LOS
ANGELES — Clad in a yellow gown, blue foot covers, hair net, face mask and
latex gloves, Paula Cannon pushed open the door to the animal room. "I hate
this smell," she said, wrinkling her nose.News (Updated
August 29, 2010)
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FRIDAY, Aug. 27 (HealthDay
News) -- The brain can be a convenient hiding place for HIV, the virus that
causes AIDS.
That's the finding of
Swedish researchers who analyzed samples from about 70 HIV-infected patients
who'd been taking anti-HIV drugs. The tests showed that about 10 percent of the
patients -- a larger proportion than expected -- had traces of HIV in their
spinal fluid but not in their blood.
Another study by the
researchers found that 60 percent of 15 HIV-infected patients treated with
medication for several years showed signs of inflammation in their spinal fluid,
although the levels were lower than they were without treatment.
Anti-HIV drugs can
prevent the virus from multiplying, but the virus also infects the brain and can
cause damage if the infection isn't treated, according to lead researcher Dr.
Arvid Eden, a doctor and researcher at the
"Antiviral treatment
in the brain is complicated by a number of factors, partly because it is
surrounded by a protective barrier that affects how well medicines get in,"
It is unclear whether
small quantities of the virus in spinal fluid represent a risk for future
complications, researchers said. Still, the findings indicate that "we need
to take into account the effects in the brain when developing new drugs and
treatment strategies for HIV infection,"
Researchers at the
After 20 years of
researching HIV, Professor Louis Mansky is hoping his latest research will lead
to a new treatment. He says, "We can count all the cells that have been
infected."
His team recently found a
way to treat the virus, using drugs already on the market.
Drugs, Decitabine and
Gemcitabine, are currently used to treat cancer. But when combined in lab
experiments, researchers wanted them to do something else for HIV. Steve
Patterson, a researcher says, "To force the virus to mutate at a much
higher rate and kill itself off."
They say that's exactly
what happened. Prof. Mansky says, "Together, in combination, at
concentrations or at doses much lower than what's used for cancer chemotherapy,
these things work in our models very, very well."
The beauty of this is
that the drugs are already approved by the FDA, saving them lots of time and
money. Prof. Mansky says, "The hope is that these drugs can be, um, uh,
more quickly developed into new anti-HIV drugs."
Of course, plenty more
research needs to be done, including clinical trials in humans. And they also
hope to put the drugs in pill form. Right now, they're only given through an IV.
But for now, they're quite optimistic about the discovery.
Prof. Mansky adds,
"We hope that we'll be able to translate this into some effective
therapy."
These researchers have
studied the cancer drugs in mice and also found positive results, but it will
take some time before they can test people. One big question will be whether the
drugs have any long-term side effects on patients.
ANI / Wednesday, August
25, 2010
Scientists have
identified the key components of a protein called TRIM5a that destroys HIV in
rhesus monkeys.
Senior researcher Edward
M Campbell, of Loyola University Health System, said that the finding could lead
to new TRIM5a-based treatments that would knock out HIV in humans.
In 2004, other
researchers reported that TRIM5a protects rhesus monkeys from HIV. The TRIM5a
protein first latches on to a HIV virus, then other TRIM5a proteins gang up and
destroy the virus.
Humans also have TRIM5a,
but while the human version of TRIM5a protects against some viruses, it does not
protect against HIV.
Researchers hope to turn
TRIM5a into an effective therapeutic agent. But first they need to identify the
components in TRIM5a that enable the protein to destroy viruses.
"Scientists have
been trying to develop antiviral therapies for only about 75 years. Evolution
has been playing this game for millions of years, and it has identified a point
of intervention that we still know very little about,"
TRIM5a consists of nearly
500 amino acid subunits. Loyola researchers have identified six 6 individual
amino acids, located in a previously little-studied region of the TRIM5a
protein, that are critical in the ability of the protein to inhibit viral
infection. When these amino acids were altered in human cells, TRIM5a lost its
ability to block HIV-1 infection.
By continuing to narrow
their search, researchers hope to identify an amino acid, or combination of
amino acids, that enable TRIM5a to destroy HIV.
Once these critical amino
acids are identified, it might be possible to genetically engineer TRIM5a to
make it more effective in humans. Moreover, a better understanding of the
underlying mechanism of action might enable the development of drugs that mimic
TRIM5a action,
In their research,
scientists used Loyola's wide-field "deconvolution" microscope to
observe how the amino acids they identified altered the behaviour of TRIM5a.
