Subtyping was based on a partial HIV-1 pol sequence of 987 nucleotides, encoding the whole protease and amino acids 1–230 of RT. This region was amplified by RT-polymerase chain reaction and sequenced using infrared-labelled primers learn more as previously described

[21,22]. Sequences were first analysed using the National Center for Biotechnology Information HIV-1 subtyping tool to quickly discriminate between B and non-B strains. Non-B sequences were subsequently aligned with sequences from the most recent reference data set from the Los Alamos National Laboratory website (http://hiv.lanl.gov/) using BioEdit 7.0.5 (http://www.mbio.ncsu.edu/BioEdit/bioedit.html) and ClustalX 1.83 (http://bips.u-strasbg.fr/fr/Documentation/ClustalX/). The resulting alignment was analysed with the Phylip package version 3.67 (http://evolution.genetics.washington.edu/phylip.html)

and a neighbour-joining tree was built based on the F84 substitution model. The reliability of the tree topology was assessed by bootstrapping using 1000 replicate data sets. Sequences that could not be unequivocally assigned ABT-199 mouse to a pure subtype or CRF were considered as possible recombinants and examined using Simplot 3.5.1 (http://sray.med.som.jhmi.edu/SCRoftware/simplot/) to identify the recombination pattern. Similarity plots and bootscans were generated by comparing the sequence under investigation with those of reference strains using a sliding window of 300 nucleotides with 20-nucleotide steps. Subtype assignment of each recombination

fragment was confirmed through phylogenetic analysis using the same parameters as for the whole sequences. For URFs, we further examined the degree of similarity of the pol sequences to other HIV-1 sequences, using the BLAST search engine (http://www.ncbi.nlm.nih.gov/blast/) with default settings. Standard nonparametric methods (the Wilcoxon signed-rank test) were used to compare median age, HIV-1 RNA levels and CD4 cell counts in patients with B and non-B subtypes. Categorical variables in these two groups were compared using χ2 or Fisher’s exact test. The crude and Mantel–Haenszel adjusted odds ratios of having a non-B subtype Thymidine kinase were also calculated. Univariate analysis was performed using χ2 and logistic regression. A subsequent multivariate analysis was performed on all variables, using the same tests with a full model. The Cochran–Armitage test for trend was used to determine if an association, when present, was linear. In all tests, a P-value below 0.05 was considered significant. HIV-1 subtype was determined for all patients, revealing an overall prevalence of non-B clades of 11.4% (417 of 3670 patients). Continent of origin (92.2% Europe, 4.5% Africa and 3.3% other), route of infection (35.6% heterosexual, 32.9% IDU, 26.3% MSM and 5.2% other) and gender (70.4% male) were known for 97% (n=3561), 53.5% (n=1963) and 98.1% (n=3602) of individuals, respectively.

[34-36] The expression of TLR4 mRNA and protein was detected in Mφ, endometrial epithelial cells and stromal cells.[10, 31, 32] Reverse transcription polymerase chain reaction analysis also demonstrated the expression of CD14, MD2 and MyD88 mRNA in both endometrial epithelial cells (EEC) and endometrial stromal cells (ESC).[32] The expression levels of TLR4, CD14 and MD2 appeared Galunisertib mouse to be

higher in ESC compared with those in EEC. However, the expression levels of MyD88 were similar between ESC and EEC. Treatment of endometrial stromal cells with LPS significantly increased the production of a number of macromolecules, such as hepatocyte growth factor (HGF), vascular endothelial cell growth factor (VEGF), IL-6, IL-8 and tumor necrosis factor (TNF)-α in a dose-dependent fashion.[32, 37, 38] A

significantly more growth-promoting effect of LPS was observed on endometrial cells derived from women with endometriosis when compared with similar cells derived from control women.[37, 38] The stimulatory effect of LPS was inhibited by the addition of neutralizing antibodies for TLR4 and also by an LPS antagonist, polymyxin B.[10] This indicates that Mφ, ESC and EEC express TLR4 and respond to LPS through TLR4. In fact, we recently demonstrated that both ESC and EEC were able to significantly proliferate in response to LPS and this growth-promoting effect of LPS

