Sheehan and colleagues5 described a case of intramedullary spinal cysticercosis in a 16-year-old American woman who traveled to Mexico 10 years before the presentation. This patient lived just outside Washington, DC. She adhered to a Kosher diet and denied consuming pork. For our patient, we analyzed cox1 gene of mtDNA for the identification of the haplotype of the unstained histopathological specimens.1 The cox1 sequence data revealed that it was completely the same as the haplotype of Korea and China1 in Asian genotype.6 Since this patient has never visited Korea and China and the haplotype of T solium in Thailand differs from Korea and China, so far as we know it is most likely that she acquired the infection in Laos during

click here one of her previous trips. It suggests that the haplotype of Korea and China may be distributed widely in Asia including Laos. It is unlikely that she acquired the spinal cysticercosis during her most recent trip, because the symptoms had begun before her recent trip and the parasite had already degenerated into the tissue specimen.

Probably, she had a chronic infection that became progressively symptomatic prompting her recent presentation to the hospital. This approach to use unstained pathological specimens can become a powerful tool to assess where the patient became infected, especially in the case of patients who traveled to multiple endemic countries or who had never visited such regions but got accidental infections in developed countries from some others who were either visitors from Rutecarpine endemic areas or residents after traveling to such endemic areas.1,7,8 NCC can be divided into I-BET-762 manufacturer parenchymal, leptomeningeal, intraventricular, and spinal cysticercosis according to the location of involvement.9 Most often the brain is affected and is involved in 60% to 92% of all patients with cysticercosis.10 Spinal NCC is rare compared with intracranial NCC involving the brain, basal cisterns, and ventricles. In 1963, Canelas and colleagues11 reported a 2.7% incidence of spinal NCC in 296 cases of NCC. Since that

time, others have suggested that the incidence of spinal NCC is up to 5%;5 however, an incidence of <1% to 3% is most often reported among more recent case series.3,12 A differential diagnosis of the spinal cystic lesions includes spinal tumors, epidermoid tumors, echinococcosis, arachnoid/colloid cysts, and meningoceles. Accurate diagnosis of NCC is based on neuroimaging studies, laboratory analysis of the cerebrospinal fluid, and antibody detection in the serum. A set of diagnostic criteria has been proposed to help clinicians and health workers with the diagnosis of NCC.13 One of the absolute or gold standard criteria for the diagnosis of NCC is histological demonstration of the parasite in biopsy or operation material. Histologically, encystment of cysticercus larva is seen. The cyst is comprised of the outer layer, covered by hair-like projections.

Sheehan and colleagues5 described a case of intramedullary spinal cysticercosis in a 16-year-old American woman who traveled to Mexico 10 years before the presentation. This patient lived just outside Washington, DC. She adhered to a Kosher diet and denied consuming pork. For our patient, we analyzed cox1 gene of mtDNA for the identification of the haplotype of the unstained histopathological specimens.1 The cox1 sequence data revealed that it was completely the same as the haplotype of Korea and China1 in Asian genotype.6 Since this patient has never visited Korea and China and the haplotype of T solium in Thailand differs from Korea and China, so far as we know it is most likely that she acquired the infection in Laos during

GSK126 manufacturer one of her previous trips. It suggests that the haplotype of Korea and China may be distributed widely in Asia including Laos. It is unlikely that she acquired the spinal cysticercosis during her most recent trip, because the symptoms had begun before her recent trip and the parasite had already degenerated into the tissue specimen.

