Registration for a live webinar on 'Precision medicine treatment for anticancer drug resistance' is now open.
See webinar detailsWe noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- The disease process of HIV
- Better HIV treatment options are available
- Areas that current therapy cannot address
- Addressing the cure for HIV: a literary review
- Outline
- How do we measure persistent HIV?
- Why HIV persists: establishment of latency
- HIV persists in all tissues
- How to measure HIV reservoirs?
- HIV measuring assays depend on its life cycle
- Where to measure HIV reservoirs?
- Why do we expect a cure to be possible?
- Sustained remission of ART is rare but observed
- Leading questions in cure research
- Low decay of CD4+ T cells post therapy
- How does HIV persist on ART?
- What type of virus persists?
- One, two or three reservoirs?
- Proliferation as a mechanism of persistence
- Breaking the cycle of HIV persistence dynamics
- Questioning strategies' fundamental assumptions
- Tissue sanctuary sites after ART?
- Is the mechanism for HIV persistence the same?
- Measuring the clinical impact of cure strategies
- What are the strategies for an HIV cure?
- Cure strategies
- Step model to a cure
- Path to a cure (1)
- Can we decrease persistent HIV on ART?
- Innate vs. adaptive anti-HIV response (1)
- Type I IFN immunotherapy in HIV-1 disease
- IFN-alpha increases NK response
- RCTs of therapy interruption in chronic HIV-1
- Main clinical and virological findings
- IFN-alpha decreases integrated HIV
- Rectal biopsies of individuals on IFN therapy (1)
- Rectal biopsies of individuals on IFN therapy (2)
- Peg-IFN-alpha2b+ ART with ART interruption
- Randomized trial: NCT00594880
- Path to a cure (2)
- Can we clear HIV on ART after ART interruption?
- Overview of cure-directed strategies
Topics Covered
- The disease process of HIV
- The rationale for a cure in 2018
- Conceptual overview of HIV cure research
- Leading questions in cure research
- Stages in cure-directed studies
- Examples of cure-directed study designs
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Montaner, L. (2018, November 29). HIV cure: harnessing innate and adaptive strategies [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/AIFD3916.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Luis Montaner has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: Periodic Reports: Advances in Clinical Interventions and Research Platforms
Transcript
Please wait while the transcript is being prepared...
0:00
I am Luis Montaner at the Wistar Institute and the discussion
today studies to harness innate and adaptive strategies towards an HIV cure.
0:12
We can start by reviewing the disease process of
HIV infection itself to know that in the context of acute infection there
is a seeding of HIV virus throughout the body that is
signaled by a very high viral load and a sudden CD4 loss.
The disease process itself,
underlies a period of several years in which there is
a steady-state between the amount of virus and the immune system.
Now, the amount of the HIV reservoir which we're going to discuss in the future,
is thought to be in some respects established in
an individual basis through the dynamics of the immune system and
the viral infection in a steady-state within the
individual where several factors can contribute to the level of viremia
that a person will have which in turn is expected
to reflect the level of the reservoir once therapy is initiated.
Of course, therapy prevents what otherwise would be the rise in viral load with
what would be a decrease in CD4 count followed by opportunistic infections and death.
Now, the objective of therapy is to prevent this outcome.
But the initiation of therapy relative to
this immunological decay is also considered to be a factor
that will affect the level of the reservoir that
one would retain after the initiation of therapy.