tolaasii, which are naturally resistant to phage infection (Munsch & Olivier, 1995; Yoon et al., 2011). The aim of this study was to isolate bacteriophages that are effective against P. tolaasii and some other pathogenic pseudomonads. The isolation, purification, and host range of these bacteriophages, as well

as the morphology and the complete genome sequence analysis of the Bf7 bacteriophage – having one of the widest host ranges of them – are described. Bacterial strains used for the host range determination of bacteriophages Idelalisib derived from the Belgian Co-ordinated Collections of Micro-organisms (BCCM/LMG, Gent, Belgium), from the Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH (DSMZ, Braunschweig, Germany), and from decaying sporocarps of oyster mushroom, isolated previously from a Hungarian mushroom farm (Sajben et al.,

2011) (Table 1). Pseudomonas tolaasii Sirolimus causes yellowing of the oyster mushroom sporocarp during cultivation; therefore, we used necrotic caps to isolate bacteriophages against the pathogen. Infected mushrooms (5 g of each) were smashed, diluted in 10 mL SM buffer (100 mM NaCl, 8 mM MgSO4, 50 mM Tris–HCl, pH 7.5, and 0.01% gelatin in distilled water), and incubated overnight at 25 °C with gentle agitation. The mushroom particles and bacterial cells were removed by centrifugation at 4000 g for 20 min at 4 °C, then the supernatant was centrifuged at 20 000 g for 60 min at 4 °C to collect the phages. Chloroform was added after the centrifugation to eliminate the residual bacterial cells. 150 μL from this mixture was added to 50 μL of P. tolaasii LMG 2342T culture (OD620 nm = 1) incubated previously at 25 °C for 18 h. The mixture was diluted in 6 mL of soft Triptic Soy Base (TSB) agar (0.7%), overlaid on 2% agar plates and allowed to solidify. The phage plaques were detected after 18 h of incubation at 25 °C. To select for phages with increased host range, these plaques were diluted in SM buffer, and the previously described method was

repeated with a culture of Pseudomonas putida DSM 9278. After this step, the resulting plaques derive from bacteriophages that are able to infect both previously applied pseudomonads. Single plaques were collected, and then phage stocks were prepared using P. putida as an indicator strain and stored at 4 °C. Phage titers were determined Anacetrapib by the double agar layer method (Adams, 1959) with minor modifications. Soft TSB with 0.7% agar was used for the top layer. Ten-fold serial dilutions were prepared from the phage lysates and added to the host bacteria. The mixture was poured onto the bottom agar layer consisting of LB medium. Number of plaques was scored after 18–24 h incubation at 25 °C. To evaluate the host range of the isolated phages, a collection of Pseudomonas strains (Table 1) were tested for sensitivity by the spot lysis assay (Day & Marchesi, 1996) performed with minor modifications. Bottom agar layers were prepared with 2% agar without nutrient source.

, 2010). Among 116 such genomic loci was an andA locus encoding anthranilate dioxygenase (see below). This locus carries an andA operon consisting of four structural genes, andAcAdAbAa. This locus also carries a divergently transcribed regulatory gene, andR, encoding a protein belonging to a AraC family of transcriptional regulators (Fig. 1a). In our IVET screening, this locus was the most repeatedly identified (51 times among the 713 IVET-positive clones) and was drastically induced (more than 100-fold induction rate) in the soil (Nishiyama et al., 2010). The gene organization and nucleotide sequence

of the ATCC 17616 andA locus are very similar to those from B. cepacia DBO1 (Chang UK-371804 research buy et al., 2003), and the deduced amino acid sequences shared

