Aidsepidemie afgeblazen

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Op vrijdag 25 juli 2008 16:28 schreef ATuin-hek het volgende:
Wellicht interessant voor dit topic:
http://www.nu.nl/news/167(...)t_fors_gestegen.html

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Op vrijdag 25 juli 2008 16:28 schreef ATuin-hek het volgende:
Wellicht interessant voor dit topic:
http://www.nu.nl/news/167(...)t_fors_gestegen.html

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Op vrijdag 25 juli 2008 16:34 schreef soylent het volgende:

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Als ik het artikel van de Lancet binnen heb zullen we een fijne discussie over de methodologie opzetten

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Anti-HIV therapy boosts life expectancy more than 13 years
Improvements due to modern antiretroviral cocktails
Rising life expectancies for AIDS patients.

BIRMINGHAM, Ala. – The life expectancy for patients with human immunodeficiency virus (HIV) has increased by more than 13 years since the late 1990s thanks to advancements in antiretroviral therapy, according to researchers at the University of Alabama at Birmingham (UAB) and Simon Fraser University in Vancouver, British Columbia.

Improved survival has led to a nearly 40 percent drop in AIDS deaths among 43,355 HIV-positive study participants in Europe and North America, bolstering the call for improved anti-HIV efforts worldwide, the study authors said.

The study is published in the British medical journal The Lancet. It was compiled by The Antiretroviral Therapy Cohort Collaboration, which includes UAB, Simon Fraser University and more than a dozen other research sites around the world.

The authors looked at changes in life expectancy and mortality among the 43,355 HIV patients taking a cocktail of drugs called combination antiretroviral therapy (cART). Data was compiled from a total of 14 studies in Europe and North America.

"Since their introduction in 1996 cART regimens have become more effective, better tolerated and easier to follow," said Michael Mugavero, M.D., an assistant professor in UAB's Division of Infectious Diseases and a co-author on the study.

"We are now seeing the benefits of years of research, hard work and efforts to make these medications widely available. This has led to dramatic improvements in life expectancy, but patients who start cART with more advanced HIV infection do not have the same level of benefit," Mugavero said.

The new Lancet study found cART yielded a 13.8-year life-expectancy increase – from 36.1 years in study participants who began therapy during the 1996-1999 period, to 49.9 years in participants who began therapy during the 2003-2005 period.

Despite the good results, the study found life expectancy for HIV patients is far lower on average than the general population, which includes all those with other chronic illnesses. For example, an HIV-positive patient starting cART at age 20 will live to 63, about 20 years shorter than the average life span of non-infected adults.

With nearly half of all patients diagnosed with advanced HIV infection, the life expectancy benefits of cART are not fully realized, said Mugavero and lead study author Robert Hogg, Ph.D., of Simon Fraser University. Improved AIDS testing and increased access to care is needed.

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Combo Therapy Boosts HIV Life Expectancy
Study Shows HIV Patients Are Living Longer Since Start of Antiretroviral Drug Therapy
By Jennifer Warner
WebMD Health News
Reviewed by Brunilda Nazario, MD

July 24, 2008 -- A 20-year-old diagnosed with HIV can now expect to live 13 years longer than the same person diagnosed with the virus that causes AIDS in 1996, according to a new study on HIV life expectancy.

Researchers credit the dramatic rise in life expectancy for people with HIV to advances in the "gold standard" for HIV treatment: combination antiretroviral drug therapy. The therapy utilizes a cocktail of various drugs that targets the virus in different ways to lower the level of HIV circulating in the body. The mix of drugs in the cocktail is modified as the virus becomes resistant or side effects of the HIV treatment become problematic.

The study shows that since the introduction of combination antiretroviral drug therapy for HIV in 1996, the average life expectancy has increased from 36.1 years in 1996-1999 to 49.4 years in 2003-2005. In addition, death rates for people with HIV who received combination antiretroviral drug therapy dropped by about 40% during the same period.

"These advances have transformed HIV from being a fatal disease, which was the reality for patients before the advent of combination treatment, into a long-term chronic condition," write researcher Robert Hogg, of the British Columbia Centre for Excellence in HIV/AIDS, in Vancouver, Canada and colleagues in The Lancet.
Combination Therapy and HIV Life Expectancy

Although previous studies have shown that combination antiretroviral drug therapy has led to significant increases in survival and quality of life for people with HIV, researchers say the impact on life expectancy on a population-wide level has not been examined until now.

In the study, researchers followed three groups of HIV-positive people in Europe and North America who began antiretroviral drug therapy in 1996-1999, 2000-2002, and 2003-2005, respectively. There were 18,587 patients in the first group, 13,914 patients in the second group, and 10,854 in the third group.

Overall, 4.7% of the participants died during the course of the study. The average mortality rate decreased from 16.3 deaths per 1,000 person-years in 1996-1999 to 10 deaths per 1,000 person-years in 2003-2005, a drop of about 40%.

Researchers found the average life expectancy for a 20-year-old diagnosed with HIV increased by more than 13 years during the study.

