05 v/v Tween 80. The CFU was determined by plating 100 μL of serial dilutions onto Petri dishes containing Middlebrook 7H10 agar, supplemented with Tween 80 and albumin–dextrose–catalase (ACD). These dilutions were stored at −80 °C and were subsequently used for virulent challenges. Ten Holstein cows recruited from herds of a cattle farm in Shandong province, China, were used for this study. The five infected animals were selected on the basis of the skin-fold thickness response to bovine tuberculin in the single intradermal tuberculin test (SITT). The SITT reactor animals were selected where the skin-fold thickness response to bovine pure protein derivative (PPD) exceeded

at least 4 mm. All of these animals were also tested positive in a whole-blood interferon-γ (IFN-γ) enzyme immunoassay

(Bovigam, Y-27632 datasheet Prionics AG), which is based on the use of the Bovigam avian PPD- and Bovigam bovine PPD-stimulating antigens. None of the infected subjects had any symptom of active tuberculosis. The five noninfected control animals were selected from a herd without a recent history of tuberculosis and were PPD tested and IFN-γ EIA negative. ELISA assays were performed according to the manufacturer’s instructions (Bovigam, Prionics AG). Briefly, whole heparinized blood was mixed in a 24-well culture plate in a 1 : 1 ratio with RPMI 1640 medium Apitolisib (Invitrogen), and then blood was stimulated with avian PPD or bovine PPD (25 000 IU each tuberculin) in 100 μL in three replicates. Phosphate-buffered saline (PBS) was used as a negative control (nil antigen). The results are calculated as mean nil antigen, avian and bovine PPD absorbance values for each sample. Blood plasma collected from cattle, within 3–30 days postapplication of the skin test, having an OD value greater than that of avian PPD and nil (PBS) antigen by over 0.100 indicates the presence of M. bovis infection (Supporting Information, Table S1). PBMCs were separated from acid citrate dextrose (ACD) anticoagulated blood of cattle (five infected and five noninfected) by OptiPrep (Asix-Shield, Norway) isothipendyl gradient centrifugation according to

the manufacturer’s protocol. From 10 mL of blood, we obtained approximately 2–5 × 106 PBMCs. To derive monocytes, PBMCs were plated in six-well plates (Costar, Corning), 5 × 106 cells per well, containing RPMI-1640 (Invitrogen) with 10% fetal calf serum (FCS; Hyclone), 2 mM l-glutamine, 10 mM HEPES and antibiotics (100 U mL−1 penicillin and 100 U mL−1 streptomycin) for 2 h at 37 °C, 5% CO2. Nonadherent cells were removed by washing with PBS. Then, adherent cells were incubated for 5 days at 37 °C, with 5% CO2 to obtain MDMs. MDMs (2 × 105 cells per well) were washed with PBS three times to remove antibiotics before infection. Cells of treatment groups were challenged with M. bovis (MOI=10 : 1) for 4 h at 37 °C, with 5% CO2.

83% of the sequences. Fecal samples were dominated by members of the phylum Bacteroidetes (62%) and the Firmicutes (35%), while skin samples had a relatively even distribution of Firmicutes (39%), Bacteroidetes (31%) and Actinobacteria (25%). Soil samples contained many phyla including the Bacteroidetes (32%), Acidobacteria (27%) and Proteobacteria [Alphaproteobacteria (10%), Betaproteobacteria (6.5%), Gammproteobacteria (5.2%) and Deltaproteobacteria

(2.7%)]. The unique distribution of phyla was also seen in the overall community composition as NMDS visualization of pairwise UniFrac distances showed clustering by individual sample rather than temperature or length of storage (Fig. 1). Sample types also differed with respect to community diversity levels, with soil bacterial communities harboring the highest levels, followed by fecal and skin samples (Faith’s PD=40, buy Daporinad 11 and 10, respectively). As noted below, each pair of subsamples within a given sample type had bacterial communities that differed with respect to their composition and diversity and these differences were irrespective of the storage conditions (see Table 1). Bacterial communities Dabrafenib ic50 in the fecal samples did not change appreciably with different storage conditions and retained their unique composition even after

