Therapeutic drug development in oncology has reached new heights in recent years with the emergence of targeted agents. To date however, clinicians have limited registered therapeutics for treatment only, i.e. trastuzumab and lapatinib. This phenomenon is not specific to breast cancer. We must ask ourselves - why is this the case? Where do the obstacles lie and what needs to change to move forward efficiently?
The answers are complex in nature and solutions involve establishing sincere partnerships. Future targeted and non-targeted therapy trials hold the key. The uptake of tissue sampling for biomarker analyses and translational research to progress the understanding of cancer biology is integral to this.
A change in direction of trial design is also required. Inherent difficulties with conventional trial design and drug evolution stratagems in their application to targeted therapeutics exist. They are part of the reasons why drugs fail at the costly phase III stage. Options include using validated alternative clinical endpoints and the neoadjuvant setting to test early drug signals.
The explosion of targeted agent trials and advances in genomics has generated vast amounts of data. However, efforts to exploit such data to improve standards in patient outcomes have lagged behind research efforts. Data sharing environments are called for involving co-operation with industry and academia to re-use data to test hypotheses, generate new biomarkers and clinical trials and set contemporary benchmarks in cancer therapy.
Collaboration must exist between pharmaceutical companies and academia. The progress of clinical trials in the future will strongly rely on co-operation between governments/regulatory bodies and the research industry to break down administrative barriers, assist in acquiring knowledge about standards of care in different countries, provide flexibility of drug registration and establish a partnered cost relationship for expensive targeted therapies.
These new streamlined drug development methods and partnerships need to be adopted by the pharmaceutical industry academia, regulatory bodies and government in order to progress effective clinical research.
Of course, the above only touches the surface of these complex issues. The many aspects involved in Barriers to Effective Care will be discussed as part of the Clinical Science Symposia on Wednesday 21 March, from 16:00 to 17:30( ESC)
27 January 2012
Los científicos piden reanudar el estudio de la gripe aviar para evitar una pandemia
El jefe de investigación de uno de los estudios que han demostrado que el virus de la gripe aviar (H5N1) puede ser transmitido a través de gotas en el aire, Yoshihiro Kawaoka, ha solicitado hoy reanudar sus ensayos clínicos, interrumpidos después de que el Gobierno de Estados Unidos pidiera a las revistas científicas Science y Nature que no publicaran los detalles de la investigación "para que no sean usados por bioterroristas".
Kawaoka, de la Universidad de Tokio (Japón) y de Wisconsin-Madison (Estados Unidos), aceptó de forma voluntaria retrasar durante 60 días la publicación de su investigación para dar tiempo al debate sobre la seguridad o el riesgo que pueda suponer hacer público su trabajo. También lo hizo Ron Fouchier, virólogo del Centro Médico Universitario Erasmus, jefe de otro equipo que también ha hallado las mutaciones que harían contagiosa la gripe aviar. Pero ahora, en declaraciones a Nature, el japonés ha decidido subrayar la importancia del estudio y asegura que detenerlo sería "irresponsable y peligroso", ya que el virus de la gripe aviar es mortal y "puede causar pandemias".
Kawaoka cita como ejemplo de la peligrosidad de este virus al brote que hubo en España durante la segunda década del siglo pasado. "Mató a un número estimado de entre 20 y 50 millones de personas en todo el mundo", mantiene. En su morfología actual solo se puede contraer a través de un contacto cercano con patos, pollos u otras aves que porten el virus, y en ningún caso puede ser traspasado a través de personas infectadas. Pero según la investigación de Kawaoka, hay tres mutaciones inducidas por el virus que pueden volverse transmisibles a través del aire entre hurones, que son considerados buenos modelos de cómo funciona la gripe en los humanos. Si esas mutaciones llegaran a transmitirse entre humanos, “podría desatarse una pandemia letal”, advierte el científico.
Desde Holanda, el virólogo Ron Fouchier defiende también la necesidad de publicar estas investigaciones. “Si no compartimos la información con el resto de la comunidad científica, será difícil prevenir una posible pandemia”, afirmó a EL PAÍS la semana pasada. “Trabajamos en condiciones de máxima seguridad biológica y hay riesgos, claro que sí. Pero es mayor el beneficio que supone prevenir una posible pandemia de gripe aviar. Estas trabas entorpecen el desarrollo científico. En EE UU, sin embargo, el peligro de bioterrorismo les parece enorme”, añadió.