was abrogated after pretreatment of cells with anti-TLR4 antibody.[8, 10, 39] Because there are other Panobinostat molecular weight exogenous and endogenous ligands for TLR4 Digestive enzyme in addition to LPS, we presume that blocking of TLR4 alone is more effective in order to suppress inflammatory response in the pelvic environment and cell growth. A recent study[32] demonstrated that LPS was able to stimulate TLR4- and CD14-mediated increased production of IL-8 by ESC. This effect of LPS was associated with the activation of NF-κB as examined by nuclear translocation of NF-κB in ESC. On the other hand, LPS alone did not stimulate IL-8 secretion in EEC. However, LPS did stimulate IL-8 secretion from EEC in the presence of soluble CD14. These findings indicate that the TLR4 system may represent local immunity in the human endometrium with different modes of TLR4 actions between ESC and EEC. We presume that an innate immune system and ovarian steroid hormones may participate either alone or in an orchestrated fashion in the growth regulation of endometriosis. The different macromolecules as secreted by Mφ in the pelvic environment are believed to enhance the growth of endometriosis. However, the initial inflammatory mediator that stimulates Mφ for the production of different cytokines and growth factors was poorly described.

, 2003; Grüner et al., 2004; Cowman & Crabb, 2006; Iyer et al., 2007a, b). Little is known about how the large RH transmembrane proteins mediate their function during erythrocyte invasion, but a crucial step appears to be the proteolytic cleavage during the invasion process (Ogun & Holder, 1994; Triglia et al., 2009). Members of RH have been identified in all Plasmodium species analyzed so far, indicating the conserved function and importance of this protein family to the

malaria parasite (Iyer et al., 2007a; Rodriguez et al., 2008). In the rodent malaria parasite Plasmodium yoelii, ERK inhibitor which has been widely used as a model to study host–parasite interactions (Landau & Gautret, 1998), the RH protein, termed Py235 (235 kDa in mass), has been shown to be a potential virulence factor that allows the parasite to invade a wider range of host erythrocytes (Freeman et al., 1980; Holder & Freeman, 1981). Py235 is also involved in the clonal phenotypic variation of merozoites (Preiser et al., 1999), enabling the parasite to evade immune responses and adapt to changes in Copanlisib the host environment during the invasion step (Snounou et al., 2000). Previously, a 94 kDa domain of Py235 of P. yoelii, which is highly conserved among the RBLs, has been found to selectively bind ATP and ADP, and is termed the nucleotide-binding domain (NBD94, Ramalingam et al., 2008). The amino acid sequence

483FNEIKEKLKHYNFDDFVKEE502 in NBD94 has been identified as a nucleotide-binding region as shown by photoaffinity labeling of the nucleotide analogue 8-N3-3′-biotinyl-ATP (Ramalingam

et al., 2008). The preference of MgATP over MgADP recognition is associated with specific structural alterations in the C-terminal domain of NBD94 as depicted by spectroscopic comparison of NBD94 and its C-terminal truncated form, NBD941–550, in which no nucleotide-dependent alteration could be observed (Ramalingam et al., 2008). This nucleotide effect in the recombinant protein is potentially significant, as demonstrated by a strong binding of Py235 to RBCs in the presence of MgATP, which becomes considerably reduced either in the presence of MgADP or in the absence of nucleotides heptaminol (Ramalingam et al., 2008). Based on these traits and the absence of significant ATPase activity of NBD94, this domain was suggested to serve as an ATP/ADP sensor during the invasion process (Ramalingam et al., 2008). More recently, the low-resolution solution and crystallographic structure of the smallest structural unit, able to bind nucleotides, and its coupling module, the hinge region, have been determined, respectively (Grüber et al., 2010). The crystal structure of the hinge region, including residues 566–663, called NBD94566–663, consists of two helices 97.8 and 48.6 Å in length, linked by a loop. The region NBD94444–547 (residues 444–547 of NBD94) has been identified to form the nucleotide-binding segment, specific for ATP and ADP.

The chi-square test investigated association of these Selleckchem SGI-1776 groups with demographic variables (age, gender, nationality, and place of residence) and business trip characteristics: length of trip (1–2, ≤28, and >28 d), time before departure that trip was planned (≤2 or >2 mo), time before departure that travel health advice was sought, if at all (<15 or ≥15 d), and source