In addition, the study showed several factors were associated with HIV life expectancy, including:

* Those treated later in the course of their infection had lower life expectancy than those treated early on.
* Participants with lower infection-fighting white blood cell counts tended to have a lower life expectancy than others (32.4 years compared with 50.4 years).
* Those who became infected with HIV through injected drug use had a shorter life expectancy (32.6 years) than those who became infected with HIV in other ways (44.7 years)
* Women had a slightly longer life expectancy than men (44.2 vs. 42.8 years), which researchers say is probably due to the fact that women, on average, started their HIV treatment earlier in the course of HIV infection than men.

In a commentary that accompanies the study, David A. Cooper of the National Centre in HIV Epidemiology and Clinical Research at the University of New South Wales in Sydney, Australia, says that with the advent of combination antiretroviral therapy the outlook for people with HIV has become less bleak and diagnosis has moved away from being an immediate death sentence.

"During the past 10 years, the discourse with patients has changed. They want to know how long they have to live. They want to plan their lives better. Should they consider life insurance, health insurance, or superannuation for retirement?"

Despite these positive results, researchers say more work is needed to close a nearly two-decade gap in life expectancy: An HIV-positive person who started on combination antiretroviral drug therapy at age 20 can expect to live to age 63 compared with an HIV-negative person in a wealthy country, who can expect to live around 80 years.

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UT pathologists believe they have pinpointed Achilles heel of HIV

Human Immunodeficiency Virus (HIV) researchers at The University of Texas Medical School at Houston believe they have uncovered the Achilles heel in the armor of the virus that continues to kill millions.

The weak spot is hidden in the HIV envelope protein gp120. This protein is essential for HIV attachment to host cells, which initiate infection and eventually lead to Acquired Immunodeficiency Syndrome or AIDS. Normally the body's immune defenses can ward off viruses by making proteins called antibodies that bind the virus. However, HIV is a constantly changing and mutating virus, and the antibodies produced after infection do not control disease progression to AIDS. For the same reason, no HIV preventative vaccine that stimulates production of protective antibodies is available.

The Achilles heel, a tiny stretch of amino acids numbered 421-433 on gp120, is now under study as a target for therapeutic intervention. Sudhir Paul, Ph.D., pathology professor in the UT Medical School, said, "Unlike the changeable regions of its envelope, HIV needs at least one region that must remain constant to attach to cells. If this region changes, HIV cannot infect cells. Equally important, HIV does not want this constant region to provoke the body's defense system. So, HIV uses the same constant cellular attachment site to silence B lymphocytes - the antibody producing cells. The result is that the body is fooled into making abundant antibodies to the changeable regions of HIV but not to its cellular attachment site. Immunologists call such regions superantigens. HIV's cleverness is unmatched. No other virus uses this trick to evade the body's defenses."

Paul is the senior author on a paper about this theory in a June issue of the journal Autoimmunity Reviews. Additional data supporting the theory are to be presented at the XVII International AIDS Conference Aug. 3-8 in Mexico City in two studies titled "Survivors of HIV infection produce potent, broadly neutralizing IgAs directed to the superantigenic region of the gp120 CD4 binding site" and "Prospective clinical utility and evolutionary implication of broadly neutralizing antibody fragments to HIV gp120 superantigenic epitope."

First reported in the early 1980s, HIV has spread across the world, particularly in developing countries. In 2007, 33 million people were living with AIDS, according to a report by the World Health Organization and the United Nations.

Paul's group has engineered antibodies with enzymatic activity, also known as abzymes, which can attack the Achilles heel of the virus in a precise way. "The abzymes recognize essentially all of the diverse HIV forms found across the world. This solves the problem of HIV changeability. The next step is to confirm our theory in human clinical trials," Paul said.

Unlike regular antibodies, abzymes degrade the virus permanently. A single abzyme molecule inactivates thousands of virus particles. Regular antibodies inactivate only one virus particle, and their anti-viral HIV effect is weaker.

"The work of Dr. Paul's group is highly innovative. They have identified antibodies that, instead of passively binding to the target molecule, are able to fragment it and destroy its function. Their recent work indicates that naturally occurring catalytic antibodies, particularly those of the IgA subtype, may be useful in the treatment and prevention of HIV infection," said Steven J. Norris, Ph.D., holder of the Robert Greer Professorship in the Biomedical Sciences and vice chair for research in the Department of Pathology and Laboratory Medicine at the UT Medical School at Houston.

The abzymes are derived from HIV negative people with the autoimmune disease lupus and a small number of HIV positive people who do not require treatment and do not get AIDS. Stephanie Planque, lead author and UT Medical School at Houston graduate student, said, "We discovered that disturbed immunological events in lupus patients can generate abzymes to the Achilles heel of HIV. The human genome has accumulated over millions of years of evolution a lot of viral fragments called endogenous retroviral sequences. These endogenous retroviral sequences are overproduced in people with lupus, and an immune response to such a sequence that resembles the Achilles heel can explain the production of abzymes in lupus. A small minority of HIV positive people also start producing the abzymes after decades of the infection. The immune system in some people can cope with HIV after all."

