovirus typing is usually accomplished by hemagglutination-inhibition
and/or neutralization with type-specific antisera. Since adenovirus can be
excreted for prolonged periods, the presence of virus does not necessarily
mean it is associated with disease.
Treatment: Most infections are mild and require no therapy or only
symptomatic treatment. Because there is no virus-specific therapy, serious
adenovirus illness can be managed only by treating symptoms and
complications of the infection.
Prevention: Vaccines were developed for adenovirus serotypes 4 and 7, but
were available only for preventing ARD among military recruits. Strict
attention to good infection-control practices is effective for stopping
nosocomial outbreaks of adenovirus-associated disease, such as epidemic
keratoconjunctivitis. Maintaining adequate levels of chlorination is
necessary for preventing swimming pool-associated outbreaks of adenovirus
conjunctivitis.
For further information, please contact the Respiratory and Enteric Viruses
Branch, National Center for Infectious Diseases, at 404-639-3607 (telephone)
or 404-639-4960 (facsimile).
References:
American Academy of Pediatrics. Adenovirus Infections. In: Peter G, ed. 1997
Red Book: Report of the Committee on Infectious Diseases. 24th ed. Elk Grove
Village, IL: American Academy of Pediatrics; 1997: 131.
Horwitz MS. Adenoviruses. In: Fields BN, Knipe DM, Howley PM, eds. Fields
Virology. 3rd ed. Philadelphia: Lippincott-Raven; 1995: 2149-71.
Foy HM. Adenoviruses. In: Evans A, Kaslow R, eds. Viral Infections in
Humans:
epidemiology and control. 4th ed. New York: Plenum; 1997:119-38.
September 2003 • Volume 189 • Number 3
Is adenovirus a fetal pathogen?
Ahmet A. Baschat, MDa* Jeffrey Towbin, MDa Neil E.
Bowles, PhDa Christopher R. Harman, MDa Carl P. Weiner, MDa • Previous
article in Issue
Objectives The purpose of this study
was to test the relationship between adenovirus genetic material in the
amniotic fluid and adverse pregnancy outcome. Study design This was a
prospective, observational study of women who were referred in the second
trimester of gestation for either genetic amniocentesis or evaluation of
fetal malformation. A 2-mL aliquot of amniotic fluid was subjected to
multiplex polymerase chain reaction for a panel of viruses that included
adenovirus and human genome controls. Fetuses with an abnormal karyotype
were excluded from analysis.
Results The prevalence of adenovirus
was similar in normal (39/652) and anomalous fetuses (23/364; 2 test,
P=.376). There was significant seasonal variation in the prevalence in both
normal and anomalous fetuses (2 exact test, P<.001), but no significant
difference between groups. The monthly proportion of patients who underwent
amniocentesis remained constant throughout the year (mean, 8.3%; 2 test,
P=.67). Central nervous system anomalies and echogenic liver foci were
significantly more common among fetuses with positive amniotic fluid
polymerase chain reaction results for adenovirus (P<.005, respectively).
Conclusion Adenovirus is found in a
similar prevalence and seasonal variation in sonographically normal and
abnormal pregnancies. Although a specific fetal presentation was not
identified, echogenic liver lesions with or without hydrops and neural tube
defects were significantly more common in the presence of adenovirus. The
significance of these findings deserves further study.
From the Department of Obstetrics,
Gynecology, and Reproductive Sciences, Center for Advanced Fetal Care,
University of Maryland,a and the Department of Molecular and Human Genetics,
Baylor College of Medicine.b Baltimore, Md, and Houston, Tex USA Presented
at the Twenty-Third Annual Meeting of the Society for Maternal-Fetal
Medicine, San Francisco, Calif, February 3-8, 2003.
*Reprint requests: Ahmet Alexander
Baschat, MD, Department of Obstetrics and Gynecology, University of
Maryland, Baltimore, 405 W Redwood St, 4th floor, Baltimore, MD 21201.;
Email: aabaschat@hotmail.com
Copyright © 2003 by Mosby, Inc.
doi:10.1067/S0002-9378(03)00720-8
Is adenovirus a fetal pathogen?
Ahmet A. Baschat, MDa*
Jeffrey Towbin, MDa
Neil E. Bowles, PhDa
Christopher R. Harman, MDa
Carl P. Weiner, MDa
Abstract
Objectives The purpose of this study was to test the relationship between
adenovirus genetic material in the amniotic fluid and adverse pregnancy
outcome.
