ASHM Report Back

Clinical posts from members and guests of the Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM) from various international medical and scientific conferences on HIV, AIDS, viral hepatitis, and sexual health.

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Jason Asselin gave us a comprehensive overview of ACCESS, a national registry designed to pull HIV data from primary health care, sexual health clinic and the laboratory.


  • his study included patients who had viral load testing within the last 12 months
    • the last VL for the year was used to allow more patients to be included
    • VL testiong as part of diagnosis was excluded
  • demographics: males were older, females were younger
  • results
    • citeria for undetectable VL was met for 71% (2009) => 87% (2014)
    • porportion of patients with a high viral load decreased
    • similar outcomes for M vs F
    • patients <40 years old were less like to achieve VL suppression compared to older patients
  • weaknesses
    • does not capture patients who did not engage in health service
  • ACCESS will be rolled out nationally from Jul ’16 – Jun’19
    • we can look forward to more comprehensive data

A brief blog reviewing the Bernard Fields Lecture. Monday 22nd Feb.

T Cells Control of HIV: Implications for Vaccines and Cure.

Speaker: Dr Bruce D Walker (Harvard, MA, USA)

In summary CD8 T cell immunity is still undergoing vital research in assessing how it impacts on overall immunity specifically relating to HIV. Can it help us in a cure or vaccine development? 

Known that CD8 T Cells can kill infected cells before progeny virions are produced. Yang 1997 showed that In vitro CD8 cells can kill HIV infected cells.

In order to assess T Cell response in initial pre peak viremia infection they are studying HIV infected babies in Durban, South Africa. FRESH program was implemented. It was noted within these patients that the rate of increase in viral load was similar across all new infection babies, but the actual peak viral load number and time to reach that in an individual varied.

 From current findings they have found that CD8 cells increase their activity within the human body just after initial exposure to HIV, a substance known as PD-1 is expressed and the more of this that is expressed over time there appears to be some correlation with the immune system getting turned down in regards to response. This was apparently similar to what has been noticed with cancer modulating cells and immune response impact.

They have been able to show that HIV some how activates CD8 activity –they hypothesize that perhaps active CD8 T cells are HIV specific. It was noted that an increased level of CD8 cell activated initial stages of infection was linked with a lower viral load set point.

Two other markers noted to be of relevant were, BCL-2 and perforin. As BCL-2 was activated CD8 cells underwent increased apoptosis, and similarly as there was a loss in perforin there was a progressive decline in CD8 functionality.

Overall early treatment does impact the overall quality of the immune response. To further hypothesis but if CD8 cell functions were maintained by commencing treatment in the pre-viremia stages of infection exposure could this help in the development of a cure and it’s effectiveness.

At the conclusion of the talk, despite being moderately confused with the biochem aspects, I got the impression that for now in order to help the development of future effectiveness of a potential cure we need to maintain baseline immunity of newly diagnosed HIV positive patients as much as possible, and prevent the exhaustion or destruction of CD8 cells after peak viremia.

I’m not sure if I would use this particular pitch to promote early commencement of ARVs in patients or for increased testing programs to detect earlier, but it’s food for thought as to why there is a possible other reason to suppress viral loads as early as possible.


Most cells infected with HIV are CD4's- what makes these cells persist long term.?

CD4cells have attributes of expanded cellular clones. The larger the cluster the older it is.

In HIV controllers, most are restricted to a particular tissue site.

Infected cells can traffick out into the blood and expand.

Can infected CD4cells capable of producing virus clonally expand in Vivo?

Where does virus replication occur in HIV controllers?Blood and lymphoid tissue are v. Different reservoirs.Rare sequences survived to traffick out of blood and into lymphoid tissue.

Are there any sequence similarities between lymph nodes at different sites?

The reservoir contains an archive of viral evolution

I have been party to a couple of discussion recently where there has been conjecture about the implications of an elusive undetectable viral load. Before I am attacked as a naysayer, I am not suggesting that total viral suppression is not the aim of antiviral therapy. It is and always has been. But some attention is now being directed at transient, persistent and recurrent low-level viral load. Along with virological and clinical implications, this may also have social and emotional costs for people living with HIV.

Some patients, particularly those who have been significantly pre-treated, no matter how compliant, do not achieve complete viral suppression. Others experience intermittent blips or periods of viraemia. What are the implications of these events? It is important to understand this as fully as we can because we must give people living with HIV reasoned and reasonable information; it fundamentally underpins the thinking behind approaches to cure research and, from a public health and prevention perspective, we must be careful not to alienate people.

Poster 136 (Silva, J. from Portugal, present a retrospective observational analysis of low-level viraemia and its immunological and virological significance. It was a relatively large study of 2,161 patients 93% on ART 19% had low level viraemia 52% of whom were adherent. The mean VL was 46 (21 - 190) with an average CD4 of 665 (126 - 2,393). There was no documented virological failure, yet 51% had transient viraemia defined as one detectable VL in the study period, 40% had persistent (constantly detectable) virus and 9% had intermittent (2 occasions of detectable VL with undetectable VL in between).

Their conclusion was "in the absence of significant differences in immunological and virological outcomes and the absence of virological failure, suggests a scarce impact of low level viraemia in patient prognosis." This is qualified by suggesting that prospective and more accurate data are required. A number of oral presentations recommended treatment adherence counselling, rather than automatic switching in the presence of low level viraemia.


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