Mechanisms of HIV Non-progression; Robust and Sustained CD4+ T-cell Proliferative Responses to P24 Antigen Correlate With Control of Viraemia and Lack of Disease Progression After Long-term Transfusion-acquired HIV-1 Infection

Wayne B. Dyer; John J. Zaunders; Fang Fang Yuan; Bin Wang; Jennifer C. Learmont; Andrew F. Geczy; Nitin K. Saksena; Dale A. McPhee; Paul R. Gorry; John S. Sullivan

Disclosures

Retrovirology 

In This Article

Conclusion

Our studies have demonstrated that host and viral genetic factors can contribute to delayed disease progression, but the single immunological factor that functionally defined non-progression was Gag-specific CD4 T cell proliferation. The maintenance of this p24-specific response does not require detectable viral replication for antigenic stimulation.[41] Detectable p24-specific T cell proliferation defines the immunocompetent recall response to viral antigen, and when spikes of viral replication were detected in these individuals, these cells likely provided T cell help for maintaining functional antiviral effector responses by other CD4 and CD8 T cells, including non-cytolytic antiviral mechanisms,[41] and may also provide T cell help for efficient generation of NAb by HIV-specific B cells. We have demonstrated that a decline in this protective p24 response in slow progressors either preceded or coincided with classic signs of disease progression.

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