Study design This was a prospective, observational study of women who were
referred in the second trimester of gestation for either genetic
amniocentesis or evaluation of fetal malformation. A 2-mL aliquot of
amniotic fluid was subjected to multiplex polymerase chain reaction for a
panel of viruses that included adenovirus and human genome controls. Fetuses
with an abnormal karyotype were excluded from analysis.
Results The prevalence of adenovirus was similar in normal (39/652) and
anomalous fetuses (23/364; 2 test, P=.376). There was significant seasonal
variation in the prevalence in both normal and anomalous fetuses (2 exact
test, P<.001), but no significant difference between groups. The monthly
proportion of patients who underwent amniocentesis remained constant
throughout the year (mean, 8.3%; 2 test, P=.67). Central nervous system
anomalies and echogenic liver foci were significantly more common among
fetuses with positive amniotic fluid polymerase chain reaction results for
adenovirus (P<.005, respectively).
Conclusion Adenovirus is found in a similar prevalence and seasonal
variation in sonographically normal and abnormal pregnancies. Although a
specific fetal presentation was not identified, echogenic liver lesions with
or without hydrops and neural tube defects were significantly more common
in the presence of adenovirus. The significance of these findings deserves
further study.
Publishing and Reprint Information TOP
From the Department of Obstetrics, Gynecology, and Reproductive Sciences,
Center for Advanced Fetal Care, University of Maryland,a and the Department
of Molecular and Human Genetics, Baylor College of Medicine.b Baltimore, Md,
and Houston, Tex USA
Presented at the Twenty-Third Annual Meeting of the Society for
Maternal-Fetal Medicine, San Francisco, Calif, February 3-8, 2003.
*Reprint requests: Ahmet Alexander Baschat, MD, Department of Obstetrics and
Gynecology, University of Maryland, Baltimore, 405 W Redwood St, 4th floor,
Baltimore, MD 21201.; Email: aabaschat@hotmail.com
Copyright © 2003 by Mosby, Inc.
doi:10.1067/S0002-9378(03)00720-8
Adenoviral Vectors Show Promise as Vaccine Carriers for
Newborns
http://www.medscape.com/viewarticle/463284?mpid=20190
NEW YORK (Reuters Health) Oct 21 - E1-deleted adenovirus vectors carrying a
rabies antigen can induce a protective antibody response when given orally
or intranasally to newborn mice, new research shows. "These new vaccines
we've developed trigger the production of protective antibodies in newborn
mice during a time in their lives when traditional vaccines are commonly
less effective," senior author Dr. Hildegund C. J. Ertl, from the University
of Pennsylvania in Philadelphia, said in a statement.
"This has potentially important public-health implications, especially in
the developing world," Dr. Ertl noted. "In addition, these are oral
vaccines, which could make them easier to distribute and administer in those
same areas," he added.
The findings, which are reported in the October 15th issue of The Journal of
Immunology, are based on a study of newborn mice given a human or chimpanzee
adenoviral vector coupled to a rabies virus glycoprotein. The researchers
included the chimpanzee adenoviral vector because many mothers in the
US carry antibodies against human adenovirus. If these antibodies are
passed to the newborn, they could, in theory, inactive a vaccine
based on a human adenoviral vector.
The authors found that both vaccines induced detectable levels of
anti-rabies antibodies. Furthermore, animals that received either vaccine
were protected against subsequent challenge with rabies virus.
Surprisingly, the human adenovirus vaccine seemed to be just as effective as
the one based on chimpanzee adenovirus.
"Even in the presence of maternal antibodies against human adenovirus, the
human adenovirus vaccine remained effective," Dr. Ertl noted. "Although
unexpected, this was good news, because it increases the repertoire of
vaccine types potentially suitable for infant vaccination."
J Immunol 2003;171:4287-4293.
Its unexpected because no one knows how the immune system works.
http://www.channel4.com/health/microsites/0-9/4health/food/ove_fatvirus.html
Channel4.com
Could fat be catching?
by Jenny Bryan
Could a fat virus be responsible for the epidemic of obesity that is
sweeping the USA and seems to be spreading to Britain? Obesity scientist,
Dr Nikhil Dhurandhar thinks that it is and has some intriguing research
findings to back him up. But he knows that other obesity specialists
cannot believe it's that simple.
'The concept of a virus causing obesity is so far away from mainstream
causes of obesity that it's going to take much more convincing and
evidence simply because it's a very different idea. But we'll do it,'
predicts Dr Dhurandhar, Wayne State University, Detroit, Michigan. In the
USA 61% of people are now officially classed as obese (with a body mass
index, BMI, of over 30) or overweight (BMI of 25-30). The situation is
scarcely any better in the UK, with about 20% of people obese and over
40%
overweight. If you look at a map of obesity in the USA, you can watch the
epidemic spreading rather like a forest fire from the east coast to the
west over the last 20 years. And it is this, says Dhurandhar, which
suggests that there could be an infection.
it started with chickens .