Probably, she had a chronic infection that became progressively symptomatic prompting her recent presentation to the hospital. This approach to use unstained pathological specimens can become a powerful tool to assess where the patient became infected, especially in the case of patients who traveled to multiple endemic countries or who had never visited such regions but got accidental infections in developed countries from some others who were either visitors from Carteolol HCl endemic areas or residents after traveling to such endemic areas.1,7,8 NCC can be divided into Epacadostat parenchymal, leptomeningeal, intraventricular, and spinal cysticercosis according to the location of involvement.9 Most often the brain is affected and is involved in 60% to 92% of all patients with cysticercosis.10 Spinal NCC is rare compared with intracranial NCC involving the brain, basal cisterns, and ventricles. In 1963, Canelas and colleagues11 reported a 2.7% incidence of spinal NCC in 296 cases of NCC. Since that

time, others have suggested that the incidence of spinal NCC is up to 5%;5 however, an incidence of <1% to 3% is most often reported among more recent case series.3,12 A differential diagnosis of the spinal cystic lesions includes spinal tumors, epidermoid tumors, echinococcosis, arachnoid/colloid cysts, and meningoceles. Accurate diagnosis of NCC is based on neuroimaging studies, laboratory analysis of the cerebrospinal fluid, and antibody detection in the serum. A set of diagnostic criteria has been proposed to help clinicians and health workers with the diagnosis of NCC.13 One of the absolute or gold standard criteria for the diagnosis of NCC is histological demonstration of the parasite in biopsy or operation material. Histologically, encystment of cysticercus larva is seen. The cyst is comprised of the outer layer, covered by hair-like projections.

P values of <0.05 were considered significant. Statistical analysis was performed using spss version 17 software (SPSS Inc., Chicago, IL). All experiments were carried out at least in triplicate. Table 1 shows the MICs of allicin and fluconazole against C. albicans ATCC 14053 and some clinical isolates. The results are representative of two

independent experiments arranged in triplicate. The MIC50 and MIC90 of these isolates ranged from 0.05 to 0.78 μg mL−1 and 0.1 to 12.5 μg mL−1, respectively for allicin, and from 0.25 to 4 μg mL−1 and 2 to 16 μg mL−1, respectively, for fluconazole. All samples were sensitive to fluconazole and drug resistance was not seen. The potency of allicin and fluconazole in decreasing the cell number of C. albicans ATCC

14053 after 0, 2, 4, 6, 8, 12 and 24 h was significant compared PD0332991 mw with the control growth (Fig. 1). Figure 1a and b indicate the inhibitory effect of allicin and fluconazole on different inoculum sizes of C. albicans. The significant reduction of Candida treated with allicin and fluconazole started after 4-h incubation (P<0.01) in comparison to untreated control for both inoculum sizes (Fig. 1). Candida albicans cells grown in RPMI 1640 medium at 35 °C showed typical yeast cells with a smooth surface after 24 h, but cells treated with increasing concentration of allicin or fluconazole displayed changes Selleckchem Inhibitor Library in surface morphology, with the cell surface becoming rough and irregular. According to Lemar et al. (2005) the main reason for this phenomenon could be a decreased cytoplasmic volume. It was also observed in the present study that higher concentrations of the antifungal agents (such as 10 × MIC) destroyed the cell surface, inducing puncture in allicin-treated samples and causing cell lysis in fluconazole-treated samples (Fig. 2). The results of fungal load determination Tenofovir in vivo in the liver, kidney and spleen at different time points indicated a significant

reduction of CFU g−1 of the tissue (P<0.001) starting from the second day postinfection for different dosages of the antifungals. In addition, the reduction of Candida cells CFU in tissues after 28 days postinfection ranked from 5 mg kg−1 day−1 fluconazole >1 mg kg−1 day−1 fluconazole >5 mg kg−1 day−1 allicin >1 mg kg−1 day−1 allicin (Table 2). As described before, the mortality and morbidity of the treated mice were evaluated for 28 days postinfection. Table 3 also shows the mean survival time (MST) of mice treated with different drugs. Moreover, based on statistical analysis of log rank=13.449 in this study, comparison of the mean of survival time between treated and control groups indicated significant differences (P<0.05) (Fig. 3). Previous reports have demonstrated the antifungal activity of allicin in vitro against Aspergillus, Trichophyton and Candida spp. (Yamada & Azuma, 1977; Aala et al., 2010). On the other hand, the antifungal potential of allicin against Aspergillus spp. was presented by Shadkchan et al.