14 days of storage (Fig. 1 and Table 1). Fecal 2 was dominated by the Bacteroidaceae (c. 75%), while Fecal 1 had a more even distribution of the six most abundant taxa across all temperatures selleck screening library (Fig. 2). Although the relative abundances of a few individual taxa were affected by temperature (Fig. 2), this did not have a significant effect on the overall community composition. The UniFrac distance between bacterial communities from the two hosts was significantly greater (permanova, P=<0.001) for both weighted and unweighted UniFrac than the distance between samples stored at different temperatures and durations (P>0.1, Table 1). This minimal effect of storage on the overall structure of the communities is evident from Fig. 1, which shows that replicate samples tended

to cluster by host. Likewise, the phylogenetic diversity of the fecal samples remained consistent across the temperatures (Table 2). Our results extend those reported by Roesch et al. (2009), who found minimal differences in community composition and relative taxon abundances after 72 h of storage at the one temperature tested (room temperature) for three of the four samples in their study. In summary, even though we did observe shifts in the abundance of some taxa in our small sample set under different storage conditions, this did not mask interpersonal differences in the overall fecal bacterial community composition, and did not affect our ability to differentiate the host origin of the two fecal samples.

So now as my jet lag stupor disappears and I become less emotional about my trip home, practicality sets in. After completing these musings, my next task will be to write

to the airline and ask for those 100,000 miles back that I used to fly from Asia. Now, what are the chances of that? The author states that she has no conflicts of interest to declare. “
“Background. In countries with high rates of measles immunization, imported cases of measles represent an important continuing source of measles infection. Methods. Airlines and state health departments report cases of suspected measles AG-014699 research buy in international travelers to the Centers for Disease Control and Prevention Quarantine

Stations. We reviewed these reports, maintained in an electronic database, to determine the demographic and epidemiologic characteristics of international air travelers infected with measles. Results. We reviewed 35 confirmed cases of measles in air travelers and analyzed their demographic and epidemiologic characteristics. The median age of case travelers was 17 (range: 4 months–50 years). These travelers arrived from all regions of the world, including 10 countries with immunization rates of measles-containing PD-166866 vaccine below 90% and five others experiencing local outbreaks. Of 17 travelers for whom immunization status was known, 2 had been adequately immunized with at least two doses of a measles-virus containing vaccine, 9 were inadequately immunized, and an additional 6 infants had not been immunized because of age. Conclusions. Measles importations cAMP continue in the United States. Travelers should be aware of the importance of assuring up-to-date immunizations, especially when visiting countries experiencing a local measles outbreak. In addition,

parents traveling with infants, and their physicians, should be aware of recommendations regarding the early administration of a dose of measles-containing vaccine for infants at least 6 months old traveling internationally. In carrying out responsibilities to prevent the introduction and spread of contagious diseases into the United States, personnel of the Division of Global Migration and Quarantine, US Centers for Disease Control and Prevention (CDC), receive reports of suspected and confirmed cases of measles in international travelers entering US ports as provided for by federal public health law and state agreements through the Council of State and Terrritorial Epidemiologists. These reports, from international vessel or aircraft captains, state and local health officials, US Customs and Border Protection officers, and foreign Ministries of Health, have been collected in an electronic database, the Quarantine Activity Reporting System (QARS), since August 1, 2005.

In the two reported cases,

symptoms appeared between 11 and 14 days after exposure, respectively. This is much shorter than might be expected according to the literature. Both patients presented with fever, cough, urticaria, and eosinophilia, manifestations that are most commonly associated with acute schistosomiasis (Katayama fever)6 and occasionally with other helminth infections in returned travelers.7 Helminth infections SB203580 supplier are difficult to diagnose during the invasive stage. In the reported cases, the diagnosis was made about 3 weeks after the onset of symptoms by positive agar-plate stool cultures in both patients, the presence of Strongyloides stercoralis larvae in the stools of one patient and a serologic Raf inhibitor diagnosis in the other.1 When faced with a returned traveler from the tropics with eosinophilia, an helminth infection should be at the top of a differential diagnosis. Not only are serologic tests frequently not positive early in the infection but also they may lack specificity, particularly in the case of strongyloidiasis8; both schistosomiasis and filariasis may lead to false positive tests for strongyloidiasis. Repeat stool examinations (and urinalyses