They attached fluorescent
proteins to TRIM5a to, in effect, make it glow. In current studies, researchers
are fluorescently labeling individual HIV viruses and measuring the microscopic
interactions between HIV and TRIM5a.
"The motto of our
lab is one of Yogi Berra's sayings -- 'You can see a lot just by looking,'"
The findings will appear
on the cover of September 15, 2010 issue of the journal Virology.
URL of the article:
http://www.dnaindia.com/scitech/report_new-finding-could-lead-to-novel-hiv-treatments_1428591-all
2010-08-27
Scientists have revealed
that vitamin A and beta-carotene supplements are unsafe for HIV-positive women
who breastfeed because they may boost the excretion of HIV in breast milk
-thereby increasing the chances of transmitting the infection to the child.
Epidemiologist Eduardo
Villamor of the University of Michigan School of Public Health says transmission
of HIV through breastfeeding happens because breast milk carries viral particles
that the baby ingests.
Supplementing
HIV-positive women with vitamin A and beta-carotene appears to increase the
amount of the virus in milk.
This may be partly
because the same nutrients raise the risk of developing subclinical mastitis, an
inflammatory condition, which causes blood plasma to leak into the mammary gland
and viral particles to then leak into the milk, he says.
The results are
significant because they provide biological explanations for a previous report
that supplementation with these nutrients increased chances of mother-to-child
HIV transmission.
"So there are now
strong arguments to consider the implications of supplementation to pregnant or
lactating women who are HIV-positive. It does not look like it's a safe
intervention for them," said Villamor.
Mother-to-child HIV
transmission is a huge problem in developing countries where HIV is prevalent,
Villamor said. In 2008 alone, there were 430,000 new infections and more than 95
percent of those resulted from mother-to-child transmission. Most were in
sub-Saharan
In one of the studies,
1,078 HIV-infected women were divided into four groups. The test groups received
either 5,000 IU of vitamin A and 30 mg of beta-carotene everyday during
gestation and the lactation period, or a control regimen.
The dose for
beta-carotene was higher than the amount usually provided by the diet, according
to Villamor. Smaller doses might not have the same effect.
Villamor said tests
trying to separate the effects of each nutrient showed that beta-carotene seemed
to increase the amount of HIV in breast milk independent of vitamin A, but an
effect of vitamin A alone cannot be ruled out.
The findings are
potentially controversial because vitamin A is an important supplement for
postpartum women in countries where HIV infection is highly prevalent, but
supplementation programs may not take into account a woman's HIV status.
"The takeaway is
that daily supplementation of HIV-infected pregnant or lactating women with
vitamin A and beta-carotene at the doses tested is probably not safe and efforts
need to be strengthened on preventing mother-to-child transmission through other
interventions such as anti-retroviral regimens," Villamor said.
The findings appear in two separate articles in the American Journal of Clinical Nutrition and the Journal of Nutrition. (ANI)
By Rachel Bernstein,
LOS
ANGELES — Clad in a yellow gown, blue foot covers, hair net, face mask and
latex gloves, Paula Cannon pushed open the door to the animal room. "I hate
this smell," she said, wrinkling her nose.
The stink came from
scores of little white mice scurrying about in cages. Some of the cages were
marked with red biohazard signs, indicating mice that had been injected with
HIV.
Yet, in some of the
animals — ones with a small genetic change — the virus never took hold.
Like mouse, like man?
Maybe so.
In early 2007, a patient
in
It worked. Sixty-one days
after the patient's transplant, his virus levels were undetectable, and they've
stayed that way.
Since news of the man's
cure broke, HIV patients have been telephoning doctors to ask for bone marrow
transplants. But it's not that simple. The treatment is too risky and
impractical for widespread use.
"A bone marrow
transplant — it's a horrible process you would not wish on your worst enemy
unless they needed one to save their life," said Cannon, a biology
professor at USC's Keck School of Medicine. There are grueling treatments to
prepare a patient for transplant; the danger of rejecting the marrow; and the
risk of graft-versus-host disease, wherein the marrow attacks the patient.
And that's assuming the
patient can find a matching donor — a difficult proposition in itself — with
the right HIV-resistant genetic constitution, which is present in only about 1
per cent of the Caucasian population.
But there could be
another way.
Instead of sifting
through the sands for a rare donor and then subjecting a patient to the dangers
of a bone marrow transplant, Cannon and her colleague Philip Gregory, chief
scientific officer at the Richmond, Calif.-based biotech company Sangamo
BioSciences, began to think: They could use gene therapy instead, to tweak a
patient's own cells to resistance — and recovery.
The mouse
"cure," they say, suggests they're on the right track.