Cheeses

have a number of advantages over fresh fermented products (such as yoghurt) as a delivery system for viable probiotic to GI tract. Cheeses tend to have a higher pH and more solid consistency where the matrix of the cheese and its relatively high fat content may offer protection to probiotic bacteria during passage through the GI tract. Cheese also has high buffering capacity than yoghurt (Gardiner et al., 1998). Overall, the major points to be addressed while incorporating probiotics into foods are the selection of a compatible probiotic strain/food type combination; using food processing conditions that are compatible with probiotic survival; ensuring that the food matrix supports Talazoparib chemical structure probiotic growth (if fermentation is required); selecting a product matrix, packaging, and environmental conditions to ensure adequate probiotic survival over the product’s supply chain and during shelf storage; and finally ensuring that addition of the probiotic does not adversely impact on the taste and Neratinib supplier texture of the product. Probiotics are normally added to foods as a part of the fermentation process. The emphasis for prolonged survival of probiotics

in the food matrix has resulted in the alteration in the functionality and efficacy of the food product. In order to exert health benefits, probiotic bacteria must remain viable in the food carriers and survive the harsh condition of GI tract, with a minimum count of 106 CFU g−1. The nature of food carrier can affect the stability of the probiotic microorganisms during GI transit. Although dairy-based products are suggested to be the main carriers for the delivery of probiotics, other nondairy-based products such as soy and fruits can be exploited as a potential carrier of probiotic microorganisms because of the increasing

demand for new flavor and taste among consumers. A brief idea about the variety Dimethyl sulfoxide of products that serve as carriers for probiotics is given in Table 4. B. animalis, L. acidophilus, L. brevi, L. paracasei L. acidophilus, L. casei, Bifidobacterium Lactobacillus, Bifidobacterium, Streptococcus thermophilus L. acidophilus, L. casei, Bifidobacterium L. casei, L. rhamnosus GG, L. paracasei, L. acidophilus LA39 The regulatory status of probiotics as a component in food has to be established on an international level. A regulatory framework should be established to better address probiotic issues, including efficacy, safety, labeling, fraud, and claims. Probiotic products shown to confer defined health benefits on the host should be permitted to describe these specific health benefits. Surveillance systems (trace-back, postmarketing) should be put in place to record and analyze adverse events associated with probiotics in food and monitor long-term health benefits.

“
“Uncontrolled viral replication and antiretroviral treatment (ART) may independently contribute to hepatic mitochondrial toxicity. The present study

was designed to explore the longitudinal effects of treatment modifications on hepatic mitochondrial function by means of noninvasive 13C-methionine breath test (MeBT) diagnostics. A total of 113 HIV-infected patients underwent two consecutive MeBTs over an interval of 11.8±3.5 months. Forty-nine patients remained on stable ART or no therapy; 28 participants switched ART; 27 patients (re)initiated ART, and nine individuals underwent a structured treatment interruption (STI) of ART between MeBTs 1 and 2. Breath test results were expressed as cumulative percentage dose of 13CO2 recovered after 1.5 h test time (cPDR1.5h). Initiation of ART in treatment-naïve individuals and patients on Z-VAD-FMK in vivo STI was associated

with a significant improvement of hepatic mitochondrial function (P<0.05). Cessation of ART or a prolonged delay in initiating therapy in treatment-naïve patients in turn led to a significant decline of 13C-exhalation compared with baseline (P<0.05). A marked increase in 13C-exhalation click here was observed in individuals who switched from stavudine or ddI to tenofovir or abacavir (+170%; P<0.001), while no differences between MeBTs 1 and 2 were found in individuals on ART who had remained on stable regimens or in those who changed a protease