Kawaoka, de la Universidad de Tokio (Japón) y de Wisconsin-Madison (Estados Unidos), aceptó de forma voluntaria retrasar durante 60 días la publicación de su investigación para dar tiempo al debate sobre la seguridad o el riesgo que pueda suponer hacer público su trabajo. También lo hizo Ron Fouchier, virólogo del Centro Médico Universitario Erasmus, jefe de otro equipo que también ha hallado las mutaciones que harían contagiosa la gripe aviar. Pero ahora, en declaraciones a Nature, el japonés ha decidido subrayar la importancia del estudio y asegura que detenerlo sería "irresponsable y peligroso", ya que el virus de la gripe aviar es mortal y "puede causar pandemias".
Kawaoka cita como ejemplo de la peligrosidad de este virus al brote que hubo en España durante la segunda década del siglo pasado. "Mató a un número estimado de entre 20 y 50 millones de personas en todo el mundo", mantiene. En su morfología actual solo se puede contraer a través de un contacto cercano con patos, pollos u otras aves que porten el virus, y en ningún caso puede ser traspasado a través de personas infectadas. Pero según la investigación de Kawaoka, hay tres mutaciones inducidas por el virus que pueden volverse transmisibles a través del aire entre hurones, que son considerados buenos modelos de cómo funciona la gripe en los humanos. Si esas mutaciones llegaran a transmitirse entre humanos, “podría desatarse una pandemia letal”, advierte el científico.
Desde Holanda, el virólogo Ron Fouchier defiende también la necesidad de publicar estas investigaciones. “Si no compartimos la información con el resto de la comunidad científica, será difícil prevenir una posible pandemia”, afirmó a EL PAÍS la semana pasada. “Trabajamos en condiciones de máxima seguridad biológica y hay riesgos, claro que sí. Pero es mayor el beneficio que supone prevenir una posible pandemia de gripe aviar. Estas trabas entorpecen el desarrollo científico. En EE UU, sin embargo, el peligro de bioterrorismo les parece enorme”, añadió.
**Publicado en "EL PAIS"
Gladstone scientists identify protein that contributes to symptoms of Parkinson's disease
Scientists at the Gladstone Institutes, an independent and nonprofit biomedical-research organization, have identified a protein that exacerbates symptoms of Parkinson's disease -- a discovery that could one day lead to new treatments for people who suffer from this devastating neurodegenerative illness. In a paper being published online in Neuron, Gladstone Investigator Anatol Kreitzer, PhD, and Talia Lerner, PhD, who worked at Gladstone while completing her graduate studies at the University of California, San Francisco (UCSF), describe how a protein called RGS4 normally helps regulate the activity of neurons in the striatum -- the part of the brain that controls movement. But in experimental models of Parkinson's disease, RGS4 does the opposite by actually contributing to problems with motor control. The result is a deterioration of movement and motor coordination, which are the hallmark symptoms of Parkinson's. More than 10 million people suffer from Parkinson's worldwide, including the boxer Muhammad Ali and the actor Michael J. Fox.
Scientists have long known that a drop in dopamine -- an important chemical in the brain -- is associated with Parkinson's. And for decades patients have taken a drug called Levodopa to boost the brain's dopamine levels. Unfortunately, however, Levodopa's efficacy begins to fade as the disease progresses. So scientists have begun looking for other targets for which they can develop new therapeutic strategies.
"About 60,000 Americans are diagnosed with Parkinson's annually, and dopamine-based therapies often do not provide a long-term solution," said Dr. Kreitzer, who is also an assistant professor of physiology and neurology at UCSF, with which Gladstone is affiliated. "Our discovery that RGS4 may play a role in the development of Parkinson's symptoms, helps us lay the groundwork for a new therapeutic strategy -- independent of dopamine."
Drs. Kreitzer and Lerner found that RGS4 is required for dopamine to regulate brain circuits during learning. But when dopamine levels drop dramatically, as in Parkinson's, RGS4 becomes overactive and disrupts these circuits -- thereby leading to Parkinson's symptoms. Therefore, they tested whether removing RGS4 could prevent these symptoms.
Drs. Kreitzer and Lerner treated mice lacking RGS4 with a chemical that lowers dopamine levels, mimicking the effects of Parkinson's. They then monitored the mice's motor skills -- including their ability to move freely in an open arena and traverse a balance beam -- and compared them to Parkinson's mice in which RGS4 remained intact.