Now, with $14.5 million
from the California Institute for Regenerative Medicine, the San Francisco-based
stem cell research-funding center created by 2004's Proposition 71, Cannon,
Gregory and researchers at the City of
Cannon and other HIV
researchers insist that, despite cancers and deaths associated with past gene
therapy trials, it's the right way to target the disease. They cite recent
successes, including treatments that cured children with the "bubble
boy" syndrome and helped blind children regain their vision.
"I don't think
anyone would want to do gene therapy if there were an alternative," said
Caltech biologist David Baltimore, one of the many L.A.-based researchers
pursuing gene therapy strategies to prevent or cure HIV. "I think it's
absolutely necessary. Nothing else will work."
Since AIDS emerged in the
early 1980s, development of anti-HIV medications has turned the disease from a
virtual death sentence into a chronic, manageable condition.
But the clamor for a cure
hasn't quieted.
Vaccine trials have
failed; drug-resistant strains are on the rise; and the meds, which can have
uncomfortable side effects such as fatigue, nausea and redistribution of body
fat that creates a so-called buffalo hump, cost about $20,000 a year.
A bone marrow transplant
is about five times as expensive, but it would have to be done only once.
The question was, could
researchers create bone marrow stem cells that — just like the marrow the
In 2006, Gregory asked
Cannon if she was interested in testing whether a tool his company developed,
called a zinc finger nuclease, could do the trick.
Zinc finger nucleases are
genetic scissors, cutting DNA at a specific site — say, in the middle of the
CCR5 gene. When the cell glues the gene back together, it usually makes a
mistake, resulting in a gene that no longer works.
"It just jumped out
at me as, 'Oh my gosh, that's actually something that could work,' " Cannon
said.
The team spent about a
year optimizing the procedure for treating delicate stem cells with the CCR5
snippers.
They tested the method
using so-called humanized mice — ones engineered to have a human immune system
— because HIV doesn't infect normal mice. When stem cells were treated with
the molecular scissors before being injected into mice, the resulting immune
system lacked CCR5, exactly as the scientists had hoped.
These mice acted just
like the
Ready to make the leap
from mouse to man, Gregory found a third leg for the team: researchers at City
of
"They brought
Paula's data to us and we said, 'Wow, this looks fantastic,' " said Dr.
John Zaia, City of
Researchers there are now
working toward clinical trials, optimizing every element of the treatment for
safety, effectiveness and reproducibility.
On a wiltingly hot
afternoon in July, lab manager Lucy Brown maneuvered a computer mouse across
three screens speckled with red, yellow and green dots.
The computer was hooked
to a flow cytometer — a collection of black boxes, green wires and silver
knobs that can detect subtle differences between cells and separate them at a
rate of 50,000 per second. This is how the scientists will separate stem cells
from patients' blood once trials are underway, to be sure that the genetic fix
in the CCR5 gene was made, and kept.
Upstairs, machines with
mazes of sterile tubes and pumps stood ready to prepare cells for CCR5-snipping.
Here, the scientists will purify the bone marrow stem cells, increasing their
numbers first to 5 per cent of total cells, up from a measly 0.1 per cent in the
starting mixture, and then to 99 per cent. At this point they can begin testing
methods to clip the cells' DNA.
When all is perfected,
the scientists will have a precise recipe for producing batches of engineered
stem cells, including exactly how long the cells should be treated, how much of
each chemical needs to be added, how pure the cells need to be, and thousands of
other details.
"We are literally
writing the book on how you do this," said David DiGiusto, director of City
of
To receive FDA approval
for clinical trials — a goal they hope to achieve in three to four years —
the researchers must prove that they can safely and reliably prepare the cells.
Once they get the green light, the first cases will probably be people like the
They'll modify the
patients' cells in the stringently sterile manufacturing lab that DiGiusto
designed with details such as cove molding and seamless floors so there are no
corners or cracks to collect dust. Anyone who enters must wear a full bunny
suit, much like the one Cannon wears in her mouse room, to keep from
contaminating the delicate cells.
Some have advertised the
effort as a quest for the elusive "C" word, but Cannon doesn't quite
see it that way.
"People say we're
trying to cure HIV," she said. "I think of it more as, we're just
trying to make the body live quite happily and healthily with a small amount of
virus."
Malaria
Carole Leach-Lemens
Published: 25 August 2010
In HIV-exposed and
HIV-infected infants aged six to 15 months breastfeeding significantly lowered
the risks of getting malaria according to Neil Vora and colleagues in a
prospective study of infants in Tororo, a high malaria transmission rural area
in south eastern Uganda, published in the advance online edition of the Journal
of Acquired Immune Deficiency Syndromes.
