aureus 8325-4 and DU 1090 were cultured in TSB at 37 °C to an optical density at 600 nm of 0.5. Fifty-milliliter culture aliquots were centrifuged, http://www.selleckchem.com/products/MK-2206.html washed with PBS, and resuspended in 1 mL PBS (2 × 108 CFU per 30 μL)

for histopathology experiments. For cytotoxicity studies, 5 mL of culture described above was resuspended in 10 mL of Dulbecco’s modified Eagle’s medium (DMEM; Invitrogen, CA). The minimal inhibitory concentrations (MICs) of apigenin for S. aureus were evaluated using the broth microdilution method according to CLSI guidelines (CLSI, 2005). Briefly, apigenin was diluted in a 96-well plate over the concentration range of 4-1024 μg mL−1 using double dilution method. Following inoculation with 5 × 105 CFU mL−1 of overnight broth cultures in each well, the plate was inoculated at 37 °C for 24 h. The MIC was defined as the lowest concentration at which the growth of S. aureus was inhibited. Staphylococcus aureus strain 8325-4 was cultured in TSB medium at 37 °C, shaken at 200 r.p.m. to an optical density (OD600 nm) of 0.3, and aliquoted into five 250-mL flasks in a volume of 100 mL. Apigenin dissolved in DMSO was added to the four cultures to obtain final concentrations of 1, 4, 16, and 64 μg mL−1. 1% DMSO was added to the control culture. The bacteria were cultured at 37 °C with constant shaking, and cell growth

was measured by reading the OD600 nm values every 30 min. Hemolytic activity was measured as described previously (Worlitzsch et al., 2001; Qiu et al., 2010a) using rabbit Selleckchem NVP-BKM120 erythrocytes. Briefly, S. aureus cultures with different concentrations of apigenin were harvested when grown to the postexponential growth phase by centrifugation

(5500 g, 4 °C, 1 min), and the residual cells were removed using a 0.2-μm filter. A 0.1 mL volume of bacterial culture supernatants were brought up to 1 mL with the addition of PBS and 25 μL defibrinated rabbit erythrocytes for 30 min at 37 °C. The unlysed blood cells were removed by centrifugation (5500 g, room temperature, Calpain 1 min). Following centrifugation, the hemolytic activity of the supernatants was detected by measuring the optical density at 543 nm. Medicine-free culture supernatant served as the 100% hemolysis control. The percent of hemolysis was calculated by comparison with the control culture supernatant. The culture supernatants collected previously were used in Western blot analysis. Samples were boiled with Laemmli sample buffer for 10 min, and then 25 μL of the sample was fractionated by SDS-PAGE (12% polyacrylamide gels; Laemmli, 1970). The Western blot protocol was performed as described previously (Qiu et al., 2010a, b). Proteins were transferred onto polyvinylidene fluoride membranes (Roche, Basel, Switzerland) using a semi-dry transfer cell (Bio-Rad, Munich, Germany). The membrane was blocked for 2 h with 5% bovine serum albumin (Amresco) at room temperature.

Overall RMSE reflects GSI-IX concentration the average of the difference waveform derived by subtracting the instantaneous position of the target from the participant’s location. This score was calculated separately for random and repeated sequences and averaged for all trials within a block (Wulf & Schmidt, 1997; Boyd & Winstein, 2004b; Vidoni & Boyd, 2009). The difference between overall RMSE during random and repeated sequence tracking reflects implicit learning and was used to evaluate reductions in tracking errors across practice and at retention. Random tracking performance was assessed

using the second random sequence (Boyd & Winstein, 2004b; Boyd & Linsdell, 2009). As overall RMSE reflects both spatial accuracy and temporal lag, improvement on each of these components of movement was also assessed (Boyd & Winstein, 2004a).Time lag of tracking is the time (in milliseconds) corresponding Z-VAD-FMK chemical structure to the maximal cross-correlation coefficient and represents the temporal distance from the target. Spatial error is the residual RMSE score that remains following adjustment of the participant’s cursor position to account for the time lag of tracking. Time lag scores in larger negative numbers indicate greater time lag of tracking, while a zero value represents no tracking

