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January 29, 2012)
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By Claire Bates
25th January 2012
A gum swab test used to
diagnose HIV is just as accurate as the traditional blood screening, according
to a new study.
Researchers at
The OraQuick HIV1/2 does
not use saliva, but rather absorbs antibodies directly from the blood vessels in
the mucous membranes of the mouth.
The test draws out HIV
antibodies, if they are present, from the tissues of the cheek and gum within 20
minutes.
Study leader Dr Nitika
Pant Pai, at
'Although previous studies
have shown that the oral fluid-based OraQuick HIV1/2 test has great promise,
ours is the first to evaluate its potential at a global level.'
The study, published in
this week's issue of The Lancet Infectious Diseases, has major implications for
countries that wish to adopt self-testing strategies for HIV.
The oral HIV test has
become one of the most popular tests because of its acceptability and ease of
use. It is non-invasive, pain-free, and convenient.
'Getting people to show up
for HIV testing at public clinics has been difficult because of visibility,
stigma, lack of privacy and discrimination.
'A confidential testing
option such as self-testing could bring an end to the stigmatization associated
with HIV testing', said Dr Pai.
High risk populations fuel
the expansion of HIV epidemics but they face widespread discrimination, violence
and social marginalisation from healthcare services.
UNAIDS estimates that
globally, 90 per cent of men who have sex with men lack access to the most basic
sexual health services.
'Oral HIV tests can be a
powerful tool for high risk populations, but self-testing must be accompanied by
linkage to care to achieve good health outcomes,' said the study's co-author Dr
Rosanna Peeling, at the
By PLoS Guest Blogger
January 26, 2012
Guest blogger Dr Christian
Lienhardt discusses the International Roadmap for Tuberculosis Research a
framework outlining priority areas for investment in TB research.
With 8.8 million new cases
and 1.4 million deaths worldwide in 2010, TB remains an unacceptable burden of
human suffering and loss, overwhelmingly borne by poor and vulnerable people
living in low or middle income countries. The tools available for TB control are
old, lack effectiveness, and are not readily accessible in many settings. In
most highly affected countries the diagnosis of pulmonary TB still relies on
sputum microscopy, a century old technology that only detects half of cases.
Current treatment of tuberculosis, which was developed in the 1970s, demands
close supervision, is difficult to use in people living with HIV, and cannot be
used in patients infected with multi-drug resistant strains. The only TB vaccine
(BCG), first used in 1922, is variable in its efficacy to protect adults from
pulmonary TB. More effective and widely accessible tools are needed to make a
greater impact on the global TB burden in order to reach the goal of eliminating
TB by 2050, defined as less than one case per million population in the Global
Plan to Stop TB 2011-2015.
Fortunately there is hope,
thanks to notable progress in the development of new tools for TB control over
the last decade. In diagnostics the recent introduction of Xpert MTB/RIF – a
DNA-based molecular assay that can diagnose TB and the presence of
rifampicin-resistance in 100 minutes – is a major breakthrough. For treatment,
nine new drugs are currently in phases I to III clinical trials. For vaccines,
four novel candidates are presently in phase II clinical trials and two have
recently entered phase IIb trials.
These advance alone are,
however, insufficient. A recent mathematical model suggests that to effectively
control and eliminate TB by 2050 a combined and synergistic implementation of
several novel strategies is needed. These strategies include improved diagnosis
of drug-susceptible and drug-resistant TB, shorter treatment of overt TB cases,
scaled-up treatment of latently infected persons, and mass vaccination campaigns
using a more effective vaccine. This could be obtained only through massive
synergistic efforts in all areas of research and development.
“What research is
required to Stop TB?”
Research across the full
continuum – from basic science for discovery, to development of new
diagnostics, drugs and vaccines, and their optimal uptake for better TB control
– is necessary to enable the revolution in TB control technology needed to
achieve the goal of TB elimination by 2050. For this, we need to improve our
understanding of the basic science that will fuel the development of new
diagnostics, drugs and vaccines, and we need to ensure that the newly developed
tools are acceptable and affordable to be effectively used where they are
needed. To achieve these objectives all aspects of research must be properly
addressed and funded in a harmonized way.
To support this, the TB
Research Movement engaged in the development of a coherent and comprehensive
roadmap for global TB research towards TB elimination that encompasses all
aspects of research. This roadmap was developed through a coordinated process
including a multidisciplinary
This roadmap provides an
architecture on which transformational and outcome-oriented research areas can
be constructed. It is intended to promote organization of cross-disciplinary
teams and attract all research-related constituents to the field, especially
those in BRICS countries, who have a vital role to play. It provides a common
platform for donors, researchers, implementers, and advocates by identifying the
most important research questions.