of travel health advice (company or external). Results were considered statistically significant at p < 0.05 and all analyses were performed using sas Version 9.2. Surveys were returned by 63% (n = 383) of the 608 self-registered FBT in Rijswijk. Twenty-eight respondents did not meet the inclusion criterion of traveling to a malaria-endemic country in the preceding 2 years, and a further 27 FBT did not finish the questionnaire. Only the 328 completed questionnaires that adhered to our inclusion criteria were used for analysis. Demographic characteristics of the study cohort are described in Table 1. The vast majority of FBT were male (n = 311; 95%) and aged between 46 and 60 years (n = 205; 63%), and the most common nationality was Dutch (n = 146; 45%). No statistical association of demographic characteristics

with knowledge level was found. ALK phosphorylation Most FBT (n = 232; 71%) sought travel health advice before their trip. The most common reason given for not seeking advice among those who did not (n = 47; 49%) was that the Resveratrol FBT “knew what to do.” FBT with a longer duration of stay were more likely to consult health advice (p = 0.01). The vast majority of trips were planned less than 2 months before departure (n = 269; 82%), and almost one third (n = 89; 27%) of business travel was arranged within just 2 weeks of departure (Figure 1). FBT who had sought company travel health advice perceived risk significantly more accurately than those seeking advice from external sources (p = 0.03). However, seeking company travel health advice was also significantly associated with an increased tendency

to overestimate the risk of typhoid (odds ratio = 2.03; 95% confidence interval = 1.23–3.34). Among countries with a sufficient sample size (n ≥ 10), the most common destinations of Nigeria (n = 142) and Malaysia (n = 67) produced mean knowledge scores of 4.2 and 3.7 out of 11, respectively. FBT visiting Gabon (n = 23) scored highest, with an average of 4.7 correct responses out of 11. The accuracy of perceived risk for each disease is presented in Figure 2. Correct responses were those agreeing with the actual disease risk. Incorrect responses were those that either overestimated or underestimated risk. On an average, underestimation of risk was 23% more common than overestimation. The majority of individuals underestimated risk for polio (52%), dengue fever (55%), cholera (57%), and influenza (67%). Just 4% of FBT underestimated risk of HIV.

However, the measured values of TPP+ distribution also indicated that ionophores had only a minor influence on membrane potential. Some acidification of the cytoplasm occurred, but the total protonmotive force was

only decreased by about 20%. In contrast, the ATP pool fell by 75%. It should be noted that the experiments were performed with late-exponential or stationary-phase cells to reflect the conditions that pertain predominantly in the rumen (Hobson & Wallace, 1982). It seems improbable that the mechanisms differ in more active bacteria, as in mid-exponential phase, although the magnitude of the gradients and pools may be different. Russell and his colleagues ABT-199 in vitro have made similar observations with other species of ruminal bacteria. The high apparent intracellular concentrations of Na+ and K+ were similar to those measured in S. bovis (Russell, 1987). Ruminal bacteria have been described as mildly halophilic, based on their requirements of Na+ for growth (Caldwell et al., 1973; Caldwell & Hudson, 1974). The membrane potential fell by < 10% when monensin

was added to S. bovis, although intracellular pH was affected to a greater extent (Russell, 1987). The protonmotive force of a ruminal Peptostreptococcus was unaffected by monensin, yet the ATP pool fell by two-thirds (Chen & Russell, 1989). It therefore appears that it is not the collapse of transmembrane ion gradients that causes the toxic effect of ionophores on intact bacteria, but the energy expenditure required to support the increased energy demand of homoeostatic selleck screening library mechanisms maintaining the gradients. Any extra demands induced by adding different cations may therefore have an influence on the efficacy of an ionophore, even if the ion is not translocated by the ionophore. In conclusion,

it may be possible to enhance the efficacy of ionophores by adding salts of mineral cations to the diet. However, the spectrum of antibacterial activity against different species, upon which ionophore depends for its nutritional effects, may well be different P-type ATPase when the added cations are present, depending on the ion gradients present in different species. Thus, the nutritional effects of the ionophores (Chen & Russell, 1989) may not be the same at different cation concentrations. The present results also have implications for mechanisms by which ruminal bacteria may become resistant to ionophores. Adaptive resistance to ionophores involves changes in the permeability of the cell envelope (Newbold et al., 1992; Callaway & Russell, 1999), which may well affect changes in transmembrane ion gradients. One of the fears concerning the use of antimicrobials in livestock production is that transmissible resistance factors will arise and by transfer to human pathogens will render antibiotic therapy ineffective (Goodrich et al., 1984). However, there is no evidence that such resistance arises by exposure to ionophores such as monensin (Russell & Houlihan, 2003; Phillips, 2007).