time lag between participant and target. Lower RMSE scores indicate less overall error and show improved motor performance. Statistical analyses were performed in three steps. First, improvement in performance during the acquisition phase (days 1–4) was assessed for overall RMSE, spatial error and time lag using separate 3 (Group: 1 Hz, 5 Hz, Control rTMS) × 12 (Block: 1–12) mixed-measures anovas for the random and repeated sequences. Group was treated as a between-subjects factor and Block was treated as a repeated measures factor. In all cases the dependent variables (overall RMSE, spatial error and time lag) were log transformed as Maulchy’s sphericity test revealed that raw scores across blocks violated the sphericity assumption for each dependent variable and both sequences. Second, implicit sequence-specific

learning at oxyclozanide retention was examined for overall RMSE, spatial error and time lag using three separate 3 (Group: 1 Hz, 5 Hz, Control rTMS) × 2 (Sequence: Random, Repeated) mixed-measures anovas. Group was treated as a between-subjects factor and Sequence was treated as a repeated measures factor. As implicit sequence-specific learning is defined as lower error/less lag during repeated compared with random sequence tracking, significant Group × Sequence interactions were investigated using contrasts comparing repeated vs. random sequence tracking performance within each group to determine if implicit sequence-specific learning was evident in each group. Bonferroni correction was applied with the corrected threshold of P = 0.033 to correct for multiple comparisons.

Multidrug resistant (MDR) phenotype was determined as described previously (Tumbarello et al., 2007). The disks used for confirmation test were obtained from Beijing Tiantan Biological Products Corporation (China). Escherichia coli (ATCC 25922) and K. pneumoniae (ATCC 700603) were used selleck chemicals as quality control strains. Plasmid DNA was extracted and purified by the alkaline lysis method using a commercial plasmid DNA purification kit (Tiangen Biotech Co., Ltd, China). Detection of genes encoding blaSHV/TEM/CTX-M groupI/CTX-M groupIV enzymes was performed by PCR with the primers listed in Table S1, Supporting

information. The specific PCR assay of CTX-M group II, III, and V was implemented with the relevant primers (Nagano et al., 2003; Pitout et al., 2004; Chmelnitsky et al., 2005). Further amplification for K. pneumoniae carbapenemase (KPC) in speculative isolates (MIC of imipenem or meropenem of ≥ 2 μg mL−1), another pair

of primers was used (Yigit et al., 2001). PCR products were subjected to bidirectional nucleotide sequencing using an automated DNA sequencer (ABI 3730XL, Weiterstadt, Germany). The nucleotide sequences or deduced protein sequences were analyzed via both Basic Local Alignment Search Tool (blast) program (http://www.ncbi.nlm.nih.gov/BLAST) and web site on the nomenclature of ESBLs (http://www.lahey.org/studies). The genetic relationship between all qualified K. pneumoniae isolates was determined by MLST with seven housekeeping genes (Diancourt et al., Staurosporine 2005). Chromosomal DNA was obtained by the alkaline lysis method using a commercial genomic DNA purification kit (Tiangen Biotech Co., Ltd) according to the manufacturer’s instructions. Allele Docetaxel in vitro sequences and sequence types (STs) were verified at the http://www.pasteur.fr/recherche/genopole/PF8/mlst/Kpneumoniae.html

web site. The phylogenetic relationships among the different STs were established according to a dendrogram generated using the unweighted pair group method with arithmetic mean (UPGMA) algorithms and eBURST analysis (http://pubmlst.org/perl/mlstanalyse). Categorical variables were evaluated by the chi-square test. Values are expressed as percentages of the group from which they were derived (categorical variables). Two-tailed tests were used to determine statistical significance. P value of < 0.05 was considered significant. All statistical analysis was performed by the spss statistics program, version 16.0, for Windows (SPSS Inc., IBM). In total, 183 ESBL-producers were screened. Of the 183 study isolates, seven isolates were negative for ESBL production by the double-disk synergy test and 18 isolates were excluded by the rpoB confirmatory test. Thus, 158 K. pneumoniae was included for further characterization. The frequency of occurrence of ESBL-producers in the six areas ranges from 28.8% to 64.4% (Fig. S1). Complete medical records were available for review from 133 of 158 patients.