Dhurandhar's story starts in Bombay in the 1980s with a mysterious
epidemic that wiped out hundreds of thousands of chickens. The birds were
found to be infected with an adenovirus called SMAM-1. Adenoviruses are
very common. There are at least 40 types that affect humans and they
cause about 1 in 20 cases of chest infection.
What was intriguing about the Indian chickens with SMAM-1 was not so much
that they were probably killed by an adenovirus infection, but that they
died plump, with a large pale liver and large kidneys. They weren't thin
and emaciated as you might expect an animal with a virus to be.
Working in India, Dhurandhar deliberately infected some more chickens
with the same virus and, sure enough, these birds also put on weight. He
decided to pursue his research in the USA, but the US government wasn't
keen on him importing a virus that had wiped out a large portion of the
Indian chicken population.
Instead, Dhurandhar borrowed a human adenovirus, called Ad-36, from the
US collection and set to work infecting first chickens and then rhesus
monkeys and marmosets. Like the chickens, infected animals started to put
on weight. Six months after they were infected, three male
marmosets put on three times as much weight and doubled their body fat
compared to three animals that were not infected. It was a very small
study, but the results were still impressive.
It wouldn't be ethical to infect humans with Ad-36 to see if they got
fat. But, as the virus does occur naturally in the human population,
Dhurandhar decided to compare infection rates in people who were fat with
those who weren't. He tested 500 people in three cities. Thirty per cent
of obese people screened positive for the Ad-36 virus, compared with only
5 to 10% of those who were not overweight.
how the fat virus might work
Dhurandhar - and his critics - wanted to know how a fat virus might work.
Dhurandhar showed that Ad-36 appeared to increase the size and number of
fat cells in infected animals. In the laboratory, his experiments
suggested that Ad-36 encourages pre-fat cells with the potential to
become fat cells to do just that. Three times as many pre-fat cells
became fat cells when they were exposed to Ad-36 compared with fat cells
that weren't exposed to the virus.
twin studies
As part of his studies to try and convince other obesity researchers
about the importance of the fat virus, Dhurandhar turned to a set of
identical twins, Christyn and Beth. Born with exactly the same genes,
there was no chance that one twin was genetically more likely to put on
weight than the other. Until they went to college, the twins did indeed
remain a very similar weight - as do nearly all sets of identical twins.
But in the two years after Christyn left home to go to college, she
became two and a half stone heavier than her twin. Blood tests showed
that, while Beth remained Ad-36 negative, Christen had, at some point,
been infected with the virus. Did the virus make her put on weight or did
she just eat more and exercise less when she went to college? Who knows,
but Dhurandhar blames it on the virus.
Others remain skeptical.
'The idea that a virus may be causing obesity seems intrinsically
unlikely,' says Professor Stephen Bloom, from Imperial College, London.
'Obesity has been growing at a constant rate for about 50 years and the
causes are pretty obvious. People have been eating much more and taking
less exercise. Why do you need to invent some strange story about a
virus?'
Virologist, Professor William Russell, from the University of St
Andrews,points out that adenoviruses have never been linked with a
long-term illness, like obesity. They cause short-term infections and
disappear. It's important to keep an open mind but, at present, the
evidence just does not stack up, he says.
a vaccine against obesity?
In the USA, some scientists are more prepared to accept that viruses
could be involved. 'Viruses can lie dormant for many years and we've seen
the crossover of the HIV virus, for example, from animals to humans. We
may be seeing a similar thing now with the obesity virus,' suggests Dr
John Foreyt from Baylor College, Texas. 'We really don't know why people
get fat or why people are skinny. There's so much that is unknown and
that's why we need new theories and people looking at why our bodies are
the way they are,' he says. One possible hypothesis is that, in the late
'70s, someone working on a chicken farm in India had the Ad-36 virus and
came in contact with birds with SMAM-1. The two viruses got together,
exchanged genetic material, and turned into a hybrid virus capable of
infecting humans and making them fat. There is nothing, of course, to
confirm this series of events, but Dr Dhurandhar now has research grants
to help him develop his theories. He has his sights set on a vaccine
against the fat virus, but accepts that could be some way off:
'It would be absolutely fascinating to have a vaccine to prevent at least
some types of obesity virus - that's my dream,' he says.
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