high similarities (85–96%). The study of DBO1 suggested that the AndR protein was a positive regulator of the andA promoter, as the andR mutant failed to grow on anthranilate, and that the andA promoter was upregulated by anthranilate but neither by benzoate nor by salicylate (Chang et al., 2003). However, it remained unclear whether tryptophan, a compound from which anthranilate can be formed (Fig. 1b), needs to be metabolized to induce andA promoter. The ferric uptake regulator (Fur) is a global transcriptional regulator for the iron regulon in many Gram-negative bacterial species (Faulkner & Helmann, selleck chemicals llc 2011). Our preliminary microarray analysis of ATCC 17616 revealed the transcriptional down-regulation of andAc in the fur mutant (our unpublished observation). As no canonical Fur binding site (Fur box) was located upstream of the andA operon (Yuhara et al., 2008), it was assumed that this operon is under the indirect control of Fur. We found in the present study that the ATCC 17616 andA operon is involved in the catabolism of tryptophan and anthranilate, and that the proliferation of ATCC 1716 in soil was dependent on andA. We also report the requirement of andR function and the moderate dependence of (Cornelis et al., 2009) fur function for the induction of andA promoter in

the soil. The bacterial strains and plasmids used in this study are listed in Table 1. Escherichia coli cells were grown at 37 °C in Luria-Bertani (LB) broth (Maniatis et al., 1982) and B. multivorans cells at 30 °C in 1/3 LB broth (0.33% tryptone, 0.16% yeast extract, and Axenfeld syndrome 0.5% NaCl) or in M9 minimal medium (Maniatis et al., 1982). When used, succinate, tryptophan, and anthranilate were added to the media at a final concentration of 20 mM. 2,2′-Dipyridyl was added at a final concentration of 0.1 mM. Antibiotics were added to the media at the following concentrations: ampicillin at 50 μg mL−1 and kanamycin (Km) at 50 μg mL−1 for E. coli, and Km at 200 μg mL−1 and tetracycline (Tc) at 50 μg mL−1 for B. multivorans. When necessary, diaminopimelic acid (DAP) and lysine were added at 100 μg mL−1. To count LacZ+ and LacZ− colonies on agar plates, 40 μg mL−1 of X-gal was added to the media.

[26] These form the foundation for Table 2. Similar actions have been proposed by groups including the World Health Organization.[10] Lambert and colleagues argue that, since name similarity is easily and cheaply measured, steps should be taken to monitor and reduce similarity as a way to reduce the likelihood of drug name confusions to improve medication safety. This is sound advice, but difficult to implement on a national or international scale.[11] A number of organisations have produced broad strategies aimed at preventing drug confusion (JCAHO, ISMP and the US National Coordination Council for Medication Error Reporting).[12,14] There is considerable overlap with previously described strategies.

Additional recommendations include the unambiguous labelling of injectable and IV drug containers, and proposing that all prescriptions clearly specify medication LBH589 supplier strength, dosage, route of administration and frequency, even where there is only one accepted option. Finally, there is a strong endorsement for collaboration among all stakeholders to facilitate the design of packaging and labelling that minimises error. In addition to the actions proposed in Table 2, further processes recommended to reduce problems for pharmacists to use with error-associated

medications[29] include keeping patient medication profiles current, with sufficient information for pharmacists to evaluate the appropriateness Everolimus order of medication orders, reading product labels at least three times (e.g., when a product is selected, packaged and returned to the shelf) and counselling patients in order to provide an opportunity to ensure that an order has been dispensed correctly and that the patient understands the proper use of the medication.[29] Finally, a medication safety issue brief for hospitals and health networks[25] suggests

that actions to reduce errors from look-alike, sound-alike drugs should include organisations evaluating their formularies to identify medications that are prone to name confusion and Osimertinib chemical structure that errors involving look-alike, sound-alike drugs are tracked, with the results used to educate staff. They also suggest providing drug name spelling with verbal orders, providing the intended use of the drug with the order, and conducting a ‘failure mode and effects analysis’ for all drugs being considered for inclusion on a formulary. Obstacles to changing names, labels or packages include: the nature of the problem; that standards for names, labels and packages do not incorporate human factors principles; and that most of the information on labelling and packaging problems is not systematic and comprehensive. There is also a barrier in the regulatory structure governing pharmaceuticals. Regulatory agencies do not yet ‘own’ the problem – they do not see it falling into their jurisdiction.