Two recent classical tone-shock conditioning magnetoencephalographic (MEG) studies shed some light on the spatiotemporal characteristics of the so-called conditioned response [CR; a representation of the associated unconditioned stimulus (UCS); Moses et al., 2010] and on the temporal characteristics of shock conditioning and contingency reversal during auditory processing (Kluge et al., 2011). The spatiotemporal dynamics underlying human auditory emotion processing independent of the CR still remain quite elusive. This appears predominantly consequent upon the dynamic

nature of affective sounds revealing their meaning only after signal integration over time (Bradley & Lang, Fulvestrant 2000). Bröckelmann et al. (2011) addressed this constraint of signal

convolution by using different ultra-short click-like tones that revealed their identifying characteristic almost instantaneously. Emotional significance was assigned to these tones by means of MultiCS conditioning, a novel and highly challenging affective associative learning procedure (see Steinberg et al., 2012b). Auditory evoked magnetic fields (AEFs) in response to multiple different click-like tones (CS) were compared before and after conditioning with pleasant, unpleasant or neutral auditory scenes (UCS). The results demonstrated the brain’s remarkable capacity to differentiate multiple emotionally relevant from non-relevant tones after brief learning in a rapid and highly resolving fashion. Affect-specific amplified CS processing was evident IDH inhibitor during the auditory N1m (100–130 ms) and the preceding P20–50 m (20–50 ms) component. Motivated attention, automatically and selectively engaged by emotion-associated tones (Lang et al., 1998a,b; Vuilleumier, 2005), modulated neural activity within a distributed frontal–parietal–temporal

network more generally implicated Amobarbital in the prioritised processing of behaviourally relevant or physically salient stimuli (Corbetta & Shulman, 2002; Fritz et al., 2007). Here, we aimed to investigate whether effects of rapid and highly differentiating affective processing would generalise to cross-modal conditioning of multiple CS with a single electric shock and thus a UCS which is frequently applied in human (Sehlmeyer et al., 2009) and animal neuroscience research. AEFs were measured in response to 40 click-like tones before and after four contingent pairings of 20 stimuli with an electric shock (CS+), while the other half remained unpaired (CS−). Based on our previous findings, we hypothesised a modulation of early AEF components (N1m, P20–50m) within a distributed frontal–parietal–temporal attention network differentiating multiple shock-conditioned tones from unpaired tones. In line with aversive learning studies that reported right-lateralised increased activation to CS+ (Hugdahl et al., 1995; Morris et al., 1997) or greater left-hemispheric responses to CS− (Morris et al., 1998; Rehbein et al.

For this reason, immunomodulatory treatment was stopped with consecutive deterioration of disease. However, because of the prompt healing and the preserved muscle reflexes, we had to revise our hypothesis. The ulcer in this case was associated with ENL and the neuropathy was due to leprosy because the tendon reflexes of the lower extremities could easily be elicited. One of the hallmarks of the leprosy neuropathy is that reflexes are not altered unless being at the end stage of the disease. Third, years

of corticosteroids Cyclopamine supplier for presumed sarcoidosis probably modified the clinical presentation of leprosy toward lepromatous forms. The clinical spectrum of leprosy is determined by the underlying immunological response of the host against M leprae. The dynamic nature of the disease may lead to spontaneous fluctuations in clinical states that are known as leprosy reactions.1,8 ENL is classified as a systemic inflammatory reaction with features of vasculitis

that may occur in the course of leprosy primarily during the treatment find more of lepromatous and borderline lepromatous subtypes. It is classified as a type-II reactional state and often shows chronic relapsing course. Dactylitis is one of the hallmark features of ENL and can be associated with generalized illness, painful erythematous skin nodules, and various forms of organ involvement such as nerves, kidneys, lymph nodes, eyes, joints, spleen, and liver.9 Thalidomide is the treatment of choice for the management of ENL mainly in relapsing or steroid depending course. Niclosamide Efficiency is based on its anti-tumor necrosis factor (TNF)-α activity because elevated levels of anti-TNF-α may play a major role in the pathogenesis of ENL. Precaution is recommended in women of child-bearing age. Short courses of steroids are effective in the

management of ENL. They are required if neuritis is present. As our case shows, steroid dependence is a difficult condition to manage. Effective treatment has also been observed with clofazimine. It has the limitation of being slow to act and not being useful in all manifestations of ENL.10–13 In conclusion, the diagnosis of leprosy is particularly challenging in people of nonendemic regions. Travelers returning from endemic areas who present with unexplained sarcoidosis-like symptoms should be investigated for mycobacterial infection. Once diagnosis is made, patients with leprosy would be best treated by doctors who have knowledge on this disease. As shown in this case report, it is always a difficult challenge to treat patients with leprosy especially when they present with leprosy reactions. The authors state they have no conflicts of interest to declare. “
“The aim of this study was to evaluate the presence of wild poliovirus or sabin-like poliovirus in 152 stool samples from migrants in the Accommodation Center in Italy and liquid waste from the sewage systems.