in case of Schistosoma haematobium schistosomiasis) may be necessary to detect parasites in the first few weeks after exposure. Even then, tests may be negative because of a long prepatent period (eg, 2 mo in schistosomiasis). Chronic strongyloidiasis is usually asymptomatic or gives rise to mild gastrointestinal symptoms, most often peptic ulcer-like symptoms. Of greater concern is its potential to become a fulminant, fatal illness in appropriate circumstances. Strongyloides hyperinfection syndrome and dissemination result from decreased cell-mediated immunity, including that associated with corticosteroid treatment and HTLV1.5,9 Ibrutinib order Disseminated strongyloidiasis carries mortality rates from 50% to 87%, even with treatment.3 This

infection is now considered the leading cause of death from a parasitic disease in the United States.10 In Western countries chronic, usually asymptomatic, strongyloidiasis was classically associated with immigration. However, it is now increasingly seen in tourists. In a series of 43 travelers with strongyloidiasis in Canada, the infection was associated with visiting friends and relatives in 37% of the cases, tourism in 30%, and immigration in 21%.11 These results may illustrate an epidemiological change in the acquisition of strongyloidiasis in Canada; on the other hand, they may be the result of referral bias. However, it is interesting to note that in an older series of 76 persons in Canada with confirmed strongyloidiasis, nonmigrants made up only 4% of the cases, whereas 96% were persons who had immigrated a median of 48 months (range 2–480 mo) prior to presentation.

pseudintermedius exfoliative toxins. This work was supported by Grants-in-Aid for Scientific Research

(to K.N. and J.H.) and by Grants-in-Aid for Scientific Research on Priority Areas ‘Applied Genomics’ (to M.S.) and ‘Comprehensive Genomics’ (to M.H.) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. K.I. and J.H. contributed equally to this study. “
“Trichoderma spp. are well-known biocontrol agents because of their antimicrobial activity against bacterial and fungal phytopathogens. However, the biochemical mechanism of their antiviral activity remains largely unknown. In this study, we found that Trichokonins, antimicrobial peptaibols isolated from Trichoderma pseudokoningii SMF2, could

induce defense responses and systemic resistance in tobacco (Nicotiana STA-9090 concentration tabacum var. Samsun NN) against tobacco mosaic virus (TMV) infection. Local Trichokonin (100 nM) treatment selleck compound led to 54% lesion inhibition, 57% reduction in average lesion diameter and 30% reduction in average lesion area in systemic tissue of tobacco compared with control, indicating that Trichokonins induced resistance in tobacco against TMV infection. Trichokonin treatment increased the production of reactive oxygen species and phenolic compounds in tobacco. Additionally, application of Trichokonins significantly increased activities of pathogenesis-related enzymes PAL and POD, and upregulated the expression of several plant defense genes. These results suggested that multiple defense pathways in tobacco were involved in Trichokonin-mediated TMV resistance. We report on the antivirus mechanism of peptaibols, which sheds light on the potential of peptaibols in plant viral disease control. In past decades, attention has been paid to the development of biological control agents that are efficient, reliable and safe to the environment

(Lyon & Newton, 1997). Among the biological control agents that have shown a satisfactory degree of control of pathogens, some Trichoderma spp. are well-known for their ability to reduce disease incidence by inhibiting growth and development of fungal and Astemizole bacterial plant pathogens and inducing plant defense reactions (Yedidia et al., 1999; Segarra et al., 2009). Although the antimicrobial activity of Trichoderma spp. against fungi and bacteria and the involved mechanisms have been widely studied (Howell, 2003; Harman et al., 2004), the antiviral effect of Trichoderma spp. and the underlying biochemical and molecular mechanisms are still unknown. Peptaibols, mainly identified from Trichoderma spp., play an important role in the antimicrobial activities of these biocontrol fungi (Daniel & Filho, 2007). At present, 316 peptaibols have been identified, >60% of which are from Trichoderma spp. (http://www.cryst.bbk.ac.uk/peptaibol/home.shtml).