As expected, Parkinson's mice with RGS4 intact exhibited major problems with movement. They lacked coordination and often remained frozen in place for long periods of time. When attempting to cross the balance beam, many had repeated slips and falls, while others could not even attempt the task.
But Parkinson's mice without RGS4 performed fluid, coordinated movements with no major problems, even though they also had lower dopamine levels. The vast majority crossed the balance beam without any missteps. Many of the physical traces of Parkinson's had disappeared.
"By discovering how the removal of RGS4 affects brain circuitry at the molecular level, we gained a deeper understanding of the protein's role -- both normally and in Parkinson's disease," said Dr. Lerner. "We've also shed light on a previously unknown mechanism by which the dopamine depletion causes the symptoms of Parkinson's disease. We are optimistic that our work could pave the way for a much-needed alternative to Levodopa -- such as a drug that has the ability to inactivate RGS4 in Parkinson's patients."
Scientists have long known that a drop in dopamine -- an important chemical in the brain -- is associated with Parkinson's. And for decades patients have taken a drug called Levodopa to boost the brain's dopamine levels. Unfortunately, however, Levodopa's efficacy begins to fade as the disease progresses. So scientists have begun looking for other targets for which they can develop new therapeutic strategies.
"About 60,000 Americans are diagnosed with Parkinson's annually, and dopamine-based therapies often do not provide a long-term solution," said Dr. Kreitzer, who is also an assistant professor of physiology and neurology at UCSF, with which Gladstone is affiliated. "Our discovery that RGS4 may play a role in the development of Parkinson's symptoms, helps us lay the groundwork for a new therapeutic strategy -- independent of dopamine."
Drs. Kreitzer and Lerner found that RGS4 is required for dopamine to regulate brain circuits during learning. But when dopamine levels drop dramatically, as in Parkinson's, RGS4 becomes overactive and disrupts these circuits -- thereby leading to Parkinson's symptoms. Therefore, they tested whether removing RGS4 could prevent these symptoms.
Drs. Kreitzer and Lerner treated mice lacking RGS4 with a chemical that lowers dopamine levels, mimicking the effects of Parkinson's. They then monitored the mice's motor skills -- including their ability to move freely in an open arena and traverse a balance beam -- and compared them to Parkinson's mice in which RGS4 remained intact.
As expected, Parkinson's mice with RGS4 intact exhibited major problems with movement. They lacked coordination and often remained frozen in place for long periods of time. When attempting to cross the balance beam, many had repeated slips and falls, while others could not even attempt the task.
But Parkinson's mice without RGS4 performed fluid, coordinated movements with no major problems, even though they also had lower dopamine levels. The vast majority crossed the balance beam without any missteps. Many of the physical traces of Parkinson's had disappeared.
"By discovering how the removal of RGS4 affects brain circuitry at the molecular level, we gained a deeper understanding of the protein's role -- both normally and in Parkinson's disease," said Dr. Lerner. "We've also shed light on a previously unknown mechanism by which the dopamine depletion causes the symptoms of Parkinson's disease. We are optimistic that our work could pave the way for a much-needed alternative to Levodopa -- such as a drug that has the ability to inactivate RGS4 in Parkinson's patients."
*Source: Gladstone Institutes
Mechanism sheds light on how the brain adapts to stress
Scientists now have a better understanding of the way that stress impacts the brain. New research, published by Cell Press in the January 26 issue of the journal Neuron, reveals pioneering evidence for a new mechanism of stress adaptation and may eventually lead to a better understanding of why prolonged and repeated exposure to stress can lead to anxiety disorders and depression. Most stressful stimuli cause the release of corticotropin-releasing hormone (CRH) from neurons in the brain. This is typically followed by rapid changes in CRH gene expression. In more practical terms, as soon as the CRH-containing neurons run out of CRH, they are already receiving directions to make more. CRH controls various reactions to stress, including immediate "fight-or-flight" responses as well as more delayed adaptive responses in the brain. Regulation of CRH activity is critical for adaptation to stress, and abnormal regulation of CRH is linked with multiple human psychiatric disorders.
"Despite the wealth of information regarding the physiological role of CRH in mediating the response to stress, the molecular mechanisms that regulate expression of the CRH gene, and thereby CRH synthesis, have remained largely elusive," explains senior study author, Dr. Gil Levkowitz, from the Weizmann Institute of Science in Israel. "In our study, we used mouse and zebrafish model systems to identify a novel intracellular signaling pathway that controls stress-induced CRH gene expression."
