A latent reservoir for HIV in resting memory CD4+ T cells is established early in the course of HIV infection, blocking efforts to eliminate the virus and achieve cure. Within this reservoir, cellular quiescence is the major mechanism maintaining HIV latency. Understanding how this reservoir is established during perinatal infection and maintained through adolescence and young adulthood, despite long-term virologic suppression and in the absence of HIV specific immune responses, will aid in advancing HIV therapeutics aimed at virus eradication. The opportunity to treat HIV infection soon after infection, coupled with the unique properties of the developing neonatal immune system, distinguishes perinatal HIV infection from adult infection. The pathogenesis of HIV persistence in perinatally infected children and adolescents, along with insights into HIV latency during and after HIV remission in the Mississippi child, will be discussed.
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