However the researchers
found that breastfeeding was not protective against malaria in HIV-unexposed and
HIV-infected children of 15-24 months of age.
Co-trimoxazole
prophylaxis appeared to significantly reduce the risks of malaria when comparing
HIV-unexposed infants not taking co-trimoxazole to HIV-infected or exposed
infants taking co-trimoxazole.
Breastfeeding is
recognised as being one of the most practical and cost-effective ways of
providing the best nourishment to infants, of boosting the baby’s immunity by
providing protection from infectious disease and reducing diarrhoeal diseases as
well as respiratory illnesses. Further evidence has shown that stopping
breastfeeding early increases morbidity and mortality rates among children born
to HIV-infected mothers.
The World Health
Organization (WHO) now recommends that HIV-infected mothers exclusively
breastfeed their infants who are HIV-uninfected or of unknown status “for the
first six months of life, introducing appropriate complementary foods
thereafter, and to continue breastfeeding for the first 12 months of life.”
WHO also recommends that
all HIV-infected and mothers who are nursing take co-trimoxazole prophylaxis
(also known as trimethoprim-sulfamethoxazole or TS, Bactrim, or Septra); for
infants born to HIV-infected mothers co-trimoxazole prophylaxis should start at
six weeks of age. For children who are breastfeeding prophylaxis should continue
until breastfeeding has stopped and HIV negative status is confirmed.
Co-trimoxazole
prophylaxis is known to reduce malaria incidence in both HIV-infected adults and
children. In vitro studies have shown that breast milk proteins contain
antimalarial properties.
Little clinical evidence
exists about the effects of breastfeeding on the incidence of malaria in
children. Data that does exist does not consider the mother’s HIV status. The
high incidence of malaria and HIV in young children across sub-Saharan
A cohort of 99
HIV-unexposed children, 202 HIV-exposed children and 45 HIV-infected children
enrolled between August 2007 and April 2008 were followed prospectively. All
children were given insecticide-treated bednets. Co-trimoxazole prophylaxis was
given to both HIV-infected and HIV-exposed infants. A malaria diagnosis was made
by the presence of fever and a positive blood smear. Monthly questionnaires were
used to determine when breastfeeding stopped.
This study was part of a
larger cohort study designed to compare the effectiveness of two different
artemisinin-based therapies for treating malaria and to measure the protective
efficacy of cotrimoxazole prophylaxis against malaria in HIV-exposed and
HIV-infected children.
The median age at
enrollment for HIV-exposed children was significantly lower than for
HIV-unexposed or HIV-infected, 3.7 (IQR:2.4-6.6), 5.6 (IQR:3.5-7.4) and 4.9
(IQR:3.0-8.3) months, respectively. HIV-infected children were more likely to
live in town compared to HIV-unexposed and exposed children (36% compared to
21%, p=0.03).
The authors found that
the link between breastfeeding and malaria varied in relation to age and use of
cotrimoxazole.
Insufficient data were
available for children HIV-unexposed between the ages of six-15 months and not
breastfeeding to evaluate an association between breastfeeding and the risk of
malaria; the majority of children in this category breastfed for 15 months or
more.
No significant difference
in the incidence of malaria was seen in this category of children
(HIV-unexposed) aged 15-24 months whether they breastfed or not (7.5 compared to
6.67 episodes for each person-year, p=0.21). Following policy guidelines these
children did not get co-trimoxazole prophylaxis.
Breastfeeding, however,
was associated with a significantly lower malaria incidence rate in HIV-exposed
children taking co-trimoxazole aged between 6-15 months (1.36 compared to 2.44
for each person-year p=0.008). Since most children in this category stopped
breastfeeding before 15 months of age, in accordance with guidelines, there was
insufficient data to evaluate the association between breastfeeding and malaria.
HIV-infected children
taking cotrimoxazole showed a greater variation of when breastfeeding stopped
compared to the other groups. In those aged between 6-15 months breastfeeding
was associated with a significantly lower incidence of malaria (1.13
compared to 3.76 for each person year, p=0.002) whereas in those aged 15-24
months there was no significant difference between those who breastfed and those
who did not. Why breastfeeding is protective in the younger age group and not
the older is uncertain.
After controlling for
age, breastfeeding status and place of residence the risk for malaria in
children taking cotrimoxazole prophylaxis (HIV-infected and HIV-exposed) was
significantly lower than in those not taking prophylaxis (HIV-unifected) RR
=0.42 95% CI: 0.34-0.52, p<0.001.