inhibitor (PI) or nonnucleoside reverse transcriptase inhibitor (NNRTI) component. The present data suggest that hepatic mitochondrial function in HIV disease is a dynamic process with a high regenerative capacity and highlight the pathogenic relevance of HIV replication. Our findings suggest that modern ART per se does not negatively impact hepatic mitochondrial function. Increasingly, deaths among Janus kinase (JAK) HIV-infected persons are caused by hepatic complications [1,2]. Indeed, the majority of liver-related morbidity within the D:A:D cohort has been attributed to viral hepatitis coinfection. In the next few decades, a shift of morbidity to metabolic liver diseases is likely, analogous to the rising prevalence of the metabolic syndrome within the HIV-negative population [3]. The putative pathogenic role of antiretroviral therapy (ART) in this context is contested. Although the introduction of combination ART (cART) has reduced overall hepatic morbidity in both HIV-monoinfected and HIV/hepatitis C virus (HCV)-coinfected individuals, data on the long-term hepatotoxic effects of ART are absent. Two recently published cross-sectional trials showed a prevalence of nonalcoholic fatty liver disease in HIV-monoinfected patients of about 30%, which seems to be higher than calculated for the age-adjusted HIV-negative population [4,5].

Forty-two (77.8%)

of 54 patients with AHC who received therapy started it before week 12. Further characteristics of both populations are listed Gemcitabine clinical trial in Table 1. The IL-28B genotypes were in Hardy–Weinberg equilibrium (P=0.791 for AHC and 0.821 for CHC). The prevalence of the rs12979860 CC genotype was 47.5% among patients with AHC and 45.8% in those with CHC (P=0.778) (Table 1). In the group of individuals with AHC, 31 subjects with genotype CC (81.6%) were infected with HCV genotype 1 or 4 and 7 (18.4%) with genotype 2 or 3. Among CT/TT patients with AHC, 32 (76.2%) were infected with genotype 1 or 4 and 10 (23.8%) with genotype 2 or 3, respectively (P=0.948). In the group of patients with CHC, 119 (54.6%) of those with rs12979860 genotype CC were carriers of HCV genotype 1 or 4, while

99 (45.4%) were infected with HCV genotype 2 or 3. Of those harbouring rs12979860 genotype CT/TT, 200 (77.5%) bore HCV genotype 1 or 4 and 58 (22.5%) genotype 2 or 3 (P<0.001). A more detailed genotype distribution is shown in Table 2. In the subpopulation of patients with CHC enrolled in the German cohort, the distribution of HCV anti-PD-1 monoclonal antibody genotypes was also significantly different from that found in patients with AHC. Specifically, 41 (53.9%) German patients with CHC and rs12979860 CC harboured HCV 1 or 4 vs. 65 (75.6%) of those bearing CT/TT (P=0.034). There were no significant differences in HCV plasma load among patients with different IL-28B genotypes in the overall population. Thus, the median (Q1–Q3) HCV-RNA level was 6.36 (5.68–6.88) log10 IU/mL in carriers of rs12979860 CC and 6.27 (5.59–6.79) log10 IU/mL in those harbouring CT or TT (P=0.458). However, HCV-RNA load was significantly higher in patients with AHC and the CC genotype than C59 in those with AHC and rs12979860 CT/TT (Table 3). ALT levels in the entire population were higher in patients with the CC genotype [83 (58–165) in CC carriers vs. 74 (45–126) in CT/TT carriers; P=0.022]. The relationships between the IL-28B genotype and several parameters in the AHC and CHC groups are listed

in Table 3. Spontaneous clearance of HCV, as defined in this study, was documented in eight (10.1%) of the 79 patients in whom this information was available. There was no relationship between spontaneous clearance of the virus and HCV genotype. Thus, the numbers of patients who cleared HCV were as follows: six (11.3%) with genotype 1, one (12.5%) with genotype 2, one (10%) with genotype 3 and none with genotype 4 (P=0.746). The association between IL-28B genotype and spontaneous clearance did not reach statistical significance. Five (13.5%) of the patients with rs12979860 genotype CC and three (7.1%) of the patients with genotype CT or TT (P=0.349) showed spontaneous HCV clearance. The associations between IL-28B genotype and other factors are displayed in Table 3.