The transmission of maternal E. coli colonizing the newborn can occur after colonization

or infection of amniotic fluid, after membrane rupture or on passage of the neonate through the vaginal canal during delivery, and may cause early neonatal infection. Data on the features and virulence factors of infection-causing E. coli strains in mothers and babies, and colonization of genital tracts of pregnant women by this microorganism are scarce. Neonatal sepsis by E. coli is related to a limited number of phylogenetic groups B2 and D, both considered as virulent. The pathogenicity of these groups is associated with the presence of several virulence factors, some of which are contained into pathogenicity islands (PAIs) (Soto selleck products et al., 2008). The study of these E. coli strains is necessary to understand the potential risk factors for vertical transmission of neonatal infection by pregnant women and to design interventions Ganetespib purchase to address such risk factors adequately. The aim of this study was to compare the virulence factors present in E. coli isolates from the genital tract of pregnant women with those of E. coli from nonpregnant women in order to shed light on the possible differences in the virulence profiles that could

explain their capacity to cause severe infections. The study included 648 vaginal and endocervical samples from 321 pregnant and 327 nonpregnant women followed either at the antenatal visits or at the Gynecology Department of the Hospital Clinic of Barcelona. Samples from each woman were collected using sterile swabs. The samples were spread in chocolate agar (PVX, BioMèrieux, Spain). Colonies with an E. coli appearance were grown in McConkey agar (MCK, BioMèrieux) with subsequent biochemical

identification using the β-glucuronidase/indol test (DIATABS, Rosco Diagnostica, Taastrup). Escherichia coli isolates Etomidate were grown in blood agar plates (COS, Oxoid) to study their hemolytical capacity. The virulence profile was analyzed by PCR using gene-specific primers for 17 virulence genes such as hemolysin (hly), cytotoxic necrotizing factor (cnf1), autotransporter (sat1), P-fimbriae (pap genes), type 1C fimbriae (focG), yersiniabactin (fyu), heat-resistant hemagglutinin (hra), S-fimbriae (sfaS), invasin (ibeA), adhesin (iha), aerobactin (iucD), siderophores (iutA, iroN) and antigen 43 (ag43) (Table 1). PCR conditions were 94 °C for 4 min, followed by 30 cycles of 94 °C for 30 s, the corresponding annealing temperature (55–63 °C) for 30 s, 72 °C for 2 min and a final elongation of 72 °C for 5 min. Samples were run in 1.5% agarose gels and stained with SYBR Safe DNA gel stain (Invitrogen, Spain). The E.

2). Other dilutions were carried out in sterilized water and ranged from 10−2 to 10−6, depending on the degree of bacterial growth. The number of viable bacteria in each tube was determined in triplicate. They were plated on BHI agar using 50 μL volumes in triplicate. The number of colonies on agar was counted on a light board after incubation at 37 °C for 24 h. The antimicrobial effects of the tested compounds with different concentrations were compared with the appropriate Y-27632 manufacturer controls by anova.

Similar comparisons were also made among different compounds within each concentration tested. The bactericidal rate is calculated as follows: Inhibition of the three Gram-positive bacteria S. aureus, B. subtilis and B. cereus by the three chelators

is illustrated in Fig. 3. As shown in Fig. 3a, CP251 completely inhibited the growth of S. aureus at 500 μg mL−1, indicating that CP251 can be bactericidal against S. aureus at this concentration, while at the same concentration, DTPA decreased the growth of S. aureus from 3.2 × 104 to 8.5 × 102 CFU mL−1, yielding a bactericidal rate of 97.3%. CP252 decreased the growth of S. aureus to 8.75 × 103 CFU mL−1, indicating a bactericidal rate of 72.7%. DTPA exhibited marked inhibition against B. subtilis isolated from mussel, decreasing the growth of B. subtilis from 4.5 × 107 to 2.2 × 106 CFU mL−1 at 1000 μg mL−1 (the bactericidal rate was 95.1%) and to ABT-199 concentration 1.4 × 103 CFU mL−1 at 1500 μg mL−1 (the bactericidal rate was almost 100.0%). The inhibitory effects of CP251 and CP252 were found to be much

