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Resting CD4+ T-cells are critical for establishing HIV-1 reservoirs. It has been known for over two decades that resting CD4+ T-cells are refractory to HIV-1 infection, but the underlying mechanisms are not fully...
Quiescent CD4+ T lymphocytes are highly refractory to HIV-1 infection due to a block at reverse transcription.
Sterile Alpha Motif and HD domain-containing protein 1 (SAMHD1) is a recently identified host factor that restricts HIV-1 replication in dendritic and myeloid cells. SAMHD1 is a dNTPase that presumably reduces...
HIV infection results in inhibited cholesterol efflux by apolipoprotein A-I (apoA-I) in macrophages, and this impairment involves Nef mediated down-regulation and redistribution of ATP-binding cassette transpo...
Lens epithelium–derived growth factor (LEDGF/p75) is a cellular co-factor of HIV-1 integrase (IN) that tethers the viral pre-integration complex to the host cell chromatin and determines the genome wide integr...
The Moloney murine leukaemia virus (Mo-MLV) gag gene encodes three main structural proteins, matrix, capsid and nucleocapsid and a protein called p12. In addition to its role during the late stages of infection, ...
Macrophages are important target cells for the Human Immunodeficiency Virus Type I (HIV-1) in vivo. Several studies have assessed the molecular biology of the virus in this cell type, and a number of differences ...
The effect of drug resistance transmission on disease progression in the newly infected patient is not well understood. Major drug resistance mutations severely impair viral fitness in a drug free environment,...
Correlates of protection (CoPs) against infection by primate lentiviruses remain undefined. Modest protection against HIV-1 was observed in one human vaccine trial, whereas previous trials and vaccine-challeng...
Helicases hydrolyze nucleotide triphosphates (NTPs) and use the energy to modify the structures of nucleic acids. They are key players in every cellular process involving RNA or DNA. Human immunodeficiency vir...
Activation of the NF-κB transcription factors by the viral protein Tax plays a vital role in the pathogenesis of diseases associated with human T-cell lymphotropic virus type I (HTLV-I). The Tax oncoprotein un...
The Tax protein encoded by Human T-lymphotropic virus type 1 (HTLV-1) is a powerful activator of the NF-κB pathway, a property critical for HTLV-1-induced immortalization of CD4+ T lymphocytes. Tax permanently st...
The potential role of antibodies in protection against intra-subtype HIV-1 superinfection remains to be understood. We compared the early neutralizing antibody (NAb) responses in three individuals, who were su...
Our inability to cure HIV/AIDS is related to the ability of the virus to establish reservoirs during treatment. In order to develop new strategies, it is certainly essential that a suitable animal model be imp...
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
This article is part of a Supplement: Volume 9 Supplement 2
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