Dr. Levkowitz and colleagues discovered that the protein Orthopedia (Otp), which is expressed in parts of the brain associated with stress adaptation, modulated CRH gene expression and was required for stress adaptation. The researchers went on to show that Otp regulates production of two different receptors on the neurons' surface. The receptors, which receive and relay CRH production instructions, essentially function as "ON" and "OFF" switches.
"This regulation of the CRH gene is critical for neuronal adaptation to stress. Failure to activate or terminate the CRH response can lead to chronic over- or under-activation of stress-related brain circuits, leading to pathological conditions," concludes Dr. Levkowitz. "Taken together, our findings identify an evolutionarily conserved biochemical pathway that modulates adaptation to stress."
**Source: Cell Press
"Despite the wealth of information regarding the physiological role of CRH in mediating the response to stress, the molecular mechanisms that regulate expression of the CRH gene, and thereby CRH synthesis, have remained largely elusive," explains senior study author, Dr. Gil Levkowitz, from the Weizmann Institute of Science in Israel. "In our study, we used mouse and zebrafish model systems to identify a novel intracellular signaling pathway that controls stress-induced CRH gene expression."
Dr. Levkowitz and colleagues discovered that the protein Orthopedia (Otp), which is expressed in parts of the brain associated with stress adaptation, modulated CRH gene expression and was required for stress adaptation. The researchers went on to show that Otp regulates production of two different receptors on the neurons' surface. The receptors, which receive and relay CRH production instructions, essentially function as "ON" and "OFF" switches.
"This regulation of the CRH gene is critical for neuronal adaptation to stress. Failure to activate or terminate the CRH response can lead to chronic over- or under-activation of stress-related brain circuits, leading to pathological conditions," concludes Dr. Levkowitz. "Taken together, our findings identify an evolutionarily conserved biochemical pathway that modulates adaptation to stress."
**Source: Cell Press
‘Arrugas’: el dolor pasa del cómic al cine
Paco Roca (Valencia, 1969) nunca lo tuvo claro. “Me llamaban los productores, pero las propuestas desaparecían, no acababan de cuajar”. El objetivo era su cómic Arrugas (2007), una singular reflexión sobre el daño que provoca el alzhéimer, y que se convirtió en un éxito de ventas: 20.000 ejemplares, una cantidad increíble en España. “Yo creo que el público español poco a poco va abriéndose a nuestros trabajos, que lee más tebeos que los de superhéroes. Compra María y yo, Píldoras azules… No tendremos las tiradas de mercados como el francés, pero crecemos”. Arrugas, inspirado en las vivencias del padre de un amigo de Roca, y de la gente que le rodeaba, le reportó el Premio Nacional de Cómic. Mientras, Roca siguió con sus trabajos: Memorias de un hombre en pijama o El invierno del dibujante son otros dos grandes ejemplos de un talento que empezó a ser conocido en el año 2000 con GOG.
Y llegó el productor Manuel Cristóbal y se empecinó en que Arrugas fuera una película de animación dirigida por Ignacio Ferreras. El resultado, que se puede ver desde hoy en los cines, y que ha logrado ser precandidato al Oscar y candidato a dos goyas: filme de animación y guion adaptado, lo explica el mismo Paco Roca en el video.
**Publicado en "EL PAIS"
Y llegó el productor Manuel Cristóbal y se empecinó en que Arrugas fuera una película de animación dirigida por Ignacio Ferreras. El resultado, que se puede ver desde hoy en los cines, y que ha logrado ser precandidato al Oscar y candidato a dos goyas: filme de animación y guion adaptado, lo explica el mismo Paco Roca en el video.
**Publicado en "EL PAIS"
Protein in the brain could be a key target in controlling Alzheimer's
A protein recently discovered in the brain could play a key role in regulating the creation of amyloid beta, the major component of plaques implicated in the development of Alzheimer's disease, according to researchers at Temple University's School of Medicine. A group led by Domenico Pratico, professor of pharmacology and microbiology and immunology at Temple, discovered the presence of the protein, called 12/15-Lipoxygenase, in the brain three years ago.
"We found this protein to be very active in the brains of people who have Alzheimer's disease," said Pratico. "But three years ago, we didn't know the role it played in the development of the disease."
Following two years of study, the Temple researchers have found that the protein is at the top of a pathway and controls a biochemical chain reaction that begins the development of Alzheimer's.