The authors also found,
unlike in adults, no association between HIV and the risk of malaria in children
aged 6-15 months of age and taking cotrimoxazole prophylaxis. They suggest this
is because of an immature immune system; infants have still to develop partial
immunity characteristic of adults after repeated exposure.
Limitations, note the
authors, include:
Sample sizes were not
based on testing the hypothesis that breastfeeding reduces the risk of malaria,
so they were unable to analyse all possible associations when disaggregating by
age and HIV status.
The observational nature
of the study meant that analyses were not adjusted for confounding factors,
including socio-economic or nutritional status. So breast-feeding could have
been a surrogate for time spent outside, or under an insecticide-treated bednet
as well as for the nutritional status of the infants. All these factors that
would affect the risk of malaria.
The authors conclude that
“breastfeeding was protective against malaria in children born to HIV-infected
mothers, but this effect faded with age.”
They stress the need for
further research to confirm their findings as well as explain how breastfeeding
is protective against malaria.
Based on their findings,
they recommend that “HIV-infected mothers should be counselled about the
importance of breastfeeding and co-trimoxazole prophylaxis to protect their
children and themselves against malaria.”
Reference
Vora N et al.
Breastfeeding and the risk of malaria in children born to HIV-infected and
uninfected mothers in rural Uganda. J Acquir Immune Defic Syndr, advance
online publication, July 28 2010.
Recurrent bacterial
pneumonia infections in people living with HIV increase the odds of developing
lung cancer, according to a study published online August 23 in the Journal of
Acquired Immune Deficiency Syndromes.
Non-AIDS-related cancers—such as liver cancer, anal cancer and lung
cancer—are a growing concern for people with HIV. Researchers have
demonstrated that the rates of all of these cancers have increased in recent
years at the same time that AIDS-related cancers have dropped. Moreover, rates
of a number of non-AIDS-related cancers are much higher in people with HIV than
their HIV-negative counterparts. Lung cancer is no exception.
In fact, studies have shown that lung cancer is now the third most common cancer
in people with HIV. What’s more, it is two to five times more likely in
HIV-positive individuals than in HIV-negative people. People with HIV are far
more likely to smoke than the general population—the leading cause of lung
cancer in the
To help understand this phenomenon, Fatma M. Shebl, MD, PhD, and her colleagues
from the National Cancer Institute in
They found that recurrent bacterial pneumonia—defined as at least two episodes
of bacterial pneumonia in one year—was strongly associated with an increased
lung cancer risk, while tuberculosis and PCP were not. People who’d
experienced recurrent bacterial pneumonia were 63 percent more likely to develop
lung cancer than people who’d not had recurrent pneumonia. The odds of
developing lung cancer were even higher among people younger than 50 who’d
developed recurrent bacterial pneumonia.
Shebl and her colleagues did not have data on the smoking habits of the people
they studied, so they could not directly control for smoking in their analysis.
They did, however, conduct several analyses that assumed varying rates of
smoking among the cohort. When the team factored in smoking in this way, they
found that the increased risk from recurrent bacterial pneumonia—while still
strong—was no longer statistically significant, meaning that the association
could have occurred by chance.
“Lung cancer risk was significantly elevated among [people with an AIDS
diagnosis] who had recurrent pneumonia, suggesting a role for pulmonary
infections and inflammation in lung carcinogenesis,” they concluded.
“Additional studies utilizing biological markers for pulmonary infections and
inflammation, along with detailed information on smoking behaviors, are needed
to further characterize the mechanisms of increased lung cancer risk among
[people with HIV].”
By Catherine Hood on Aug
29, 2010
Dear Dr Cath,
What are the chances of
catching HIV through oral sex?
I use condoms for sex
with my boyfriend but have oral sex without.
Am I putting myself at
really bad risk?
I know there's something
you can use but I don't like the thought of using a plastic dam.
Dear reader,
It's difficult to
quantify the risk of catching HIV through oral sex because most people who catch
the virus have had unprotected intercourse too.
There are a few cases
reported in
Think of oral sex as
safer sex rather than safe sex.
The risks of catching HIV
are small but can be increased if you have sore of bleeding gums or cuts and
ulcers in your mouth or on your genitals.
It's also best not to
brush your teeth just before giving someone oral sex as this can inflame your
gums.
Using a dental dam would
be a safer option.
This is a sheet of latex
that he places between his mouth and your vulva when giving you head.
Latex friendly flavoured
lubricants may help with the taste. Likewise use flavoured condoms on him. You
may not like the taste but they will keep you safe.