The roadmap appears at a
critical moment, when funding for TB research has flattened for the first time
since 2005. A report released recently by the Treatment Action Group and
the Stop TB Partnership found that in 2010 just US$ 617.1 million was spent on
TB research and development globally, down 0.3% compared to 2009 funding levels
– while the Global Plan to Stop TB 2011-2015 calls for at least US$ 9.8
billion in TB research funds over the plan’s five-year period. It is hoped
that the research roadmap will serve as a framework for concrete actions to
synergize TB research efforts globally and catalyse the development of new
research collaborations to address difficult and as yet unanswered questions in
TB.
Dr. Christian
Lienhardt is Senior Scientific Advisor at the Stop TB Partnership and
WHO and responsible for the TB Research Movement. He has been coordinating the
development and production of the International Roadmap for Tuberculosis
Research that is presented here.
The cells that make it
possible for the immune system to remember previous attackers pack themselves
full of energy-making units known as mitochondria, (green). The extra
mitochondria may give memory T cells (right) the staying power to live much
longer than the T cells that actively fight pathogens (left). (Credit: Erika
Pearce)
WASHINGTON U.-ST. LOUIS
(US) — After defeating an infection, the immune system creates a memory of the
vanquished attacker to make it easier to identify and eliminate it in the
future.
New research finds the
cells that store these memories—memory T cells—are able to enhance their own
survival by packing themselves full of mitochondria—energy generators that
help the cells live a long time and allow them to recognize a returning invader.
The findings, published in
the journal Immunity, may aid efforts to develop vaccines and to direct the
immune system to attack cancers.
Cells typically get most
of their energy from glucose and other sugars. When those fuels run low and
oxygen is still available, mitochondria allow cells to make energy efficiently
from alternative fuel sources such as fats and amino acids.
DOI:
10.1016/j.immuni.2011.12.007
“These extra
mitochondria provide the memory T cells with the flexibility to sustain
themselves on a variety of energy sources,” says senior author Erika Pearce,
assistant professor of pathology and immunology at
T cells have multiple jobs
in fighting infection, including recognizing an invader, secreting signals that
help mobilize other immune cells and regulating the immune response to minimize
collateral damage to the body. To do these jobs, they differentiate into various
specialized T cell types, such as the memory T cell.
In earlier research,
Pearce showed that when memory T cells develop as a result of an infection, they
change the way they generate energy. Her data suggested that mitochondria likely
play an important part in this metabolic switch.
For the new study, Rianne
van der Windt, a postdoctoral researcher in Pearce’s lab, gave a drug that
forces mitochondria to work at maximum capacity to T cells that had never
encountered a pathogen, T cells that specialized in actively fighting infection
and memory T cells. She monitored the cells’ consumption of oxygen, an
indicator of how much they are using their mitochondria to make energy.
Memory T cells were the
only T cells to significantly increase their consumption of oxygen after
exposure to the drug, suggesting that they somehow maintained a considerable
reserve energy-generating capacity in their mitochondria that the other T cells
lacked.
When van der Windt
measured numbers of mitochondria in the T cells, she found that memory T cells
had many more mitochondria. She hypothesized the extra energy generating
capacity that comes with more mitochondria allows memory T cells to live for
long periods of time and to power-up again if an invader is re-encountered.
“In follow-up
experiments, we showed that production of additional mitochondria is triggered
by interleukin-15, an immune signaling factor long known to be important to
memory T cells,” says Pearce. “We also found that by genetically
manipulating T cell’s mitochondria and causing them to switch to the
energy-making methods favored by the memory cells, we could cause a higher
percentage of undifferentiated T cells to become memory cells.”
Pearce notes that T cells
that lack extra mitochondria can rapidly proliferate when the immune system is
fighting an infection, but they die off almost as rapidly when the infection is
cleared. She thinks that further consideration of what makes T cells stable
could be helpful to researchers working to use T cells to attack tumors.
These projects typically
involve removing the patient’s T cells, training them to recognize the tumor
and exposing them to an immune signaling factor that makes the cells
proliferate. The cells are then injected back into the patient.
“If these cells are
pushed too hard and don’t see the signals that normally accompany an immune
reaction, they’re all going to die fairly quickly,” Pearce says. “To
produce a lasting and effective immune response, I think we need to pay more
attention to what the mitochondria look like in T cells.”
It may be possible to use
interleukin-15 and other agents that promote creation of mitochondria to help
these cells persist longer, Pearce says. Further studies of how mitochondria are
organized in memory T cells are under way. She is also collaborating with
vaccine researchers to see if new insights into memory cells can aid the
development of preventive treatments for pathogens that have proven difficult to
vaccinate against, such as HIV and Leishmania.