Pratico said that their research has shown that 12/15-Lipoxygenase controls Beta secretase (BACE-1), an enzyme that is key to the development of amyloid plaques in Alzheimer's patients.
"For reasons we don't yet know, in some people, 12/15-Lipoxygenase starts to work too much," he said. "By working too much, it sends the wrong message to the Beta secretase, which in turn starts to produce more amyloid Beta. This initially results in cognitive impairment, memory impairment and, later, an increase of amyloid plaque."
BACE-1 has long been a biological target for researchers seeking to create a drug against Alzheimer's disease, said Pratico. But because little has been known about how it functions, they have been unsuccessful developing a molecule that could reach the brain and block it.
"We now know much better how Beta secretase works because we have found that the 12/15-Lipoxygenase protein is a controller of BACE functions," he said. "You don't need to target the Beta secretase directly because the 12/15-Lipoxygenase is really the system in the brain that tells BACE to work more or work less."
Pratico said that they have validated 12/15-Lipoxygenase as a target for a potential Alzheimer drug or therapy.
"By modulating BACE levels and activity through controlling the 12/15-Lipoxygenase, we can potentially improve the cognitive part of the phenotype of the disease, and prevent the accumulation of amyloid beta inside the neurons, which will eventually translate into less of those plaques," he said. "This is a totally new mechanism for controlling BACE."
Pratico said his group has looked at an experimental compound that blocks 12/15-Lipoxygenase function as a potential therapy to inhibit BACE function in the brain. In their lab, using animal models, they saw the drug's ability to restore some cognitive function, as well as improve learning and memory ability.
"There is an opportunity here to study this molecule and develop an even stronger molecule to target 12/15-Lipoxygenase function in the brain," he said.
**Source: Temple University
"We found this protein to be very active in the brains of people who have Alzheimer's disease," said Pratico. "But three years ago, we didn't know the role it played in the development of the disease."
Following two years of study, the Temple researchers have found that the protein is at the top of a pathway and controls a biochemical chain reaction that begins the development of Alzheimer's.
Pratico said that their research has shown that 12/15-Lipoxygenase controls Beta secretase (BACE-1), an enzyme that is key to the development of amyloid plaques in Alzheimer's patients.
"For reasons we don't yet know, in some people, 12/15-Lipoxygenase starts to work too much," he said. "By working too much, it sends the wrong message to the Beta secretase, which in turn starts to produce more amyloid Beta. This initially results in cognitive impairment, memory impairment and, later, an increase of amyloid plaque."
BACE-1 has long been a biological target for researchers seeking to create a drug against Alzheimer's disease, said Pratico. But because little has been known about how it functions, they have been unsuccessful developing a molecule that could reach the brain and block it.
"We now know much better how Beta secretase works because we have found that the 12/15-Lipoxygenase protein is a controller of BACE functions," he said. "You don't need to target the Beta secretase directly because the 12/15-Lipoxygenase is really the system in the brain that tells BACE to work more or work less."
Pratico said that they have validated 12/15-Lipoxygenase as a target for a potential Alzheimer drug or therapy.
"By modulating BACE levels and activity through controlling the 12/15-Lipoxygenase, we can potentially improve the cognitive part of the phenotype of the disease, and prevent the accumulation of amyloid beta inside the neurons, which will eventually translate into less of those plaques," he said. "This is a totally new mechanism for controlling BACE."
Pratico said his group has looked at an experimental compound that blocks 12/15-Lipoxygenase function as a potential therapy to inhibit BACE function in the brain. In their lab, using animal models, they saw the drug's ability to restore some cognitive function, as well as improve learning and memory ability.
"There is an opportunity here to study this molecule and develop an even stronger molecule to target 12/15-Lipoxygenase function in the brain," he said.
**Source: Temple University
Un metaanálisis confirma que el test de saliva para detectar el VIH tiene una precisión del 98%
Un test de saliva en lugar del análisis de sangre para detectar el virus del sida. Según un metaanálisis publicado esta semana en la revista 'The Lancet Infectious Diseases', esta herramienta tiene una precisión muy similar a la prueba tradicional, basada en el estudio de una muestra de sangre.