Similarly, Hales et al. (1998) reported the existence of two differently sized flagellin gene sequences (1.4 and 1.0 kbp) in strains of B. cepacia. These authors also revealed that the strains containing the larger flagellin gene had flagella with FK506 order relatively greater diameters. The three-dimensional structures of the type I and II flagellins in the Actinoplanes strains were predicted using SWISS-MODEL with a template structure (PDB ID

Code: 3a5x). Interestingly, each of the structures differs most markedly at the region of the knob-like projection, which has been reported to contribute to stabilizing the conformation of the flagellin protein and flagellum fibers (Malapaka et al., 2007). In addition, the type II flagellin had a relatively compact structure that may decrease the mechanical stability of parts of flagellum. This study only observed the type II flagellin in four of the Actinoplanes strains tested, all of which are considered to be motile actinomycetes (Stackebrandt & Kroppenstedt, 1987; Matsumoto et al., 2000). In contrast, the structure of the inner and outer core regions were well conserved in both flagellin proteins. These conserved structures contained the N- and C-terminal regions. The phylogenetic Selleck UK-371804 analysis was performed using the N-terminal amino acid

sequences (115 aa) of flagellin from 17 Actinoplanes species (Fig. 3). The phylogenetic tree showed that the Actinoplanes species formed three clusters, and that some of these relationships were well correlated with analyses obtained using 16S rRNA data. A. consettensis and A. humidus both had highly conserved N-terminal flagellin sequences (aa similarity of 99.3%), and the central and C-terminal regions were also similar. Furthermore, these two strains showed 100% similarity in the 16S rRNA analysis. On the other hand, both species were well characterized by a numerical taxonomical approach, and were established as distinct species without genotypic data. Until now, a polyphasic taxonomic approach including genotypic analysis is believed to determine the taxonomic position of prokaryotic microorganisms. Therefore, these two species should be clarifying

the taxonomic position using genotypic characterization. The observation that A. auranticolor did not cluster with DOK2 the other members of Actinoplanes in this study may have arisen due to horizontal transfer (Wassenaar et al., 1995; Liu & Ochman, 2007). The differences in the size of flagellin gene, and those revealed in the phylogenetic analysis imply that the N-terminal region of the flagellin gene was useful for phylogeny or evolutionary study in the genus Actiniplanes. However, it is not yet known why organisms with the type II flagellin have lost the knob-like projection on the flagella. In addition, further flagellin gene sequencing of non-Actinoplanes species are required to discuss the evolutional distribution of flagellar gene in actinomycetes.

Primary outcomes were change in CD4 cell count from baseline, and proportion of patients reaching undetectable HIV RNA levels, defined as <50 copies/mL. We collected information on study characteristics and the demographic and clinical characteristics of patients at inclusion. We contacted the authors or sponsors of eligible studies to request additional information when necessary. We used data from intention-to-treat analyses, which assessed HTS assay patients according to their assigned treatment group, regardless of their actual adherence or follow-up. We estimated treatment effects in two ways: (1)

we compared the proportion of patients with undetectable HIV RNA at W48 in the treatment and placebo groups using odds ratios (ORs) and 95% confidence intervals (CIs); (2) we compared CD4 cell count increases at W48 using standardized and nonstandardized mean differences and 95% CIs. The standardized mean differences, used for the analysis, are calculated as the ratio of the observed mean differences to an estimate selleckchem of the standard deviation obtained from pooling the standard deviations from both treatment

groups [18,19]. The nonstandardized mean differences are just the observed mean differences and were used for the interpretation. Positive mean differences in CD4 cell counts indicated superior treatment responses. Missing values were imputed as virological failure and no increase in CD4 cell count from baseline. We used a random effects model and the DerSimonian and Laird method [20] to combine virological suppression Tenoxicam proportions. We used the same random effects model and the Hedges method [18,19] to combine changes in CD4 cell count. We used a random effects meta-regression model to estimate the extent to which covariates explained heterogeneity in treatment effects. We entered the following baseline population characteristics into the model: mean age; percentage of men; percentage of individuals with AIDS-defining events; median CD4 cell count; median HIV RNA level; percentage of individuals

