Routine genotyping to identify HIV-resistant CBUs could create a bank of CB-derived stem/progenitor cells with which to treat HIV infection. HIV depletes the cells of the immune system, allowing rare DAPT mw opportunistic infections to thrive and eventually leading to the death of the individual. The virus displays selective tropism

towards the monocyte/macrophage lineage and T lymphocytes (T cells). As the viral infection depletes the host of T cells, the patient advances to the condition known as AIDS, and the decline in the number of T cells marks this progression. The viral envelope contains two major glycoproteins required for the fusion of the viral and cell membranes: glycoprotein 120 (gp120) and glycoprotein 41 (gp41). gp120 binds to a cell membrane receptor known as cluster of differentiation 4 (CD4) and a co-receptor expressed by T cells [1–3]. This binding induces a conformational change allowing the gp41 fusion peptide to interact with the lipid bilayer and form membrane pores used to transfer viral contents inside the cell for replication. The different HIV-1 strains can be distinguished by the co-receptor used to infect cells. The predominant strain found early during HIV infection, the chemokine (C-C motif) receptor 5 (CCR5)-tropic (R5) selleck screening library strain, infects cells expressing the CCR5 co-receptor

[4–6], while the chemokine (C-X-C motif) receptor 4 (CXCR4)-tropic (X4) strain binds to the CXCR4 co-receptor. There are also dual-tropic strains that use both CCR5 and CXCR4 co-receptors. Without a functional CCR5 co-receptor the HIV-1 R5 strain is incapable of infecting T cells [7,8]. Currently, the treatment for HIV-infected individuals is highly active antiretroviral therapy (HAART). Although effective, this therapy requires a daily regimen consisting of several pills. If the patient discontinues therapy, viral Glutamate dehydrogenase reservoirs in the gut-associated lymphoid tissue and in haematopoietic progenitor cells can restore the levels

of HIV and trigger T-lymphopenia [9]. Interestingly, there are individuals who are resistant to HIV-1 infection as a result of a common 32-bp deletion in both copies of the CCR5 gene [10–12]. The 32-bp deletion (Δ32) results in an early termination of translation, which produces a nonfunctional protein. CCR5 and CXCR4 are both chemokine receptors that HIV-1 uses in conjunction with CD4 to infect T cells [4,5,13]. Individuals who inherit one CCR5Δ32 allele are partially resistant to HIV infection [14]. Recently, Hutter et al. (2009) showed that long-term remission of HIV disease could be achieved in a patient with acute myeloid leukaemia following an allogeneic bone marrow transplant from a CCR5Δ32/Δ32 donor [15]. These findings demonstrate that CCR5Δ32/Δ32 donor bone marrow has the potential to be used in stem cell therapy for HIV infection.