The immunogenicity of the combination vaccine is at least as good as the monovalent vaccines[54, 55] and is particularly useful as many travelers also require hepatitis A vaccination.[18] Ambrix (inactivated HAV and recombinant HBsAg) is licensed in Europe as a two-dose schedule in children aged 1 to 15 years.[56] HCV

is a member of the Hepacivirus genus within the Flaviviridae family.[57-59] It is estimated that 3% of the world’s population is chronically infected.[60] The prevalence is estimated to be 3.2% in China, 4.8% in Pakistan, and up to 15% in parts of Asia and Africa. CHIR 99021 The highest prevalence of HCV is in Egypt (15%–22% of the population)[61-64] (Figure 2). HCV transmission generally results from parenteral exposure to contaminated blood via injecting drug use (IDU), blood transfusions, unsafe injections, medical procedures, body piercing,

or tattooing. It may also occur via perinatal transmission. Sexual transmission of HCV has been described among HIV-positive men who have sex with men, and is associated with high-risk sexual behaviors.[58, 65, 66] In approximately 20% of people no cause of infection can be established. The risk of occupational transmission of HCV needlestick injuries is around 0.3%.[67] Perinatal transmission PCI-32765 price from HCV-infected mothers occurs in 2.7% to 8.4% of births.[67] The widespread practice of paid donor blood and poor screening has led to high HCV transmission rates in the developing world. Screening for HCV in blood and blood products is not universal in many developing countries[40]: the WHO estimates that 43% of donated blood in the developing world is inadequately screened.[67]

The frequency of reuse of injection equipment without sterilization also varies, with highest rates in Southeast Asia and the Middle East (1.2%–75%).[68] Unsafe injecting practices in developing countries such as Egypt, India, and G protein-coupled receptor kinase Pakistan led to the formation of the Safe Injection Global Network (SIGN).[67, 69] The SIGN was established in 1999 and aims to achieve safe and appropriate use of injections worldwide. The WHO through collaborations with national regulatory authorities has focused on formulating national policies for: the safe and appropriate use of injections, the quality and safety of injection devices (in particular, single-use injection devices and auto-disable syringes), facilitating access to injection equipment, and achieving cost-effective use of injections. Intervention strategies targeting these core components simultaneously have improved vaccine injection safety.[67, 69] Acute HCV infection is usually asymptomatic and unrecognized, with <1% of HCV-positive individuals reporting an acute illness associated with jaundice.[70] Following infection, HCV RNA begins to replicate in the human liver and is detectable in the serum within 1 to 3 weeks.

Short-term (6 h) incubations were used to determine the effects of NaNO2 on the ability of the AOB to oxidize ammonia to nitrite. Concentrations of NaNO2 similar to that applied in previous studies of nitrite effects on N. europaea were used (Stein & Arp, 1998; Beaumont et al., 2004a, b). The final pH was significantly higher in NaNO2 amended than in unamended incubations for all three AOB, indicating less acidification and thus reduced rates of ammonia PD-0332991 purchase oxidation (Table 1). However, among the three AOB, only N. eutropha showed significantly slower rates of and less net nitrite production

when incubated in the NaNO2-amended medium, although this strain also had the fastest maximum nitrite production rate among the three strains (Table 1). Similar results were observed for N. eutropha and N. europaea cells incubated in phosphate-buffered, rather than HEPES-buffered, medium (data not shown). Thus, among the three AOB, the ammonia-oxidizing activity of N. eutropha was the most negatively affected by the presence of high nitrite concentrations. Genes selected for this study included those with demonstrated involvement in the ammonia oxidation and/or the nitrite reduction pathways of N. europaea (Klotz & Stein, 2011). The genes were amoA, encoding the α-subunit of ammonia

