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Author Topic: Vaccine and HIV science moving forward CROI 2007 in LA exciting 2 me  (Read 2481 times)

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Offline bimazek

  • Member
  • Posts: 781
This seems like good news... they have discovered ...
well.. a vaccine that can lead to longer life if given during first weeks in SIV

also other good new trends... see below...   i went thru all 1000 papers presented and found the ones that have hopeful research findings and good new science advancements...

T-Cell Based Vaccines: Promise of Clinical Efficacy?
Session Day and Time: Tuesday, 2 - 3:30 pm
Room: West Hall B
CROI 2007

How Can T-cell-based Vaccines Protect against SIV and HIV?
Mario Roederer
Vaccine Res Ctr, NIAID, NIH, Bethesda, MD, US

Background:  Acute infection by simian immunodeficiency virus (SIV) causes a massive infection of CD4 memory cells throughout the body, leading directly to their destruction. Over the first few weeks after infection, as much as 80% of the CD4 memory compartment is destroyed; this represents a significant insult to the immune system.  Indeed, the extent of the destruction of the CD4 memory compartment during this early phase predicts long-term survival. Therefore, protecting against this destruction is an important goal for prophylactic intervention, such as vaccination.

Methods:  To test this, we vaccinated nonhuman primates with a variety of vectors encoding SIV genes; these regimens induced either cellular immune responses or cellular and humoral responses.

Results:  Vaccines eliciting antigen-specific CD8 T-cell responses tempered the destruction of the CD4 memory compartment following challenge with SIV. The preservation of the memory compartment was evident at the early, post-acute time point (4 weeks), and persisted for many months. The extent of preservation was also highly inversely correlated with progression to death.

Conclusions:  These findings identify a key mechanism leading to differential rates of progression to AIDS in infected subjects. In addition, they point to the critical importance of reducing the cell-associated viral load during acute infection, through therapeutic or vaccination strategies. Finally, these studies show that a T-cell-based vaccine against HIV or SIV can have profound protective effects even in the absence of sterilizing immunity.





here a new drug that may help with the reservoirs of hiv... that is great news to me....................

A Novel Inhibitor of HIV-1 Release from Human Macrophage Reservoirs
Carolyn Luscombe*1, L Williams1, G Khoury1, D Hill2, R Ptak2, G Ewart1, and M Miller1
1Biotron Ltd, Canberra, Australia and 2Southern Res Inst, Frederick, MD, US

Background:  Current models suggest that HAART may be required for as long as 60 years in order to eradicate HIV-1 from the host. One of the major reservoirs of HIV-1 is cells of the monocyte lineage that remain generally refractory to current drug treatments. Following on from our previous findings that amiloride analogs block the Vpu ion channel activity and can inhibit HIV replication in monocyte-derived macrophages, Biotron Limited (BIT) has generated a library of >300 small-molecule compounds with significant improvements in anti-HIV-1 activity compared with the amiloride analogs.

Methods:  BIT compounds were designed to inhibit HIV-1 Vpu ion channel activity. Compounds were screened for activity in planar lipid bilayers and in our proprietary cell-based anti-Vpu assay before selected compounds were tested for ability to inhibit HIV-1BaL. Herein, we present data for BIT225 selected as our lead pre-clinical candidate based on its superior anti-HIV activity in vitro, and on its in vivo safety and pharmacology profile. Efficacy of BIT225 was also tested against other selected HIV-1 viruses, either as a stand-alone treatment or in combination with licensed antiretroviral drugs.

Results:  BIT 225 significantly reduced both the amount (measured by p24 or RT) and specific infectivity of virus particles released from HIV-1BaL infected day 14 macrophages. The EC50 for reduction of particle release was 1.1±0.4 mM and a TC50 of 212 mM, giving an antiviral index of 193, which was 16-fold greater than measured for 5-(N, N-hexamethylene) amiloride. Further studies with R5 clinical isolates and multi-drug resistant strains revealed BIT225 demonstrated broad-spectrum activity against clinical isolates from among different virus clades and selected drug resistant strains. Additionally, we investigated the ability of BIT225 to inhibit virus replication in combination with licensed HIV-1 inhibitors (efavirenz, lopinavir, or tenofovir PMPA or TDF) in HIV-1BaL-infected macrophages. Analysis of drug interactions was performed using the Prichard and Shipman MacSynergy II 3-D model for statistical evaluation of combination assays with the outcomes revealing additive or synergistic effects with no evidence of synergistic cytotoxicity with the drug concentrations evaluated.

Conclusions:  Here, we present the initial findings on our lead compound BIT225 that may represent a novel first-in-class drug with anti-HIV-1 activity.






if you catch hiv in beginning days and weeks GO ON HAART... that is how i see this........................

Slower CD4 Cell Decline following Cessation of a 3-Month Course of HAART in Primary HIV Infection
Sarah Fidler*1, G Touloumi2, J Fox1, N Pantazis2, K Porter3, A Babiker3, J Weber1, and CASCADE Collaboration
1Imperial Coll, St Mary's Hosp, London, UK; 2Athens Univ Med Sch, Greece; and 3Med Res Council Clin Trials Unit, London, UK

Background:  Our objective was to investigate whether a short course of HAART during primary HIV infection influences rate of CD4+ and viral load change.