weaker at 1500 μg mL−1. However, at a concentration of 3000 μg mL−1, CP251 isothipendyl and CP252 both showed a marked inhibitory effect on the growth of the bacterium, decreasing the growth of B. subtilis from 4.5 × 107 to 8.1 × 103 and 4.2 × 104 CFU mL−1, respectively. The bactericidal rate of both compounds at this concentration was close to 100.0% (Fig. 3b). However, all three chelators were found to have only a weak inhibitory influence against B. cereus. CP251, DTPA and CP252, respectively, decreased the growth of B. cereus from 7.45 × 107 to 1.35 × 107, 1.64 × 107 and 1.89 × 107 CFU mL−1 at 2000 μg mL−1, the corresponding bactericidal rates being 81.9%, 78.0% and 74.6% (Fig. 3c). Inhibition of the chelators against three Gram-negative bacteria P. aeruginosa, V. parahaemolyticus and E. coli is illustrated in Fig. 4. CP251 completely inhibited the growth of P. aeruginosa at a concentration of 100 μg mL−1, indicating that CP251 is bactericidal against P. aeruginosa, while DTPA decreased the growth of P. aeruginosa from 2.75 × 104 to 3.8 × 103 CFU mL−1 at 100 μg mL−1, indicating a bactericidal rate of 86.2%. CP252 decreased the growth of P. aeruginosa from 2.75 × 104 to 8.45 × 103 CFU mL−1 at 100 μg mL−1, generating a bactericidal rate of 69.3% (Fig. 4a). Compared with S. aureus, the chelators inhibited the growth of P. aeruginosa more effectively. CP251 strongly inhibited the growth of V.

A single colony of this species was transferred to fresh medium and used for all subsequent experiments. The culture was confirmed as axenic by microscopy, colony morphology and 16S rRNA cloning and analyses. To explore the ability of the isolate to metabolize

a range of electron acceptors, nitrate, Fe(III)-NTA, Fe(III)-oxyhydroxide or Fe(III)-citrate was added (20 mM) to minimal medium with either acetate or glycerol (10 mM) as an electron donor. Electron donor utilization was tested using Fe(III)-citrate (20 mM) as the electron acceptor and lactate, formate, ethanol, glucose, yeast extract, benzoate, acetate or glycerol (10 mM) as potential electron donors. The pH tolerance was assessed using Fe(III)-citrate medium (20 mM) with glycerol (10 mM) as the electron donor at pH ranging from 3.5 to 10. The pH of the medium was adjusted Selleckchem HDAC inhibitor with NaOH or HCl prior to inoculation. The 16S–23S rRNA intergenic spacer region from the bacterial RNA operon was amplified as described previously using primers ITSF and ITSReub (Cardinale et al., 2004). The amplified

products were separated by electrophoresis in Tris-acetate–EDTA gel. DNA was stained with ethidium bromide and viewed under short-wave UV light. Positive microbial community changes identified by the Ribosomal Intergenic Spacer Analysis (RISA) justified further investigation by DNA sequencing of 16S rRNA gene clone libraries. PCR products were purified using a QIAquick PCR purification kit (Qiagen, UK) and ligated directly into a cloning vector containing topoisomerase I-charged vector arms (Agilent Technologies, UK) prior Selleckchem GSI-IX to transformation into Escherichia coli-competent cells expressing Cre recombinase (Agilent Technologies). White transformants that grew on LB agar containing ampicillin and X-Gal were screened for an insert using PCR. Primers were complementary to the flanking regions of the PCR insertion site of the cloning vector. The conditions for PCR method were as follows: an initial denaturation at

94 °C for 4 min, melting at 94 °C for 30 s, annealing at 55 °C for 30 s, extension at 72 °C for 1 min, 35 cycles, followed by a final extension step at 72 °C for 5 min. The resulting PCR products were purified using an ExoSap protocol, and 2 μL of ExoSap mix (0.058 μL exonuclease I, 0.5 μL Shrimp alkaline Rapamycin order phosphatase and 1.442 μL QH2O) was added to 5 μL of PCR product and incubated at 37 °C for 30 min followed by 80 °C for 15 min. Nucleotide sequences were determined by the dideoxynucleotide method (Sanger et al., 1977). An ABI Prism BigDye Terminator Cycle Sequencing kit was used in combination with an ABI Prism 877 Integrated Thermal Cycler and ABI Prism 377 DNA Sequencer (Perkin Elmer Applied Biosystems, UK). Sequences (typically 900 base pairs in length) were analysed against the NCBI (USA) database using the blast program packages and matched to known 16S rRNA gene sequences.