monooxygenase; nirK, encoding copper-containing nitrite reductase; norB and norS, both encoding cytochrome c-dependent nitric oxide reductases; cytS, encoding cytochrome c′-β; and cytL, encoding cytochrome P460. NirK and NorB have demonstrated activity in reducing nitrite SP600125 research buy to nitrous oxide via nitric oxide in N. europaea (Beaumont et al., 2002, 2004b; Schmidt et al., 2004). The norS gene has been identified only in AOB and a few other bacteria (Stein et al., 2007; Norton et al., 2008) and encodes a nitric oxide reductase with high similarity to NorB (J. Hemp, pers. commun.). Cytochrome c′-β has a putative function in nitrogen oxide detoxification, while the evolutionarily related cytochrome P460 was shown to

oxidize hydroxylamine to nitrite in N. europaea (Elmore et al., 2007). Comparisons of similarity between nucleotide and translated protein sequences of genes in N. eutropha and N. multiformis MycoClean Mycoplasma Removal Kit to orthologues in N. europaea are shown in Table 2. Nitrosospira multiformis lacks cytochrome P460, and as it belongs to a different genus, there was less sequence similarity between N. multiformis and N. europaea than between the two Nitrosomonas strains for all genes. Incubations supplemented with NaNO2 only caused significant changes in the expression levels of three of the six functional genes examined. No significant change was detected in the levels of norB, cytL, or cytS mRNA of any AOB, suggesting no regulation of these genes by nitrite (data not shown). The levels of amoA mRNA of N. multiformis were significantly reduced in incubations supplemented with 20 mM NaNO2, but not with 10 mM NaNO2 (Fig. 1). Similarly, the levels of norS mRNA of N. europaea and N.

Tukey’s estimates of least significant differences were

calculated from the anova analysis. Pearson’s correlation coefficients between all pairs of variables were calculated. During the period of 0–9 days, the highest growth rate of the co-culture (A. niger–B. cepacia) was observed on the third day of postinoculation, after which it plateaued. Biomass of the co-culture was on average 2.1 times higher (P < 0.05) than that of the fungus and 6.9 times higher than that of the bacterium (Fig. 1a). In single cultures, A. niger growth was faster than B. cepacia. While the mycelial mass increased 2.2 times on sixth or ninth day in comparison with the third day, the bacterial mass increased only 1.3 and 1.8 times, respectively. The levels of solubilized phosphate ranged from 0.65 to 1.10 mg  mL−1. On the third day, solubilized phosphate showed an increase in 15 times in the B. cepacia culture, 27 times Selisistat cost BIBF 1120 manufacturer in the A. niger culture, and 23 times in the co-culture in relation to time zero (Fig. 1b). During the subsequent incubation periods, little increases in the amount of solubilized phosphate were observed. The averages observed at the end of the incubation period were 0.57 mg  mL−1 for the bacteria, 0.74 mg mL−1 for the fungus, and 0.76 mg  mL−1 for the co-culture (Fig. 1b). The efficiency of solubilization of CaP continually increased, and at the end of the incubation period, 100% of the

phosphate was solubilized by co-culture, while single cultures, rates of 78% with B. cepacia and 91% with A. niger were

obtained (Table 1). A similar trend was observed with the production of acid that increased considerably on the third day of incubation (Fig. 2a). This increase was maintained at sixth day in the fungal culture, and subsequently decreased. On the third day, acid produced by the co-culture (5.40 mg mL−1) was significantly greater (P < 0.05) than other cultures and the sum of acid produced individually by the fungal (4.35 mg mL−1) and bacterial (0.55 mg mL−1) cultures. The initial pH of the culture medium was 6.9 (time zero) and decreased on third day to 3.4 in the fungal culture, either 3.7 in the co-culture, and 5.0 in the bacterial culture (Fig. 2b). pH decrease was also observed at the subsequent time points; however, decreases were not as great. On ninth day, the pH values were 3.0 (A. niger), 4.2 (B. cepacia), and 3.1 (A. niger–B. cepacia). No significant difference of the pH was found between fungal and co-culture (Fig. 2b). Glucose content was dramatically reduced even after 3 days of incubation; 68, 99, and 98% reduction in glucose levels were observed in media inoculated with fungi, bacteria, and the co-culture, respectively (Fig. 3a). On the ninth day of postinoculation, glucose content was almost completely consumed in all cultures. Acid phosphatase activity ranged from 9.35 to 52.26 μg pNP h−1 mg−1 dry biomass (Fig. 3b).

