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Crucell « Terug naar discussie overzicht

Crucell Vaccine Stops AIDS in Monkeys

41 Posts, Pagina: 1 2 3 » | Laatste

Omlaag ↓

maxen 10 november 2008 09:08

www.bloomberg.com/apps/news?pid=20601...

Crucell Vaccine Stops AIDS in Monkeys, Harvard Scientist Says
By Simeon Bennett

Nov. 9 (Bloomberg) -- Crucell NV's experimental AIDS vaccine kept six monkeys from getting an animal equivalent of the disease, suggesting a decades-long search for ways to stop the deadly infection isn't yet at a dead end.

Researchers from Leiden, Netherlands-based Crucell and Beth Israel Deaconess Medical Center in Boston reduced levels of simian immunodeficiency virus, or SIV, in the monkeys as much as 250-fold and held off AIDS for more than 500 days, according to a report in the online edition of the journal Nature. They're now testing a similar form of the vaccine in 48 healthy people.

Last year, a vaccine being developed by New York-based Merck & Co., which had also appeared to benefit monkeys, failed in human testing. The problems appeared linked to a cold virus in the vaccine, which unexpectedly raised people's risk of getting AIDS. While the initial Crucell-Harvard vaccine recipe won't be used in humans because it contains the same cold virus, it does offer some promise, said Dan Barouch, the lead author and a virologist at Harvard University and Beth Israel.

``Our new data suggests we're not at the end of the road when it comes to vaccine development,'' he said in a Nov. 7 telephone interview.

Crucell is a biotechnology company that markets vaccines and antibodies to treat infectious diseases such as influenza, hepatitis A and B, and typhoid fever. The company's best-selling product is Quinvaxem, a liquid vaccine co-developed with Basel, Switzerland-based Novartis AG and launched in 2006 that protects against five childhood diseases.

Last month, Crucell month won a $30-million U.S. contract to develop vaccine to fight the Ebola and Marburg viruses.

HIV, the human immunodeficiency virus that causes AIDS, infects 2.7 million people each year, mostly in Africa.

Strong Immune Response

Barouch achieved the result by giving the monkeys two disabled cold-causing viruses six months apart. Each of these ``ferry'' viruses contained a hidden cargo: a single SIV protein that prompted the animals to produce masses of so-called ``killer T-cells'' that are primed to hunt and destroy SIV- infected cells.

A year after the first shots, the researchers gave the monkeys a lethal dose of SIV, and found their T-cells reduced SIV viral levels as much as 250-fold, stopping its spread and preventing the animals from progressing to simian-AIDS. Four of six monkeys who received placebo shots were dead by about 350 days.

``It certainly is better than the previous animal models, but we still don't know -- and it's a big if - whether this is going to translate into a meaningful and useful human model,'' Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, said in a Nov. 7 telephone interview.

Rare Virus Used

The vaccine may have worked because the researchers used a rare virus as the ferry for the first shot called adenovirus-26, to which humans don't typically have natural immunity. The ferry virus used for the second ``booster'' shot was the more common adenovirus-5, the same one used in the failed Merck trial, against which many people are immune.

Unlike Merck's monkey studies, Barouch and colleagues used only animals lacking a genetic mutation that predisposes them to fight SIV. That makes his results the ``most robust'' in years for adenovirus-based animal trials, Fauci said.

``He stacked the cards against himself,'' he said. ``It's another step in the direction hopefully that will get us to a T- cell based vaccine that would be of some use clinically.''

Barouch's team is now testing the adenovirus-26-based shot in a patient study at Brigham and Women's Hospital in Boston. They haven't yet decided which virus to use for the second shot, though it won't be adenovirus-5, and may be Ad26, Barouch said.

Both the monkey study and the ongoing human trial are funded by grants from the U.S. National Institutes of Health.

To contact the reporter on this story: Simeon Bennett in Singapore at sbennett9@bloomberg.net

Last Updated: November 9, 2008 13:00 ES

(van het HIV draadje)

maxen 10 november 2008 09:10

www.nature.com/nature/journal/vaop/nc...