"Aunque estudios anteriores han demostrado que este test (OraQuick HIV 1/2) es prometedor, el nuestro es el primero que evalúa su potencial global", afirma Nikita Pant Pai, principal autora de la investigación y científico médico de la McGill University Health Centre (MUHC), en Canadá. Se trata de un trabajo que compara análisis de todo el mundo que valoran la sensibilidad del test oral. Así es como Pant Pai y su equipo han concluido que esta prueba tiene una precisión del 99% en poblaciones de alto riesgo y del 97% en población de bajo riesgo.
Esta prueba cuenta con el visto bueno tanto de la agencia estadounidense del medicamento (FDA) como de la europea (EMA). De hecho, "en España se está utilizando para hacer cribados en grandes poblaciones, en narcosalas... Es muy útil para hacer diagnóstico rápido a muchas personas y a bajo coste", señala Juan Carlos López Bernaldo de Quirós, especialista de la unidad de Enfermedades Infecciosas del Hospital Gregorio Marañón de Madrid. "No exite riesgo para la persona que realiza el test y, dado que hay mucha gente rehacia a los pinchazos, también reduce el número de rechazos por esta cuestión".
La prueba, como recalcan los autores del metaanálisis, no es invasiva ni duele. Consiste en frotar con una pequeña paleta las encías para obtener una muestra de fluido oral y sumergirlo después en una solución. En una media de 20 minutos, el resultado estará listo.
Dado que cualquiera podría realizar esta prueba, planteada como auto-test, "es una opción confidencial que podría acabar con la estigmatización asociada a las pruebas para detectar el VIH", puntualiza Pant Pai. Hasta ahora, "conseguir que la gente se someta al cribado en las clínicas ha sido difícil por la visibilidad, el estigma y la discriminación".
Las ventajas son especialmente significativas en países subdesarrollados con alta prevalencia de esta infección, como África Subsahariana. "Además de facilitar el tratamiento rápido de los afectados, no requiere la intervención de personal sanitario, ni jeringa ni aguja, resulta más barato".
En cualquier caso, y de momento, "los test rápidos con resultado positivo deben ser confirmados con el análisis tradicional de sangre (prueba denominada ELISA), que tarda entre tres y cuatro días", matiza el doctor López Bernaldo de Quirós.
**Publicado en "EL MUNDO"
"Aunque estudios anteriores han demostrado que este test (OraQuick HIV 1/2) es prometedor, el nuestro es el primero que evalúa su potencial global", afirma Nikita Pant Pai, principal autora de la investigación y científico médico de la McGill University Health Centre (MUHC), en Canadá. Se trata de un trabajo que compara análisis de todo el mundo que valoran la sensibilidad del test oral. Así es como Pant Pai y su equipo han concluido que esta prueba tiene una precisión del 99% en poblaciones de alto riesgo y del 97% en población de bajo riesgo.
Esta prueba cuenta con el visto bueno tanto de la agencia estadounidense del medicamento (FDA) como de la europea (EMA). De hecho, "en España se está utilizando para hacer cribados en grandes poblaciones, en narcosalas... Es muy útil para hacer diagnóstico rápido a muchas personas y a bajo coste", señala Juan Carlos López Bernaldo de Quirós, especialista de la unidad de Enfermedades Infecciosas del Hospital Gregorio Marañón de Madrid. "No exite riesgo para la persona que realiza el test y, dado que hay mucha gente rehacia a los pinchazos, también reduce el número de rechazos por esta cuestión".
La prueba, como recalcan los autores del metaanálisis, no es invasiva ni duele. Consiste en frotar con una pequeña paleta las encías para obtener una muestra de fluido oral y sumergirlo después en una solución. En una media de 20 minutos, el resultado estará listo.
Dado que cualquiera podría realizar esta prueba, planteada como auto-test, "es una opción confidencial que podría acabar con la estigmatización asociada a las pruebas para detectar el VIH", puntualiza Pant Pai. Hasta ahora, "conseguir que la gente se someta al cribado en las clínicas ha sido difícil por la visibilidad, el estigma y la discriminación".
Las ventajas son especialmente significativas en países subdesarrollados con alta prevalencia de esta infección, como África Subsahariana. "Además de facilitar el tratamiento rápido de los afectados, no requiere la intervención de personal sanitario, ni jeringa ni aguja, resulta más barato".
En cualquier caso, y de momento, "los test rápidos con resultado positivo deben ser confirmados con el análisis tradicional de sangre (prueba denominada ELISA), que tarda entre tres y cuatro días", matiza el doctor López Bernaldo de Quirós.
**Publicado en "EL MUNDO"
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