The use of combination antiretroviral therapy (ART) has resulted in a substantial reduction in viremia, a rebound of CD4+ T-cells and increased survival for human immunodeficiency virus type 1 (HIV-1) infected individuals. Unfortunately, ART does not clear the infection or cure the individual from HIV-1. This is due to some unique characteristics of the virus, such as an ability to cause a latent infection in a subset of CD4+ T-cells, and a remarkable genetic variability. This allows HIV to become resistant to treatment under suboptimal conditions (i.e. adherence), and to escape the immune system. The mechanisms of latency needs to be better understood in order to achieve eradication of HIV-1 infection, and the general aim of this thesis was to study different aspects on HIV-1 latency, with a main focus on the circulating pool of HIV-1 infected resting memory CD4+ T-cells. In paper I we set out to analyze whether resting memory CD4+ T-cells could serve as a reservoir of founder or resistant viral strains in patients with or without optimal suppressed viremia. Our results indicated a turn-over and replacement of the cell-pool in untreated and suboptimally treated patients. The memory CD4+ T-cell-pool forms an archive of the viral population, but former resistant viral variants are not always found in these circulating cells. In paper II we wanted to investigate if treatment with high dose intraveneous immunoglobulin (IVIG) in combination with ART could reduce the pool of latently infected resting memory CD4+ T-cells in vivo. Our data suggested a reduction by an average of 68% of the HIV infected latent cell pool. The findings from this proof-ofconcept study suggest that the reservoir became accessible by IVIG treatment through activation of HIV-1 in the latently-infected resting CD4+ T-cells. IVIG will be further evaluated as an adjuvant to effective ART. In paper III, we investigated the impact of DNA methylation inhibitors and NFkB activators on HIV-1 latency in resting memory CD4+ T-cells. Cytosine methylation ...