Immune control of an SIV challenge by a T-cell-based vaccine in rhesus monkeys

Jinyan Liu1, Kara L. O'Brien1, Diana M. Lynch1, Nathaniel L. Simmons1, Annalena La Porte1, Ambryice M. Riggs1, Peter Abbink1, Rory T. Coffey1, Lauren E. Grandpre1, Michael S. Seaman1, Gary Landucci2, Donald N. Forthal2, David C. Montefiori3, Angela Carville4, Keith G. Mansfield4, Menzo J. Havenga5, Maria G. Pau6, Jaap Goudsmit6 & Dan H. Barouch1

1. Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA
2. University of California, Irvine School of Medicine, Irvine, California 92697, USA
3. Duke University Medical Center, Durham, North Carolina 27710, USA
4. New England Primate Research Center, Southborough, Massachusetts 01772, USA
5. TNO Biosciences, 2301 CE, Leiden, The Netherlands
6. Crucell Holland BV, 2301 CA, Leiden, The Netherlands

A recombinant adenovirus serotype 5 (rAd5) vector-based vaccine for HIV-1 has recently failed in a phase 2b efficacy study in humans1, 2. Consistent with these results, preclinical studies have demonstrated that rAd5 vectors expressing simian immunodeficiency virus (SIV) Gag failed to reduce peak or setpoint viral loads after SIV challenge of rhesus monkeys (Macaca mulatta) that lacked the protective MHC class I allele Mamu-A*01 (ref. 3). Here we show that an improved T-cell-based vaccine regimen using two serologically distinct adenovirus vectors afforded substantially improved protective efficacy in this challenge model. In particular, a heterologous rAd26 prime/rAd5 boost vaccine regimen expressing SIV Gag elicited cellular immune responses with augmented magnitude, breadth and polyfunctionality as compared with the homologous rAd5 regimen. After SIVMAC251 challenge, monkeys vaccinated with the rAd26/rAd5 regimen showed a 1.4 log reduction of peak and a 2.4 log reduction of setpoint viral loads as well as decreased AIDS-related mortality as compared with control animals. These data demonstrate that durable partial immune control of a pathogenic SIV challenge for more than 500 days can be achieved by a T-cell-based vaccine in Mamu-A*01-negative rhesus monkeys in the absence of a homologous Env antigen. These findings have important implications for the development of next-generation T-cell-based vaccine candidates for HIV-1.

eddy59 10 november 2008 09:18

Super bericht, veel toegevoegde waarde voor Crucell.
Eigenlijk wel logisch om met een voor mensen redelijk onbekend virus te werken als transport middel.
Zolang dit virus onbekend blijft heeft het grote kans op slagen denk ik.

[verwijderd] 10 november 2008 09:43

www.reuters.com/article/marketsNews/i...

Souped-up immune cells catch even disguised HIV
WASHINGTON, Nov 9 (Reuters) - Genetically engineered immune cells can spot the AIDS virus even when it tries to disguise itself, offering a potential new way to treat the incurable infection, researchers reported on Sunday.

The killer T-cells, dubbed "assassin" cells, were able to recognize other cells infected by HIV and slow the spread of the virus in lab dishes.

If the approach works in people, it might provide a new route of treating infection with the deadly human imunnodeficiency virus, the researchers in the United States and Britain said.

"Billions of these anti-HIV warriors can be generated in two weeks," said Angel Varela-Rohena of the University of Pennsylvania, who helped lead the study.

In a second, unrelated report, researchers testing Dutch biotechnology firm Crucell NV's (CRCL.AS: Quote, Profile, Research, Stock Buzz) (CRXL.O: Quote, Profile, Research, Stock Buzz) experimental AIDS vaccine said it prevented infection in six monkeys.

The animals were infected with a monkey version of HIV called SIV, and the vaccine used a virus that is dangerous to use in humans, so it is not ready for human tests.

But, writing in the journal Nature, Dr. Dan Barouch of Beth Israel Deaconess Medical Center and Harvard Medical School in Boston and colleagues said it shows there is still hope for developing a vaccine against AIDS.

The AIDS virus, which infects 33 million people globally, is especially hard to fight. Like all viruses, it hijacks cells in its victims, forcing them to become little viral factories and make more virus.

ESCAPE AND EVADE

HIV is even more insidious, attacking immune system cells called CD4 T cells, which help mount a defense. It can also disguise itself to escape CD8 killer cells, also known as cytotoxic T lymphocytes or CTLs.

"CTLs are crucial for the control of HIV infection. Unfortunately, HIV has an arsenal of mutational and nonmutational strategies that aid it in escaping from the CTL response mounted against it by its host," the researchers wrote in their report, published in the journal Nature Medicine.

One good defense allows HIV to hide a protein called HLA-I-associated antigen.

Varela-Rohena and colleagues took T-cells from an HIV patient and created a genetically engineered version that recognizes this deception.

"It is possible to improve on nature when it comes to preventing HIV CTL escape," they wrote.

Not only could the engineered T-cells see HIV strains that had escaped detection by natural T-cells, "but the engineered T cells responded in a much more vigorous fashion so that far fewer T-cells were required to control infection," Penn's James Riley, who also worked on the study, said in a statement. Continued...