on OBT regimens with GSS of 0, ≤1, or ≤2; and use of CCR5 inhibitors. Missing GSS values were considered to be 0. All analyses were performed using stata 9.0 (StataCorp LP, College Station, TX, USA). Our process for identifying eligible studies is summarized in Figure 1. By combining keywords, we identified 1121 titles and abstracts, of which 961 were not eligible. Of the remaining 160 potentially relevant studies, we examined in detail 80 clinical trials and excluded 70 of them because the design of the study was ineligible (n=50), because of lack of randomization (n=2) or data at W48 (n=17). Moreover, we excluded one clinical trial that evaluated vicriviroc and met all inclusion criteria [21], because the doses used [10 or 15 mg once a day (qd)] differed from those used in Phase III clinical trials. We finally retained 10 trials that met our inclusion criteria [12,13, 22–29]. Four of these used CCR5 inhibitors and six used other new antiretroviral drugs.

albicans growth that extended the lag phase for approximately 12 h, followed by growth at rates that were comparable to the control without an added chelator and the treatment with desferrioxamine. The growth of C. albicans was inhibited in the presence of 0.25 g L−1 DIBI for 24 h and displayed very weak growth thereafter (Fig. 3a). After 4 days, the maximum specific growth yield in the presence of 0.25 g L−1 of DIBI reached 4% of the Ymax obtained in the control culture. Candida Rapamycin purchase vini responded

differently to the presence of the same chelators (Fig. 3b). Both lactoferrin and DIBI provided complete inhibition over the 4-day incubation period. In contrast, desferrioxamine and deferiprone led to similar growth kinetics in C. vini as compared with the control with no added chelator (Fig. 3b). Compared with control incubations with no added chelator, a slight, but statistically not significant increase (P=0.05) of the maximum specific growth yields could be observed for selleck compound incubations with added deferiprone and lactoferrin (C. albicans) and deferiprone (C. vini). Growth inhibition of the two yeasts by DIBI was investigated further at a lower chelator concentration (0.17 g L−1), over

a longer incubation course (15 days) and in comparison with the well-characterized synthetic chelators EDTA and BPS (Fig. 4). Both EDTA and DIBI inhibited the growth of C. albicans leading to prolonged lag phases (3 days) and lower growth rates compared with the control, but the maximum specific growth yields observed after 15 days were

comparable to those obtained for the control (Fig. 4a). BPS addition led to longer lag phases, lower growth rates and a Ymax that only reached approximately 30% of the control growth over the experimental period. Candida vini displayed a similar inhibition response to BPS (Fig. 4b). However, the effect of DIBI on C. vini was stronger and led to a growth inhibition that was comparable to that of BPS until day 10. Candida vini also differed in its response to EDTA. Specifically, the lag phase was shorter (approximately 3 days) and the growth kinetics Fenbendazole were similar to the control with regard to the growth rate and yield (Fig. 4b). The nature of the inhibition caused by DIBI was further investigated. The inhibitory activity of C. albicans could be characterized as being both fungistatic and Fe specific because it could be prevented or reversed by adding iron to levels sufficient to saturate the added DIBI iron-binding capacity (Fig. 5) by adding iron together with DIBI at the time of inoculation or adding Fe after 20.5 h, respectively. Candida albicans is prevalent in human vaginal infections, but is also the most common opportunistic pathogen associated with human immunodeficiency syndrome (Kullberg & Filler, 2002) as well as the third most common cause of nosocomial bloodstream infections (Walsh et al., 2004). In contrast, C.

, 2010). However, knowledge of nitrogen metabolism and the genetic response

to nitrogen limitation in Mycobacteria Roxadustat chemical structure is sparse. Mycobacterium tuberculosis, the aetiological agent of tuberculosis, remains a major public health problem (WHO, 2010) and is thought to experience many different environments including nutrient limitation during the establishment of infection. Therefore, understanding how mycobacteria coordinate and adapt to fluctuating supplies of nutrients such as nitrogen could identify the survival mechanisms required in tuberculosis infection. In Escherichia coli, the transcriptomic response to nitrogen limitation is well described, involving the NtrB/C two-component regulatory system directing the transcription