Fig. S2. Anaerobic P-PO4−3 release (normalized to VSS; analogous to cell dry weight). Whilst anaerobic release averaged greater than 13.5 mg P-PO4−3 g−1 VSS for the 40 day pre-pandemic period and first 21 days of the simulated pandemic period, it went below 10

mg P-PO4−3 g−1 VSS in the 100% OC dosing period and had decreased to below 5 mg P-PO4−3 g−1 VSS by the end of the dosing period. Dotted lines represent the ends of a particular dosing regime and indicate the OC dosing level as a AZD0530 molecular weight percentage of the maximum OC dose. Fig. S3. Aerobic nitrate production (normalized to VSS; analogous to cell dry weight). Whilst aerobic nitrate production averaged over 0.85 mg N-NO3− g−1 VSS for the pre-pandemic period and the first 35 days of simulated pandemic period (excluding outlier at 31 days before start of dosing), it had decreased to below

0.4 mg N-NO3− g−1 VSS by day 42 and there was no nitrate production by day 56. Dotted lines represent the ends of a particular dosing regime and indicate the OC dosing level as a percentage of the maximum dose. Fig. S4. Particle size distribution of granules, including 10th (filled circles), 50th (open circles) and 90th (filled triangles) percentiles. Error bars represent standard error of the mean of three replicate measurements. Dotted lines represent the ends of a particular dosing regime and indicate the OC dosing level as a percentage of the maximum dose. Fig. S5. Light microscopy images of granules against RG7204 a black background taken on different days at different dosing regimes (indicated as the OC dosing level as a percentage of the maximum dose). All images were taken at the same magnification. Scale bar (Day 13 image) represents 1500 see more μm. Fig. S6. Effluent SS. Dotted lines represent the ends of a particular dosing regime and indicate the OC dosing level as a percentage of the maximum dose. Fig. S7. Shannon evenness (J) derived from T-RFLP data. Dotted lines represent the ends of a particular dosing regime and indicate the OC dosing level

as a percentage of the maximum dose. Fig. S8. Richness (S) derived from T-RFLP data. Dotted lines represent the ends of a particular dosing regime and indicate the OC dosing level as a percentage of the maximum dose. Table S1. Dosing of pharmaceuticals. N.B. Only OC was measured; the measured concentrations of OC were within 16% of their expected values for all except the lowest dose (i.e. 0.36 μg OC L−1 or 0.1% of the maximum dose), for which the measured values were different by between 27 and 75% of their expected values. Appendix S1. Reactor operation. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article.

This has important implications for the subsequent development of HCC and screening strategy [29]. HBV is directly carcinogenic and may promote the development of HCC in the absence of cirrhosis, especially in populations where HBV may have been acquired at birth and in early childhood [31]. It has also become evident that high HBV viral loads may be linked to the development of HCC [32]. It is probable that a lower CD4 cell count, particularly in the context of HBV coinfection, is associated with a higher risk of HCC [33]. HIV coinfection also accelerates the

progression of HBV infection [34]. There is a large regional variation in the proportion of people with HIV who have previously been exposed to HBV (10–90%). Retrospective series suggest that HBV is responsible for a much smaller proportion of HCC compared to HCV in HIV-positive click here individuals [29,30]. HIV-positive LY2109761 HCC patients are younger and are more often HCV positive [30,35–37]. The majority of the HIV cohort has HCV and cirrhosis. The great majority of HIV-positive HCC patients are on HAART at diagnosis and consequently

they tend to be only moderately immunosuppressed [30,35]. There appears to be no significant difference between HIV-positive and -negative patients in the Barcelona Clinic Liver Cancer (BCLC) stage at presentation [35]. Most HCCs are identified with ultrasound scanning and AFP levels [30]. The degree of cirrhosis should be assessed prior to any definitive treatment using the Child–Pugh classification. HIV-positive HCC patients are more likely to have compensated liver disease (Child–Pugh A). A CT scan of the chest, abdomen and pelvis is required to exclude metastatic disease. Initial series in HIV-positive

individuals with HCC showed that the majority of patients were not being offered active treatment and that consequently outcome was poor [30]. Although more recent work has shown an improvement in the situation [35], others report that one-third of patients remain untreated and even in those with potentially curable disease, one-quarter receive less oxyclozanide effective treatment than is indicated [38]. When HIV patients are offered active treatment they have a similar survival to their HIV-negative counterparts [35,37,39–41]. Whether HIV status is itself related to survival remains uncertain. One series comparing 65 HIV-positive and 267 HIV-negative patients with HCC found that HIV status negatively influenced outcome in both treated and untreated patients [42], whilst HIV-associated HCC patients have a higher drop-out rate pre-transplantation and appear to have a more aggressive overall disease course [36].