Researchers estimated that the probability of maintaining viral control at 24 months after discontinuing treatment was only 15%, but the cohort may hold important clues about a possible cure for HIV.
Interventions that maintain viral fitness costs could potentially slow progression.
The EBV-encoded EBNA1 protein is essential to maintain viral episomes and for viral persistence.
It is also required for maintaining viral latency.
A wealth of data now suggest that most HIV controllers maintain control of viral replication at least in part through potent HIV-specific T cell responses [6], [7], [8], [9], [10], [11], [12], [13], [14], [20], [22], observations that have spurred the development of vaccines that elicit T cell responses against HIV.
However, many HIV controllers lack a protective HLA type, have very low frequencies of HIV-specific T cells, or maintain control of viral replication even after documented escape from HLA-restricted epitopes [14], [20], [21], [22].
These results support the notion that a large majority of people on ART are achieving viral control at least in the early years on treatment and that HIV DR is maintained at a low level in Vietnam.
However, the mechanisms of viral control in these individuals are likely to be heterogeneous as many HIV controllers lack a protective HLA type, have very low frequencies of HIV-specific T cells, or maintain control of viral replication even after documented escape from HLA-restricted epitopes [14], [20], [21], [22].
Picker suspects some undefined immune response explains the viral control.
And viral control could soon become even more effective.