of approximately 100 genes (Zimmer et al., 2000). Mycobacterial genomes do not contain an NtrB/C homologue; instead the transcriptional response to nitrogen availability is thought to be mediated by the transcriptional regulator GlnR (Amon et al., 2008, 2009). The Mycobacterium smegmatis GlnR protein shares 55% amino acid identity with the GlnR response regulator of Streptomyces coelicolor (Amon et al., 2008), which regulates the expression of approximately 50 genes in response to nitrogen limitation (Tiffert et al., 2011); M. smegmatis (msmeg_5784) buy Alectinib and M. tuberculosis (Rv0818) GlnR share 73% amino acid identity. Bioinformatics analysis identified known S. coelicolor GlnR DNA binding motifs in all available mycobacterial genomes (Amon et al., 2008). Furthermore, analysis of a M. smegmatis GlnR deletion mutant confirmed that during nitrogen limitation, GlnR positively regulates the transcription of glutamine synthetase, glnA1, and two ammonium transporters, amt1 and amtB (Amon et al., 2008). Interestingly, glnR transcription levels did not

significantly alter during nitrogen limitation, suggesting glnR transcription is not regulated in response to nitrogen availability, but rather GlnR activity is subject to an alternate control mechanism such as post-translational modification (Amon et al., 2008). Genomic analysis of nitrogen metabolism in mycobacteria (Amon et al., 2009) highlights several differences between MRIP M. smegmatis and M. tuberculosis, with increased capacity for ammonium uptake in M. smegmatis and the lack of an apparent glutamate dehydrogenase in M. tuberculosis. This perhaps reflects the availability of nitrogen in the organisms’ natural environments, although their responses have not been compared directly. GlnR belongs to the OmpR family of two-component response regulators (Amon et al., 2008). Typically, OmpR-type response regulators are transcriptional activators, phosphorylated by a sensor kinase in response to extracellular stimuli (Kenney, 2002). A prominent feature of the OmpR family is a highly conserved aspartate residue, which undergoes phosphorylation by the sensor kinase.

The gold standard test for HIV infection in infancy was HIV DNA PCR on peripheral blood lymphocytes. INK-128 In a number of studies, including the large French perinatal cohort, equal or increased early sensitivity with amplification of viral RNA with no false positives

has been reported [330, 331]. Infants infected intrapartum may have low peripheral blood HIV levels, so HIV DNA/RNA may not be amplified from all infected infants at birth. Indeed a positive HIV DNA/RNA result within 72 hours of birth is taken as presumptive evidence of intrauterine transmission. Within the first few weeks of life the sensitivity of the viral diagnostic tests increases dramatically and by 3 months of age 100% of non-breastfed HIV-positive infants are likely to be detected [331]. Although HIV RNA and DNA assays have similar sensitivity, RNA assays commonly require 1 mL of plasma. If the sample requires dilution due to a low volume, which is often the case with paediatric samples, the Selleck Cabozantinib lower limit of detection will be increased (with a corresponding decrease in assay sensitivity). Ideally, the lower limit of detection should not exceed 100 copies/mL following dilution. In addition where MTCT may have occurred

in utero, subsequent maternal antiretroviral therapy with agents that cross the placenta could lead to a false-negative RNA result in an infected infant. This risk would be highest in a late-presenting mother. In this situation the infant should be tested using DNA PCR. The same considerations regarding using primers known to amplify maternal virus apply to

both RNA and DNA assays. In view of the genomic diversity of HIV, a maternal sample should always be obtained for HIV DNA or RNA amplification with, or prior to, the first infant sample to confirm that the primers Sorafenib chemical structure used detect the maternal virus. If the maternal virus cannot be detected then a different primer set and/or test should be used. There has been an increase in the number of cases, usually mothers established on antiretroviral therapy long term with fully suppressed HIV, where it has not been possible to amplify maternal DNA using four different primer sets. HIV DNA/RNA results on their infants should therefore be interpreted with caution and in the light of clinical and serological findings. Infant HIV diagnostic testing should be undertaken at birth, 6 weeks and 12 weeks of age. Evidence from the French perinatal cohort demonstrated that neonatal ART, especially if more than one drug, can delay the detection of both HIV DNA and RNA in the infant [332]. For this reason, the second and third HIV molecular tests are performed at 2 weeks and 2 months after stopping PEP, i.e. usually at 6 weeks and 12 weeks of age.