[verwijderd] 10 november 2008 09:43

"In the face of our engineered assassin cells, the virus will either die or be forced to change its disguises again, weakening itself along the way," added Andy Sewell of Britain's Cardiff University.

Perhaps having to mutate will weaken the virus, the researchers said.

They plan to test the T-cell treatment in HIV patients next year.

"We have managed to engineer a receptor that is able to detect HIV's key fingerprints and is able to clear HIV infection in the laboratory," said Bent Jakobsen, chief scientific officer at Adaptimmune Ltd, a British company launched in July that owns the rights to the technology. "If we can translate those results in the clinic, we could at last have a very powerful therapy on our hands." (Reporting by Maggie Fox; Editing by Cynthia Osterman)

[verwijderd] 10 november 2008 10:05

Tests on cell therapy to fight HIV

James Randerson, science correspondent guardian.co.uk, Monday November 10 2008 00.01 GMT The Guardian, Monday November 10 2008 Article history

Researchers have developed a new "assassin cell" therapy for treating HIV which involves engineering the patient's own immune system to fight the virus more effectively.

The therapy - which has proved effective in laboratory tests using human cell cultures - will be tested in a clinical trial of 35 patients with advanced HIV infection that is due to start next summer.

Efforts to find a traditional vaccine against HIV - the virus that causes Aids - have so far drawn a blank. "HIV mutates so quickly," said Dr Bent Jakobsen at Adaptimmune, the company in Oxford that is developing the new approach. "Gradually it gets better and better at escaping the detection of the immune system."

Jakobsen and his colleagues began to pursue a different approach after investigating a patient who had resisted his HIV infection particularly effectively. "When we tested the T cells from this patient, it looked as if he was responding to a number of those variants that normally escape the immune system," he said.

T cells are components of the immune system that attack and destroy cells within the body that are infected. In this patient, the T cell receptor protein seemed particularly good at recognising HIV antigens.

The team isolated the receptor protein and then improved its ability to recognise HIV further by randomly mutating it.

Treating patients will involve taking a blood sample and adding an engineered virus containing genes for the improved T cell receptor. The patient's own T cells then take up the genes and so are equipped with the improved receptor. These cells are then injected back into the patient.

The clinical trial of 35 patients next summer will take place at the University of Pennsylvania in Philadelphia.

aossa 10 november 2008 10:37

Breng dit bericht op de voorpagina aub. => aanbevelen.

eddy59 10 november 2008 11:01

Ik heb het bericht naar het anp gestuurd.
nieuwsdienst@anp.nl
Is iedereen echt zo sloom, dit is echt big nieuws.
Veel beter dan een nieuwe licentie hier of daar.

sappas 10 november 2008 11:16

quote:
eddy59 schreef:
Ik heb het bericht naar het anp gestuurd.
nieuwsdienst@anp.nl
Is iedereen echt zo sloom, dit is echt big nieuws.
Veel beter dan een nieuwe licentie hier of daar.

Alpen 10 november 2008 11:34

quote:
sappas schreef:
Begrijp ik het goed dat het volgend jaar al op mensen wordt getest. Het zit toch pas in de beginfase van het onderzoek.

"Barouch's team is now testing the adenovirus-26-based shot in a patient study at Brigham and Women's Hospital in Boston. They haven't yet decided which virus to use for the second shot, though it won't be adenovirus-5, and may be Ad26, Barouch said."

Zie ook betreffende PB van Crucell (3 april 08)
investors.crucell.com/C/132631/PR/200...

"The phase I clinical study will be conducted at the Brigham and Women's Hospital (BWH) in Boston and will focus on assessing the safety and immunogenicity of the vaccine. The study will involve 48 healthy volunteers."

eddy59 10 november 2008 11:40

quote:
sappas schreef:
[quote=eddy59]
Ik heb het bericht naar het anp gestuurd.
nieuwsdienst@anp.nl
Is iedereen echt zo sloom, dit is echt big nieuws.
Veel beter dan een nieuwe licentie hier of daar.

Eddy er wordt weinig aandacht besteedt aan dit bericht als ik de koers zie van 10,59 en slechts een volume van
80.931

Begrijp ik het goed dat het volgend jaar al op mensen wordt getest. Het zit toch pas in de beginfase van het onderzoek.