, Richmond, B.C., Canada), which uses the principle of immunofiltration of HIV-1 [glycoprotein 41 (gp41)] and HIV-2 (gp36) recombinant proteins. Because of the wide variety of inclusion criteria, the study was intended to include at least 500 patients over a 6-month period, starting in August 2010. By the end of this time-frame, however, fewer than 50 patients had been included in the study. We organized several meetings and coaching sessions with the different

teams taking part in the study and decided to ask the same doctors to record information about a larger number of consultations, the purpose of which was to survey how many HIV tests had actually been offered. From August Bleomycin ic50 2010 to August 2011, 224 patients were included in the study, of whom 51.0% were male and 48.0% female (1% unknown); 45.0% were Caucasian, 46.5% African and 8.5% of other ethnicity; 48.2% were of Belgian nationality, 24.0% of a sub-Saharan African nationality and 12% of a European nationality other than Belgian. In terms of fulfilling the inclusion criteria, 32% belonged to a high-prevalence group, 29% had an indicator condition, and 9% had returned from

an endemic country. A standard test was offered to 217 patients (97%). Twelve patients (6%) refused the standard test because they were not covered by national health insurance or fear of losing anonymity, and 203 standard tests were performed. The INSTI HIV-2/HIV-2 test was offered to 217 patients (97%). Thirteen patients (6%) refused rapid testing because it was too stressful or because Everolimus cost they were not ready to receive a result immediately, and 197 tests were performed. Two reactive rapid tests were confirmed by Western blot; one rapid test proved indeterminate in the case of an HIV-negative person. The characteristics of

the two individuals with a confirmed reactive HIV test were as follows. The first person was a 45-year-old black man who was born in Mauritania, and left his home country and arrived in Belgium in 1999. He Phosphoprotein phosphatase travelled to Mauritania in April 2010; at the time of inclusion and testing in January 2011, he had Belgian citizenship, presented with dermatitis and had never been tested for HIV, HBV or HCV; his CD4 count was 171 cells/μL, defining him as a very late presenter. The second person was a 40-year-old black man from the Democratic Republic of Congo. The date of his arrival in Belgium was unknown, and he had not recently travelled to an HIV-endemic country. Before being tested, he said he had never been tested before for HIV, HBV or HCV, but when confronted with a positive rapid test result, he said he knew he was HIV positive. The seroprevalence according to the demographic characteristics of the patient populations of the different centres varied from 0 − 0.

On the other hand, with an increase in Regorafenib in vivo the volume of bleeding and obstetrical disseminated intravascular coagulation (DIC) scores, packed red blood cells and

fresh frozen plasma (FFP) were administrated. As the fibrinogen level decreases early in atonic bleeding, the early administration of FFP may be important as an initial approach to treat the disease. In study 2, amniotic fluid embolism was classified into two types: that involving cardiopulmonary collapse; and that following DIC. Pathologically, the former type is conventional, in which fetal and amniotic fluid components are observed in pulmonary blood vessels. The pathological characteristics of the latter type include uterine atony, and PARP inhibitor the presence of fetal and amniotic fluid components in uterine blood vessels. In this type, fetal and amniotic fluid components are occasionally absent in the lungs.