Schopf (1994) suggests that this slow mode of evolution is in accordance with what Simpson defined in his study ‘Tempo and Mode in Evolution’ (1944). Hypobradytely would apply to species with a large population size, ecologic versatility and a large degree of adaptation to an ecological position and continuously available environment. Cyanobacteria fit this definition, being a remarkable lineage

considering their longevity, ease of dispersal (resulting in a wide cosmopolitan distribution), as seen in low-temperature ecotypes (Jungblut et al., 2010), and their ability to survive wide abiotic ranges, including intense desiccation and radiation. Also, analysis of cyanobacterial populations from hot springs and geothermal environments following a molecular ecology approach has shown that geographic isolation can play an important role in shaping phylogenies and distribution patterns in find protocol certain environments Forskolin mw (Papke et al., 2003). The need to generate additional information aimed at unraveling the evolutionary relationships within Cyanobacteria is evident. To date, approximately 50 sequenced cyanobacterial genomes (complete or in

progress) are available. However, 41 represent members of the unicellular subsection/group I, with the vast majority being representatives of only two genera: Prochlorococcus and Synechococcus. Only eight genomes of the genus-rich group IV heterocystous cyanobacteria have been sequenced despite their obvious evolutionary and ecological importance, and deeper phylogenetic inferences are needed to clear relationships within this group. This work was funded by a cooperation program between Sweden and Mexico (STINT: The Swedish Foundation for International Cooperation in Research and Higher Education) awarded to B.B., B.D. and L.I.F.: SEP-CONACyT No. 56045 (LIF), PAPIIT No. IN225709-3

(LIF) and FONSEC Rebamipide SEMARNAT CONACyT No. 0023459 (VS). The authors acknowledge L. Espinosa-Asuar (UNAM, México) and S. Lindvall (SU, Sweden) for technical assistance. “
“The community structure and diversity of endophytic bacteria in reed (Phragmites australis) roots growing in the Beijing Cuihu Wetland, China was investigated using the 16S rRNA library technique. Primers 799f and 1492r were used to amplify the specific bacterial 16S rRNA fragments successfully and construct the clone library. In total, 166 individual sequences were verified by colony PCR and used to assess the diversity of endophytic bacteria in reed roots. Phylogenetic analysis revealed that 78.9% of the clones were affiliated with Proteobacteria and included all five classes. Other clones belonged to Firmicutes (9.0%), Cytophaga/Flexibacter/Bacteroids (6.6%), Fusobacteria (2.4%), and nearly 3.0% were unidentified bacteria.

1.2 We recommend EFV in combination with TDF and FTC as first-line ART in TB/HIV coinfection. 1C   We recommend that when rifampicin is used with EFV in patients over 60 kg, the EFV dose is increased to 800 mg daily. Standard Regorafenib research buy doses of EFV are recommended

if the patient weighs <60 kg. 1C   We recommend that rifampicin is not used with either NVP or a PI/r. 1C   We recommend that where effective ART necessitates the use of PI/r that rifabutin is used instead of rifampicin. 1C CD4 cell count (cells/μL) HBV requiring treatmenta HBV not requiring treatment HCV with immediate plan to start HCV treatmenta HCV with no immediate plan to start HCV treatment a See BHIVA Guidelines for the management of coinfection with HIV-1 and hepatitis B or C virus [1] for indications Selleckchem Thiazovivin to treat hepatitis B and C. Start ART in some patients (2C) (Include TDF and FTC) Start ART (1B) (Include TDF and FTC) Start ART (1B) (Include TDF and FTC) 350–500 Start ART after HCV treatment commenced (1C) <350 Start ART before HCV treatment (1B) Discuss with HIV and viral hepatitis specialist 8.2.2.1 ● We

recommend patients with HIV and hepatitis B virus coinfection who have a CD4 cell count <500 cells/μL are treated with fully suppressive ART inclusive of anti-HBV active antivirals. 1B   ● We recommend patients with HIV and HBV coinfection who have a CD4 cell count ≥500 cells/μL and who have an HBV-DNA ≥2000 IU/mL and/or evidence of more than minimal fibrosis (Metavir ≥F2) are treated with fully suppressive ART inclusive of anti-HBV active antivirals. 1C 8.2.2.2 ● We recommend