Of lees ik het verkeerd

Groetjes,

Sappas
Inderdaad het wordt volgend jaar op mensen getest.
Vorige keer werkte het niet omdat de transporteur een bekend koude virus was waar tegen veel mensen al immune zijn. Nu gebruiken ze een vrij onbekend virus waartegen het menselijk lichaam nog geen immune stoffen heeft aangemaakt. Dit virus krijgt nu een code mee die het AIDS virus opspoort en vernietigd.
Eddy

aossa 10 november 2008 11:46

Waarom zou men persé met het Ad5 verder willen gaan (Ad5 = the most commonly used recombinant vaccine vector, adenovirus serotype 5), in deze studie mogelijk bij de herhaling van de (boost) vacinnatie.

Wat is de onderliggende reden ?
Wie en wat heeft er belang bij als zoveel mensen er reeds immuun voor zijn ?

eddy59 10 november 2008 11:50

[quote=aossa]
Waarom zou men persé met het Ad5 verder willen gaan (Ad5 = the most commonly used recombinant vaccine vector, adenovirus serotype 5), in deze studie mogelijk bij de herhaling van de (boost) vacinnatie.

Wat is de onderliggende reden ?
Wie en wat heeft er belang bij als zoveel mensen er reeds immuun voor zijn ?
Wat ik lees is dat het wel werkt zolang de dragen van de anti bodies maar onbekend is voor het menselijk lichaam zodat er een afweer reactie wordt veroorzaakt.

aossa 10 november 2008 11:57

quote:
eddy59 schreef:
[quote=aossa]
Waarom zou men persé met het Ad5 verder willen gaan (Ad5 = the most commonly used recombinant vaccine vector, adenovirus serotype 5), in deze studie mogelijk bij de herhaling van de (boost) vacinnatie.

Wat is de onderliggende reden ?
Wie en wat heeft er belang bij als zoveel mensen er reeds immuun voor zijn ?[/quote]
Wat ik lees is dat het wel werkt zolang de dragen van de anti bodies maar onbekend is voor het menselijk lichaam zodat er een afweer reactie wordt veroorzaakt.

Het Ad5 zou bij vele mensen dus niet werken wegens de vooraf opgebouwde immuniteit. Vandaar mijn vraag ... 'wie en wat heeft daar belang bij' ?

BTW @eddy59
Waarom 'quote' jij steeds in het kader ?
Antwoorden NA de laatste '/quote' aub.
Zoals je wel merkt lukt het MIJ wel !

gogogoo 10 november 2008 12:11

quote:
eddy59 schreef:
[quote=aossa]
Waarom zou men persé met het Ad5 verder willen gaan (Ad5 = the most commonly used recombinant vaccine vector, adenovirus serotype 5), in deze studie mogelijk bij de herhaling van de (boost) vacinnatie.

Wat is de onderliggende reden ?
Wie en wat heeft er belang bij als zoveel mensen er reeds immuun voor zijn ?
Wat ik lees is dat het wel werkt zolang de dragen van de anti bodies maar onbekend is voor het menselijk lichaam zodat er een afweer reactie wordt veroorzaakt.
[/quote]

eddy: even leren quoten aub. Ik heb geen idee wie wat typt.

Ga na het Quoten helemaal naar beneden in het bericht en begin pas te typen na de laatste " {/quote}". Veel succes.

eddy59 10 november 2008 12:14

[quote=aossa]
[quote=eddy59]
[quote=aossa]
Het zou dus mogelijk kunnen zijn dat ze na verloop van tijd weer een ander onbekend(griep) virusje kunnen gebruiken als transporteur voor de kuur. Het lijkt mij wel lastig om het medicijn zodanig nieuw te houden dat het voor iedere patient nieuw is en dus antistoffen gaat aanmaken.
Het klinkt in ieder geval fantastisch.
Sorry weer fout gegaan, ik ga mij beteren.

Sir Piet 10 november 2008 12:14

Ik "begrijp" dat het ad5 juist niet gebruikt zal worden maar ad26.

Alpen 10 november 2008 12:15

quote:
eddy59 schreef:
Inderdaad het wordt volgend jaar op mensen getest.

@Eddy59: Fase I is al gestart, zie eerdere posting, en
clinicaltrials.gov/ct2/show/NCT00618605

Jos

aossa 10 november 2008 12:20

Inderdaad is het ons allemaal al wel bekend.

PB Crucell April08
Start clinische test Juni08

De huidige berichten (via Bloomberg etc.) zijn naar aanleiding van publicatie in 'Nature' van gisteren zondag, 9 november.

Huppeldepepup 10 november 2008 12:31

Kopers en verkopers laten zich vandaag nauwelijks zien. Ik denk dat iedereen zijn adem inhoudt voor de cijfers morgen en weinig geboeid is door dit toch wat oude nieuws.
Eerlijk gezegd vind ik de rust voor de cijfers wel prettig. De verwachtingen zijn misschien niet té hoog gespannen.

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