Models of Protective Immunity to HIV TULP02
Type:
Learning from practice Back
Venue: Session Room 9
Interpretation: None
Time: 10:45 - 12:15
Code: TULP02
Co-Chairs: Keith Fowke, Canada
Aggrey Anzala, Kenya (TBC)
The session is designed to highlight similarities and differences in what has been learned about protective immunity to HIV from different models. The three models examined are highly exposed uninfected people, individuals who are infected with HIV but control the infection and model animal systems. The objective is to compare and contrast what we can learn from each different model.

    Presentations in this session:
10:45
TULP0201
Powerpoint (879 KB)
Learnings from studies of highly exposed uninfected individuals
Rupert Kaul, Canada

11:00
TULP0202
What animal models of HIV infection can and cannot teach us
Ruth Ruprecht, United States

11:15
TULP0203
Correlates of long term control of HIV infection in human populations
Photini Kiepiela, South Africa





Audio files:
  1. English audio file (mp3 format, 26.4 MB)

Rapporteur report

Science Track A: Biology and Pathogenesis of HIV report by Dr. Rupert Kaul

This non-abstract session aimed to generate discussion regarding the advantages and disadvantages of three major research models for the elucidation of the immune correlates of protection against HIV. These included Highly Exposed, Persistently Negative (HEPS) individuals, those with Long Term Non Progressive infection (LTNPs), and primate models.

Rupert Kaul (Canada) summarized lessons learned from a cohort of sex workers in Nairobi, Kenya who appear to resist HIV infection despite multiple exposures. Small pilot studies had linked resistance with both HIV-specific CTL and HIV-neutralizing genital IgA antibodies, and these associations have now been confirmed in larger, prospective cohort studies. The advantage of the HEPS studies was that such individuals represent "real life" resistance to HIV. However, since many immune and genetic factors have been associated with reduced susceptibility, the lesson for the future was that larger studies need to be performed, ideally in a blinded, prospective fashion. This will enable identification of the strongest protection correlates.

Ruth Ruprecht (USA) discussed primate models of protection against HIV. She emphasized that the primate model has been able to clearly demonstrate the only proven immune correlate of protection against HIV (in the form of SHIV) challenge, namely the prior passive administration of a cocktail of four neutralizing antibodies (b12, 2G12, 2F5 and 4E10). Important lessons for the future are that the primate models need to mimic the process of human infection as closely as possible, specifically through using repeated low dose mucosal challenge with an R5 virus based on an isolate from early infection, when viruses may be more easily neutralized.

Finally, Photini Kiepiela (South Africa) presented data regarding the immune correlates of HIV immune control by CTL in a large cohort of HIV-infected participants. Distinct HLA types were strongly associated with both enhanced and impaired HIV control. This may relate to the fact that different HLA alleles "direct" the host immune response against distinct regions of the virus, and that CTL directed against Gag may be much effective (immune "drivers") than those directed against Env or the accessory proteins (immune "passengers").

The comment was made (Guio Silvestre, USA) that the natural primate hosts of several HIV-like retroviruses demonstrate high viral loads and minimal HIV-specific cellular immunity, perhaps suggesting that evolution has led to the selection of virus "tolerance" rather than resistance or strong antiviral immunity. This may have important implications for the vaccine field.




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