leandrosmemorybox

nychealth:

Let’s stop HIV in New York City

  • If you are HIV-negative, PEP and PrEP can help you stay that way.
  • If you are HIV-positive, PEP and PrEP can help protect your partners.

Daily PrEP

PrEP is a daily pill that can help keep you HIV-negative as long as you take it every day.

  • Ask your doctor if PrEP (Pre-exposure Prophylaxis) may be right for you.
  • Condoms give you additional protection against HIV, other sexually transmitted infections, and unintended pregnancy.

Emergency PEP

If you are HIV-negative and think you were exposed to HIV, immediately go to a clinic or emergency room and ask for PEP (Post-exposure  Prophylaxis).

  • PEP can stop HIV if started within 36 hours of exposure.
  • You continue taking PEP for 28 days.

Many insurance plans including Medicaid cover PEP and PrEP. Assistance may be available if you are uninsured. Visit NYC Health’s website to find out where to get PrEP or PEP in New York City.

neurosciencestuff
neurosciencestuff:

Why HIV patients develop dementia

Since the introduction of the combination anti-retroviral therapy (cART) in the mid-90s, the life expectancy of HIV patients has significantly improved. As a result, long-term complications are becoming more relevant: almost every second HIV patient is affected by neurocognitive disorders, which can lead to dementia. It has not as yet been fully understood how these disorders occur. Researchers from Bochum have now successfully identified mechanisms how infected cells can activate brain-specific immune cells which subsequently display harmful behaviour and lead to the destruction of neurons. These findings may help develop biomarkers to identify risk patients and to make a therapeutic strategy possible in the long term. The study was published in the trade journal “Experimental Neurology”.

Immune cells in the brain under suspicion
“HIV-associated neurocognitive disorders” (HAND) include disorders of the cognitive functions, motor capacities as well as behavioural changes. How exactly HAND occur has not, as yet, been fully understood. “Scientists assume that HIV is harmful to cells directly and that it also triggers indirect mechanisms that lead to nerve cell damage,” explains Dr Simon Faissner (RUB clinic for neurology, St. Josef-Hospital). The researchers strongly suspect that, once activated in the brain and the spinal cord, immune cells keep up a chronic inflammation level which then results in the destruction of nerve cells. An immune activation in peripheral tissue as well as therapeutic consequences may likewise contribute to nerve cell damage in the brain.
First steps of HIV infection are sufficient
The HI virus overcomes the blood-brain barrier hitchhiking on infected immune cells, the monocytes and probably the T cells. The researchers from Bochum tested the hypothesis that HIV-infected monocytes activate specific immune cells in the brain, the so-called microglial cells. These cells, in turn, respond by releasing harmful substances, such as reactive oxygen metabolites and inflammatory signalling molecules, i.e. cytokines. To test this hypothesis, the researchers developed a cell culture system in which they initially examined the effect of HIV-infected monocytes on microglial cells. The researchers simulated the individual steps of HIV infection and measured the concentration of the cytokines released at each stage. Thus, they were able to demonstrate that releasing the viral RNA in the monocytes was a sufficient trigger for maximal microglial activation. Subsequent infection phases – reverse transcription into DNA and the resulting formation of HIV proteins – did not augment activation any further.
Released substances result in neuronal cell death
In the second step, they analysed nerve cells from rat brains to determine if the substances released by the microglial cells could lead to cell death. Compared with the control group, the amount of cell death was indeed twice as high. Studies of liquor cerebrospinalis received from HIV-infected patients have shown a positive correlation with marker of neuronal degeneration in patients who did not as yet present any neurocognitive disorders.
Detailed understanding necessary for therapeutic strategies
“Thanks to our research, we have gained a better understanding of the mechanisms of HIV-associated neurodegeneration,” concludes Prof Dr Andrew Chan. “These results are likely to contribute to HAND biomarkers becoming established. In the long term, these data may be used to develop therapeutic strategies aiming at retarding HAND progression in HIV-infected patients.” Starting points may include activation of microglial cells – a method that is applied in other autoimmune diseases of the central nervous system, for example in multiple sclerosis.
Start-up through FoRUM funds
The research, which was initiated following a collaboration between clinics for neurology and dermatology, St. Josef Hospital, as well as the Department for Molecular and Medical Virology, has been made possible through start-up funding provided by the Faculty of Medicine at Ruhr-Universität (FoRUM). The collaboration has evolved into an international consortium of clinics and basic research organisations in Bochum, Langen, Strasbourg and Mailand. One objective of the follow-up study, for which an application for EU funds is pending, is going to be an in-depth analysis of inflammatory processes in the central nervous system. The researchers will attempt to inhibit inflammatory processes with different drugs. They are, moreover, planning to study direct cell-cell interaction by means of state-of-the-art microscopy, in collaboration with the University of Strasbourg.
(Image credit: Mehau Kulyk/Science Photo Library)

neurosciencestuff:

Why HIV patients develop dementia

Since the introduction of the combination anti-retroviral therapy (cART) in the mid-90s, the life expectancy of HIV patients has significantly improved. As a result, long-term complications are becoming more relevant: almost every second HIV patient is affected by neurocognitive disorders, which can lead to dementia. It has not as yet been fully understood how these disorders occur. Researchers from Bochum have now successfully identified mechanisms how infected cells can activate brain-specific immune cells which subsequently display harmful behaviour and lead to the destruction of neurons. These findings may help develop biomarkers to identify risk patients and to make a therapeutic strategy possible in the long term. The study was published in the trade journal “Experimental Neurology”.

Immune cells in the brain under suspicion

“HIV-associated neurocognitive disorders” (HAND) include disorders of the cognitive functions, motor capacities as well as behavioural changes. How exactly HAND occur has not, as yet, been fully understood. “Scientists assume that HIV is harmful to cells directly and that it also triggers indirect mechanisms that lead to nerve cell damage,” explains Dr Simon Faissner (RUB clinic for neurology, St. Josef-Hospital). The researchers strongly suspect that, once activated in the brain and the spinal cord, immune cells keep up a chronic inflammation level which then results in the destruction of nerve cells. An immune activation in peripheral tissue as well as therapeutic consequences may likewise contribute to nerve cell damage in the brain.

First steps of HIV infection are sufficient

The HI virus overcomes the blood-brain barrier hitchhiking on infected immune cells, the monocytes and probably the T cells. The researchers from Bochum tested the hypothesis that HIV-infected monocytes activate specific immune cells in the brain, the so-called microglial cells. These cells, in turn, respond by releasing harmful substances, such as reactive oxygen metabolites and inflammatory signalling molecules, i.e. cytokines. To test this hypothesis, the researchers developed a cell culture system in which they initially examined the effect of HIV-infected monocytes on microglial cells. The researchers simulated the individual steps of HIV infection and measured the concentration of the cytokines released at each stage. Thus, they were able to demonstrate that releasing the viral RNA in the monocytes was a sufficient trigger for maximal microglial activation. Subsequent infection phases – reverse transcription into DNA and the resulting formation of HIV proteins – did not augment activation any further.

Released substances result in neuronal cell death

In the second step, they analysed nerve cells from rat brains to determine if the substances released by the microglial cells could lead to cell death. Compared with the control group, the amount of cell death was indeed twice as high. Studies of liquor cerebrospinalis received from HIV-infected patients have shown a positive correlation with marker of neuronal degeneration in patients who did not as yet present any neurocognitive disorders.

Detailed understanding necessary for therapeutic strategies

“Thanks to our research, we have gained a better understanding of the mechanisms of HIV-associated neurodegeneration,” concludes Prof Dr Andrew Chan. “These results are likely to contribute to HAND biomarkers becoming established. In the long term, these data may be used to develop therapeutic strategies aiming at retarding HAND progression in HIV-infected patients.” Starting points may include activation of microglial cells – a method that is applied in other autoimmune diseases of the central nervous system, for example in multiple sclerosis.

Start-up through FoRUM funds

The research, which was initiated following a collaboration between clinics for neurology and dermatology, St. Josef Hospital, as well as the Department for Molecular and Medical Virology, has been made possible through start-up funding provided by the Faculty of Medicine at Ruhr-Universität (FoRUM). The collaboration has evolved into an international consortium of clinics and basic research organisations in Bochum, Langen, Strasbourg and Mailand. One objective of the follow-up study, for which an application for EU funds is pending, is going to be an in-depth analysis of inflammatory processes in the central nervous system. The researchers will attempt to inhibit inflammatory processes with different drugs. They are, moreover, planning to study direct cell-cell interaction by means of state-of-the-art microscopy, in collaboration with the University of Strasbourg.

