Abstract
ObjectiveTo study the causes for the lack of clinical progression in a superinfected HIV-1 LTNP elite controller patient.Methodology and Principal FindingsWe studied host genetic, virological and immunological factors associated with viral control in a SI long term non progressor elite controller (LTNP-EC). The individual contained both viruses and maintained undetectable viral loads for >20 years and he did not express any of the described host genetic polymorphisms associated with viral control. None of four full-length gp160 recombinants derived from the LTNP-EC replicated in heterologous peripheral blood mononuclear cells. CTL responses after SI were maintained in two samples separated by 9 years and they were higher in breadth and magnitude than responses seen in most of 250 treatment naïve patients and also 25 controller subjects. The LTNP-EC showed a neutralization response, against 4 of the 6 viruses analyzed, superior to other ECs.ConclusionsThe study demonstrated that a strong and sustained cellular and humoral immune response and low replicating viruses are associated with viral control in the superinfected LTNP-EC.
Highlights
Long term non progressor elite controllers (LTNP-EC) constitute a subset of Human Immunodeficiency Virus (HIV-1) infected naıve individuals whose viral load is below 50 copies/ml for more than 10 years of infection [1]
The study demonstrated that a strong and sustained cellular and humoral immune response and low replicating viruses are associated with viral control in the superinfected LTNP-EC
We identified a case of HIV-1 SI in a LTNP-EC that was able to control both viruses and maintain undetectable viral loads for .20 years [24]
Summary
Long term non progressor elite controllers (LTNP-EC) constitute a subset of Human Immunodeficiency Virus (HIV-1) infected naıve individuals whose viral load is below 50 copies/ml for more than 10 years of infection [1]. This group constitutes around 1% of the HIV-1 infected individuals and has attracted a lot of interest for the identification of mechanisms contributing to the natural control of viral replication. Mutations or deletions in HIV-1 proteins, like Nef [2] or Env [3] and in accessory genes lead to viral control [2,4]. Other studies did not find relevant deletions or defects after analyzing viral sequences from a large cohort of the EC [7]
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