Results:  The rate of CD4+ decline following therapy cessation appeared significantly slower among treated participants than untreated controls (losses of 51, 95%CI 32 to 69 and 77, 65 to 89 cells/μL per year, respectively) 3 years after seroconversion; p = 0.011. At the same time point viral loads appeared to differ significantly (4.09 and 4.53 for treated and untreated, respectively) although this was largely based on extrapolated data. At 2 years, there was no significant difference in mean viral load levels (4.31, 4.14 to 4.48 and 4.47, 4.28 to 4.66). CASCADE seroconverters were more likely to reach CD4 <350 cells/μL or initiate clinically indicated ART (HR 1.45, 95%CI 1.02 to 2.05; p = 0.039)

Conclusions:  A short course of ART at primary HIV infection may delay CD4+ decline. However, findings need confirmation through a randomized clinical trial powered to address definitively the role of ART intervention in primary infection; this is currently underway through SPARTAC.






I LIKE THE FRENCH AND THE CANADIANS ... ALSO ENGLISH I TRUST THEIR MED SYSTEM... THIS IS BEAUTIFUL... I LOVE THIS PHRASE THEY USE...   During long-term HAART, HIV persists latently in a small pool of resting CD4 T cells    ........................ a small pool of resting CD4 T cells   a small pool of resting CD4 T cells   a small pool of resting CD4 T cells   .... THAT SOUNDS GOOD..  sounds like something could be done about a small pool...

HIV Persistence in Patients on Long-term Effective ART: Hidden Behind a Curtain of Regulatory CD4 CD25 T Cells
Tu-Anh Tran*1, H Hendel-Chavez1, E Le Nevot1, M G de Goer de Herve1, K Abbed1, O Lambotte1, J F Delfraissy1, A M Balazuc2, J Gasnault1, and Y Taoufik1
1INSERM U802, Univ Paris XI, Bicetre, France and 2Pasteur Inst, Paris, France

Background:  During long-term HAART, HIV persists latently in a small pool of resting CD4 T cells. Here we examined the place of CD4+CD25hi regulatory T cells (Tregs) in this latent reservoir.

Methods:  A total of 69 HIV+ patients highly adherent to HAART (plasma viral load <20 copies/mL for at least 2 years) were recruited for this study. We selected highly purified quiescent (HLADR–) Treg and non-Treg by magnetic beads and cell sorting. We quantified HIV DNA in cell subsets by a limiting dilution-based polymerase chain reaction  (PCR) method. We examined integrated HIV DNA by Alu-PCR and performed phylogenetic analysis of HIV DNA. Virus recovery from Treg in response to  various stimuli including valproic acid was assessed. FOXP3+ expression was analyzed by flow cytometry and quantitative PCR. Treg proliferation in response to specific and non-specific stimuli as well as susceptibility of those cells to HIV specific cytotoxic T lymphocytes (CTL) were examined.

Results:  Even after 7 years of effective HAART, we found latently infected Treg with integrated replication-competent virus. Phylogenetic analysis of HIV DNA suggested that the Treg reservoir was formed throughout the course of infection. Infected cells were more abundant in the Treg subset than in resting non-Treg. This may be related to Treg features such as hyporesponsiveness and inhibition of cytotoxic T lymphocyte-related functions upon activation. The size of the latent Treg reservoir was estimated to represent up to 30% of the total latent resting CD4+ T-cell reservoir. The histone deacetylase inhibitor sodium valproate led to virus expression in this reservoir, without significant cell activation, and HIV-peptide-expressing quiescent CD4 CD25 T cells were sensitive to specific T-cell cytotoxicity.

Conclusion:  These results identify a latent virus reservoir with specific features; purging of this reservoir may require therapeutics directly targeting virus quiescence instead of cell quiescence.

Offline Central79

  • Member
  • Posts: 527
Re: Vaccine and HIV science moving forward CROI 2007 in LA exciting 2 me
« Reply #1 on: March 24, 2007, 07:49:35 AM »
Wow - you read the 1000 abstracts of CROI?!

Do you have a full-time job as well?! Anyway - thanks for your picks - interesting to read these abstracts.
Diagnosed January 2006
26/1/06 - 860 (22%), VL > 500,000
24/4/06 - 820 (24.6%), VL 158,000
13/7/06 - 840 (22%), VL 268,000
1/11/06 - 680 (21%), VL 93,100
29/1/07 - 1,020 (27.5%), VL 46,500
15/5/07 - 1,140 (22.8%), VL not done.
13/10/07 - 759 (23.2%), VL 170,000
6/11/07 - 630 (25%), VL 19,324
14/1/08 - 650 (21%), VL 16,192
15/4/08 - 590 (21%), VL 40, 832

mistertonky

  • Guest
Re: Vaccine and HIV science moving forward CROI 2007 in LA exciting 2 me
« Reply #2 on: March 24, 2007, 09:21:09 AM »
thanks

i  m sure that that hiv will be completed eradicated (or controlled 100% by therapeutic vaccine) very soon, i believe within 2010.

 


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