Carl Hanson, Ph.D., who heads the Retrovirus Diagnostic Section of the Viral and Rickettsial Disease Laboratory of the California Department of Public Health, has shown that the abzymes neutralize infection of human blood cells by diverse strains of HIV from various parts of the world. Human blood cells are the only cells that HIV infects.

"This is an entirely new finding. It is a novel antibody that appears to be very effective in killing the HIV virus. The main question now is if this can be applied to developing vaccine and possibly used as a microbicide to prevent sexual transmission," said David C. Montefiori, Ph.D., director of the Laboratory for AIDS Vaccine Research & Development at Duke University Medical Center. The abzymes are now under development for HIV immunotherapy by infusion into blood. They could also be used to guard against sexual HIV transmission as topical vaginal or rectal formulations.

"HIV is an international priority because we have no defense against it," Paul said. "Left unchecked, it will likely evolve into even more virulent forms. We have learned a lot from this research about how to induce the production of the protective abzymes on demand. This is the Holy Grail of HIV research -- development of a preventative HIV vaccine."

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Op zaterdag 19 juli 2008 21:30 schreef Lambiekje het volgende:

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zijn de toetsen e, g, l, n en u niet helemaal wegsleten bij je. Het enige wat jij kan typen zijn die 5 letters.

Waarom post je nog uberhaupt?!! Maakt niet uit wat voor onderwerp, je bent ziekelijk aan het trollen. En nul komma nul inhoud aan discussie aan het meegeven. Ik weet zeer zeker dat jij geen enkele letter van dissidente kant hebt gelezen.

zielig heel zielig.

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Op dinsdag 5 augustus 2008 19:24 schreef Lambiekje het volgende:

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Geen wonder dat het niet aan Kochs postalaten doet.

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Aidsepidemie afgeblazen

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Op dinsdag 5 augustus 2008 19:24 schreef Lambiekje het volgende:

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oech wat een geblaat in de ruimte.
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Geen wonder dat het niet aan Kochs postalaten doet.

Het zogenaamde virus kan nog geen halve seconde buiten een lichaam leven. Maar kan wel in het lichaam constant van vorm en identiteit veranderen. Wat een jammerlijke kolder. Het VIRUS is nog NOOIT in een levend wezen gezien, geobserveerd en geisoleerd. Nonsense artikel dus.

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Op dinsdag 5 augustus 2008 19:24 schreef Lambiekje het volgende:

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oech wat een geblaat in de ruimte.
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Geen wonder dat het niet aan Kochs postalaten doet.

Het zogenaamde virus kan nog geen halve seconde buiten een lichaam leven. Maar kan wel in het lichaam constant van vorm en identiteit veranderen. Wat een jammerlijke kolder. Het VIRUS is nog NOOIT in een levend wezen gezien, geobserveerd en geisoleerd. Nonsense artikel dus.

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Op dinsdag 5 augustus 2008 20:26 schreef fruityloop het volgende:

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Geblaat? Nee kom jij dan eens met bronnen om je bovenstaande beweringen te staven..

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Op dinsdag 5 augustus 2008 19:24 schreef Lambiekje het volgende:

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oech wat een geblaat in de ruimte.

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[..]

Geen wonder dat het niet aan Kochs postalaten doet.

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Het zogenaamde virus kan nog geen halve seconde buiten een lichaam leven. Maar kan wel in het lichaam constant van vorm en identiteit veranderen. Wat een jammerlijke kolder. Het VIRUS is nog NOOIT in een levend wezen gezien, geobserveerd en geisoleerd. Nonsense artikel dus.

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The biological characteristics of HIV-1 primary isolates of different recombinant forms (RFs) and non-B subtypes from Galicia, Spain, were investigated and the relationships between biological phenotype and evolution of infection were determined. Peripheral blood mononuclear cells (PBMCs) were obtained during the follow-up of 32 patients infected with HIV-1 non-subtype B genetic forms, characterized in partial sequences of pol (protease-reverse transcriptase) and env V3 region: 12 (37.5%) circulating RFs (CRFs), 9 (28.1%) unique RFs (URFs), and 11(34.4%) non-B subtypes. Primary isolates were obtained by coculture with donor PBMCs. Syncytium-inducing (Sl) phenotype was examined in MT2 cell line and coreceptor use in GHOST and U87.CD4 cells. Fifty percent of tissue culture infective dose (TCID50) and viral phenotype based on V3 net charge and Geno2phenocoreceptor bioinformatic method were determined. Fifty-four HIV-1 primary isolates were obtained. CRF14_BG and BG URFs represented the largest group, being all Sl/ X4, independently of the CD4+ cell count, viral load, or the duration of infection. By contrast, 10 of 11 CRF02_AG viruses were NSI/R5. The prediction of co-receptor use was concordant with biological characterization in all NSI/R5 and in 23 of 26 SI/X4 isolates. The presence of SI/X4 or SI/X4,R5 isolates at early stages of the infection in addition to a decrease in CD4+ counts below 500 cells/μl between 2 and 6 years since diagnosis was observed in all patients infected with CRF14_BG and BG URFs. These data contrast with the usual progression in B subtype infections, in which SI/X4 viruses rarely predominate in the early years of HIV-1 infection.