TDF/FTC as part of a fully suppressive ART combination should be given to all patients where HBV treatment is deemed necessary. 1C   ● We recommend neither 3TC nor FTC be used as the sole active drug against HBV in ART due to the rapid emergence of HBV resistant to these agents. 1B   ● We recommend 3TC/FTC may be omitted from the ART regimen and tenofovir be given 6-phosphogluconolactonase as the sole anti-HBV active agent if there is clinical or genotypic evidence of 3TC/FTC-resistant HBV or HIV. 1D 8.2.3.1 ● We recommend all patients with HIV and hepatitis C virus coinfection be assessed for HCV treatment. GPP   ● We suggest commencing ART when the CD4 cell count is greater than 500 cells/μL in all patients who are not to commence HCV treatment immediately. 2D   ● We recommend commencing ART when the CD4 cell count is less than 500 cells/μL in all patients who are not to commence anti-HCV treatment immediately. 1B   ● We recommend commencing ART to optimize immune status before anti-HCV therapy is initiated when the CD4 cell count is between 350 and 500 cells/μL unless there is an urgent indication for anti-HCV treatment when ART should be commenced as soon as the patient has been stabilized on HCV therapy.

Overall, cruise lines sailing into North America AZD6244 mw have the onboard capability to manage varicella

cases and outbreaks and appear responsive to CDC recommendations. Cruise lines should continue to implement CDC-recommended response protocols to curtail outbreaks rapidly and should consider whether pre-placement varicella immunity screening and vaccination of crew members is a cost-effective option for their respective fleet operations. In 2009, an estimated 10,198,000 passengers embarked on cruise ships in North American seaports, with an estimated 13,442,000 passenger embarkations worldwide.[1] The cruise ship industry continues to burgeon, with a reported growth rate during 1990 to 2009 of 7.2% annually, characterized by larger fleet sizes; larger, more complex vessels; more annual voyages; and larger passenger and crew cohorts.[2] Of the reported 118 ships representing 4,212 voyages that originated in the United States during 2008, 54% of passengers embarked at seaports in Florida. The cruise ship environment is home to thousands of crew members who live and work at sea, most of whom were born outside the United States. Crew

members may originate from countries where endemic disease incidence and prevalence rates can differ markedly from those in the United States and with diverse national vaccine strategies. Crew CT99021 members’ living quarters, activities, galleys, and eating areas are separate from those of passengers, may vary by job duties, and may facilitate the introduction and spread of disease among crew who work and live closely for prolonged periods of time.[3] Communicable diseases associated with cruise ship passengers and crew are well documented.[4, 5] During a single 106-day cruise ship voyage, dermatologic and respiratory symptoms were the most common presenting complaints to the ship’s dispensary.[4] Reports of disease epidemics of public health importance aboard cruise ships include influenza

A and B,[6-12] Legionella pneumophila,[13-22] rubella,[23] and food-borne and water-borne outbreaks.[24-34] Tacrolimus (FK506) Except during 2009, a pandemic influenza year, varicella (isolated cases and outbreaks) was the vaccine-preventable disease most frequently reported to the Centers for Disease Control and Prevention (CDC) since 2005 by cruise ships sailing in US waters [CDC Division of Global Migration and Quarantine (DGMQ) Quarantine Activity Reporting System (QARS), unpublished data]. In the context of ongoing challenges associated with communicable diseases affecting cruise travelers, an extensive collaboration has developed between the cruise industry and the CDC. Since 2005, the CDC DGMQ has received numerous isolated case reports of varicella among crew members and has investigated outbreaks aboard vessels sailing into and from US seaports.

ERANET (project: BIOMOS) and the Hungarian National Technology Program (projects FAGCNTER and MFCDiagn) also supported this work. The financial supports of HUSRB/1203/214/250 and PTE ÁOK-KA-2013/23 grant are gratefully appreciated. Data. S1. Material and methods. Fig. S1. Genome map of the Erwinia amylovora phage PhiEaH1. “
“Enterococci are among the most notorious bacteria involved in the spread of antibiotic resistance (ABR)

determinants via horizontal gene transfer, a process that leads to increased prevalence of antibiotic-resistant buy 17-AAG bacteria. In complex microbial communities with a high background of ABR genes, detection of gene transfer is possible only when the ABR determinant is marked. Therefore, the conjugative multiresistance plasmid pRE25, originating from a sausage-associated Enterococcus faecalis, was tagged with a 34-bp random sequence marker spliced by tet(M). The plasmid constructed, designated pRE25*, was introduced into E. faecalis CG110/gfp, a strain containing a gfp gene as chromosomal marker. The plasmid pRE25* is fully functional compared with its parental pRE25, occurs at one to two