(Image credit: Mehau Kulyk/Science Photo Library)

alexiustoday

Crean gel que puede prevenir la transmisión del VIH, VPH y Herpes en la vagina y el recto

alexiustoday:

Científicos del Population Council han encontrado que su gel microbicida es seguro, estable, y puede prevenir la transmisión de múltiples infecciones de transmisión sexual (ITS), tanto en la vagina como en el recto en los animales, tales como: el VIH, virus del herpes simple 2 (HSV-2), y el virus del papiloma humano (VPH). El estudio también proporciona los primeros datos de que el gel es eficaz contra múltiples cepas del VIH, y que tiene un margen de eficacia en la vagina contra los tres virus de al menos ocho horas antes de la exposición. 

image

Estos hallazgos fueron publicados recién en PLoS ONE en un artículo titulado “A Potent Combination Microbicide that Targets SHIV-RT, HSV-2 and HPV”.

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alexiustoday

Una vacuna bloquea completamente la infección por VIH en monos

alexiustoday:

Una nueva vacuna relativamente simple que se puede administrar por vía oral ha logrado bloquear completamente la infección rectal con SIV, el equivalente en monos del VIH, en macacos rhesus y ha producido una rápida re-supresión de la carga viral en los monos que fueron infectados previamente con SIV. Los resultados se publicaron recientemente en Frontiers in Immunology.

image

Read More

leandrosmemorybox

materiajunkie:

"Curing AIDS? Shit, that’s like Cadillac making a car that lasts for 50 years. And you know they can do it, but they ain’t going to do nothing that fucking dumb. Shit, they got metal on the Space Shuttle that can go around the Moon and withstand  temperatures of up to 20,000 degrees, you mean to tell me you don’t think they can make an El Dorado with a fuckin’ bumper that don’t fall off?"

- Chris Rock (“Bigger and Blacker”, 1999)

alexiustoday

El VIH o su tratamiento tienen un efecto protector contra la esclerosis múltiple

alexiustoday:

Un equipo médico australiano e investigadores británicos analizaron los registros médicos de más de 5 millones de personas y ha descubierto que, o bien el VIH o medicamentos contra el VIH tienen un efecto protector contra la esclerosis múltiple (EM). Pacientes con SIDA o personas con VIH que reciben tratamiento tienen una probabilidad del 60% menos de probabilidades de recibir un diagnóstico de EM. La investigación fue publicada el 4 agosto de 2014  en el Journal of Neurology, Neurosurgery and Psychiatry.

image

Un análisis más profundo ha descubierto que aquellos con un régimen de tratamiento más largo, por 5 años o más, tenían un 80% menos de probabilidad de desarrollar EM. El descubrimiento es notable por el hecho de que no existen tratamientos curativos o preventivos para la EM y esta visión inesperada puede ser una de las vías más interesantes.

Read More


CANCER TREATMENT CLEARS TWO AUSTRALIAN PATIENTS OF HIV

Researchers have discovered that two HIV+ Australian men who were treated with stem cell transplant for cancer — one for non-Hodgkin’s lymphoma and the other for leukaemia — have become virus-free, presumably because the donor cells carried genes that confer immunity from it.
hey are still on antiretroviral therapy (ART) “as a precaution”, but those drugs alone could not be responsible for bringing the virus to such low levels, says David Cooper, director of the Kirby Institute at the University of New South Wales in Sydney, who led the discovery. A year ago, a different group of researchers had reported cases with a similar outcome.
Cooper presented details of the cases today at a press briefing in Melbourne, Australia, where delegates are convening for next week’s 20th International AIDS Conference. The announcement came just a day after the news that at least six people heading to the conference died when a Malaysia Airlines flight was shot down in Ukraine.

The HIV virus (yellow particles), seen on a white blood cell in this scanning electron micrograph. by Thomas Deernick, NCMIR

CANCER TREATMENT CLEARS TWO AUSTRALIAN PATIENTS OF HIV

Researchers have discovered that two HIV+ Australian men who were treated with stem cell transplant for cancer — one for non-Hodgkin’s lymphoma and the other for leukaemia — have become virus-free, presumably because the donor cells carried genes that confer immunity from it.

hey are still on antiretroviral therapy (ART) “as a precaution”, but those drugs alone could not be responsible for bringing the virus to such low levels, says David Cooper, director of the Kirby Institute at the University of New South Wales in Sydney, who led the discovery. A year ago, a different group of researchers had reported cases with a similar outcome.

Cooper presented details of the cases today at a press briefing in Melbourne, Australia, where delegates are convening for next week’s 20th International AIDS Conference. The announcement came just a day after the news that at least six people heading to the conference died when a Malaysia Airlines flight was shot down in Ukraine.

  • The HIV virus (yellow particles), seen on a white blood cell in this scanning electron micrograph. by Thomas Deernick, NCMIR