Among cases of clinical amniotic fluid embolism without fetal and amniotic fluid components in the lungs (or pulmonary examination findings are unavailable in life-saving settings), those involving uterine atony in the presence of fetal and amniotic fluid components in uterine blood vessels may be called uterus-type amniotic fluid embolism. The authors have no conflict of interest to declare. “
“To investigate the impact of antenatal exposure to a single course or repeated courses Atorvastatin of dexamethasone (DEX) on neonatal anthropometrics, placental morphometry and potential effect on maternal plasma levels and placental expression of vascular endothelial growth factor (VEGF). Pregnant women between 27 and 32 weeks of gestation who delivered between 28 and 40 weeks and received a single course (n = 38) or repeated courses (n = 33) of DEX were compared to gestational age-matched controls (n = 30). Maternal blood samples were obtained, and placental biopsy was taken. Area percent

of VEGF immunostaining and villous capillarization index were evaluated using image analysis. Infants exposed to repeated courses of DEX were significantly associated with decreased birthweight, body length, head circumference and placental weight compared with controls (P = 0.011, P < 0.001, P = 0.004, P < 0.001, respectively) and with the group that received a single course of DEX (P = 0.021, P = 0.020, P = 0.049, P = 0.010, respectively). There was a significant decrease in maternal VEGF plasma levels and percentage of VEGF immunostained area after repeated courses of DEX compared with controls (P < 0.001 and P = 0.001, respectively) or a single course (P = 0.028 and P = 0.002, respectively). Notably, repeated courses of DEX impaired normal increase in villous capillarization index compared with controls or a single course (P = 0.001 and P = 0.041, respectively).

On the other hand, with an increase in this website the volume of bleeding and obstetrical disseminated intravascular coagulation (DIC) scores, packed red blood cells and

fresh frozen plasma (FFP) were administrated. As the fibrinogen level decreases early in atonic bleeding, the early administration of FFP may be important as an initial approach to treat the disease. In study 2, amniotic fluid embolism was classified into two types: that involving cardiopulmonary collapse; and that following DIC. Pathologically, the former type is conventional, in which fetal and amniotic fluid components are observed in pulmonary blood vessels. The pathological characteristics of the latter type include uterine atony, and selleck chemicals the presence of fetal and amniotic fluid components in uterine blood vessels. In this type, fetal and amniotic fluid components are occasionally absent in the lungs.

Among cases of clinical amniotic fluid embolism without fetal and amniotic fluid components in the lungs (or pulmonary examination findings are unavailable in life-saving settings), those involving uterine atony in the presence of fetal and amniotic fluid components in uterine blood vessels may be called uterus-type amniotic fluid embolism. The authors have no conflict of interest to declare. “
“To investigate the impact of antenatal exposure to a single course or repeated courses Olopatadine of dexamethasone (DEX) on neonatal anthropometrics, placental morphometry and potential effect on maternal plasma levels and placental expression of vascular endothelial growth factor (VEGF). Pregnant women between 27 and 32 weeks of gestation who delivered between 28 and 40 weeks and received a single course (n = 38) or repeated courses (n = 33) of DEX were compared to gestational age-matched controls (n = 30). Maternal blood samples were obtained, and placental biopsy was taken. Area percent

of VEGF immunostaining and villous capillarization index were evaluated using image analysis. Infants exposed to repeated courses of DEX were significantly associated with decreased birthweight, body length, head circumference and placental weight compared with controls (P = 0.011, P < 0.001, P = 0.004, P < 0.001, respectively) and with the group that received a single course of DEX (P = 0.021, P = 0.020, P = 0.049, P = 0.010, respectively). There was a significant decrease in maternal VEGF plasma levels and percentage of VEGF immunostained area after repeated courses of DEX compared with controls (P < 0.001 and P = 0.001, respectively) or a single course (P = 0.028 and P = 0.002, respectively). Notably, repeated courses of DEX impaired normal increase in villous capillarization index compared with controls or a single course (P = 0.001 and P = 0.041, respectively).

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.