copies per chromosome, and can be transferred to Listeria monocytogenes and Listeria innocua at frequencies of 6 × 10−6 to 8 × 10−8 transconjugants per donor. The markers on the chromosome and the plasmid enable independent quantification of donor and plasmid, even if ABR genes occur at high numbers in the background ecosystem. Both markers were stable for at least 200 generations, PS-341 supplier permitting application of the strain in long-running experiments. Enterococcus faecalis CG110/gfp/pRE25* is a potent tool for the investigation of horizontal ABR gene transfer in complex environments such as food matrices, biofilms or colonic models. Horizontal transfer of resistance genes and antibiotic-mediated selection pressure leads to a persistence and propagation of antibiotic-resistant bacteria in clinical environments, stock breeding, or in soil (Murray, 1990; Doucet-Populaire et al., 1991; Showsh & Andrews, 1992;

Agerso & Sandvang, 2005; Kazimierczak & Methocarbamol Scott, 2007). Transfer of antibiotic resistance (ABR) determinants can cross the genus barrier and is mainly mediated by conjugative elements such as transposons and plasmids (Shoemaker et al., 2001). Enterococci are Gram-positive, catalase-negative, oxidase-negative members of the functional related group of lactic acid bacteria predominantly encountered in the gastrointestinal tract (GI-tract) of humans and animals. Enterococci harbor a variety of mobile genetic elements such as conjugative plasmids and transposons and therefore the genus Enterococcus is supposed to be a main actor in the spreading of ABR genes (Clewell, 1990). Characterization of the human microbial community has revealed a vast diversity of resistance genes, indicating that the human microbial community acts as a reservoir of ABR genes (Shoemaker et al., 2001; Sommer et al., 2009).

The use of intravenous zidovudine is suggested for women taking zidovudine monotherapy as per Recommendation 5.3.4. The use of intravenous zidovudine for women on HAART with a VL between 50 and 10 000 HIV RNA copies/mL can be considered regardless of mode of delivery.

However, continued oral dosing of their current regimen is a reasonable alternative. The effectiveness of zidovudine monotherapy in preventing MTCT was first demonstrated Pexidartinib in the ACTG 076 RCT of non-breastfeeding women in which zidovudine was initiated orally before the third trimester, given intravenously during labour and delivery, and orally to the neonate for the first 6 weeks of life, reducing MTCT by 67% [8]. Intravenous zidovudine has therefore been included in the management of all women treated with zidovudine monotherapy. However, the data on the contribution of intravenous zidovudine are poor. In a prospective study signaling pathway of all women prescribed zidovudine monotherapy during pregnancy before the publication of the ACTG 076 findings (1988–1994) in which the 8.8% transmission rate among women with CD4 cell counts >200 cells/μL is similar to that of the zidovudine monotherapy arm of ACTG 076 (8.3%), intrapartum intravenous zidovudine

was not associated with lower rates of transmission [51]. One rationale for intrapartum intravenous zidovudine in ACTG 076 was that labour would be associated with poor absorption of oral therapy. While not strictly comparable, the well-recognized rapid absorption of single-dose nevirapine during labour suggests that

the impact of labour on absorption may be overestimated. Pharmacokinetic data from an RCT of oral zidovudine monotherapy also vs. placebo indicate that adequate (therapeutic) zidovudine concentrations are achieved in cord blood with oral dosing. Although the concentrations are lower than have been reported with intravenous infusion, transmission was not associated with zidovudine cord blood concentration [52]. Intravenous zidovudine has historically been considered for women whose plasma VL has not been completely suppressed at the time of delivery. There is no evidence that the intravenous administration of zidovudine alters the rate of placental transfer but higher maternal plasma levels will be reflected in the cord blood concentrations. Intravenous zidovudine (as part of an intervention package; see Section 5: Use of antiretroviral therapy in pregnancy) has also been recommended for women who present in labour, having not received ART. However, data from the New York State HIV diagnostic service (1995–1997) suggest that intrapartum intravenous zidovudine alone does not significantly reduce transmission (10%; 95% CI 3.3–21.8%), as, provided neonatal prophylaxis is commenced within 48 h of delivery (this being the only intervention accessed), the latter has similar efficacy (9.3%; 95% CI 4.1–17.5%) [10].