, 2004). In pgsA mutant cells, the deficiency in the acidic phospholipids, phosphatidylglycerol and cardiolipin, causes retarded translocation of newly synthesized proteins across the inner membrane due to impaired activation of SecA in the translocation machinery (Dowhan et al., 2004), impairment in the production of OmpF protein and flagellin (Inoue et al.,

1997), and activation of the Rcs phosphorelay regulatory system (Shiba et al., 2004; Nagahama et al., 2006). The impairment of flagellin production in pgsA3 mutant cells is due to the transcription repression of the flagellar master operon flhDC (Kitamura et al., 1994). Our recent studies have shown that accumulation of σS is involved in the repression of the master operon. The transcriptional activity, as monitored via rpoS′-lacZ

transcriptional fusion GDC0199 Nutlin-3a mw and real-time PCR, in pgsA3 mutant cells is 2.6 times as high as in pgsA+ cells (Uchiyama et al., in press). While the enhanced transcription could conceivably be solely responsible for the accumulation, post-transcriptional accumulation has also been suggested to play an important role in the mutant cells, because the σS content in the mutant cells is significantly higher even if the same level of rpoS mRNA is expressed from a regulatable promoter (Uchiyama et al., in press). It is well known that σS is the master regulator that controls the genes expressed upon entry into the stationary phase and against general stress, including starvation (Tanaka et al., 1993; Pratt & Silhavy, 1998; Hengge-Aronis, 2002). Various levels Tacrolimus (FK506) of σS regulation are affected by various stress signals; an increased content of σS might be obtained by rpoS transcription or rpoS mRNA translation, or by inhibition of σS proteolysis (which, under nonstress conditions in logarithmic growth, is quite rapid via the ClpXP protease) (Pratt & Silhavy,

1998; Hengge-Aronis, 2002; Majdalani et al., 2002; Bougdour et al., 2006; Peterson et al., 2006). In the present study, we focus on the mechanisms for post-transcriptional σS accumulation, that is, we investigate the translation of rpoS mRNA and the proteolytic degradation of the sigma factor in mutant cells with acidic phospholipid deficiency. The E. coli K-12 strains and plasmids used in this study are listed in Table 1. New strains were constructed by P1 phage transduction and the methods described below, and their genotypes were verified by drug resistance tests, PCR amplification, nucleotide sequencing, and determination of phospholipid composition, as applicable. Strain BW25113ΔclpPX was constructed using the λ Red system (Datsenko & Wanner, 2000).

44 per 10 person-years) vs. 644 cases (0.89 per 10 person-years), respectively; P<0.0001]. The incidence of lipid-lowering drug use among HIV/HBV-coinfected ABT-199 clinical trial participants was not significantly lower [70 cases (0.77 per 10 person-years)] than among HIV-monoinfected participants. The proportions of participants developing grade 3 or 4 lipid abnormalities or lipid-lowering drug use over time are shown in Fig 1a–e and increased with duration on therapy. This was true for all lipid abnormalities combined

(Fig. 1a) and for individual measures (Fig. 1b–e). The proportion of HIV/HCV-coinfected participants with grade 3 or 4 lipid abnormalities was consistently lower for each specific measure of hyperlipidaemia and at each time-point compared with HIV-monoinfected participants. Predictors of developing any grade 3 or 4 hyperlipidaemia or lipid-lowering drug use that were statistically significant in univariate analyses included HIV/HCV coinfection, older male, earlier start year of HAART, NNRTI-containing regimen and PI-containing regimen (Table 2). HIV/HBV coinfection was not associated with development of hyperlipidaemia in the univariate analysis. Multivariate logistic regression analysis revealed that both HIV/HCV- and

HIV/HBV-coinfected participants had a decreased risk of hyperlipidaemia or lipid-lowering drug use after adjusting for age, gender and start year of HAART (Table 3), although HCV coinfection was more protective than HBV coinfection. HIV/HCV-coinfected participants were Romidepsin less likely than HIV-monoinfected participants to ever develop elevated total cholesterol, total:HDL cholesterol ratio, LDL cholesterol and triglycerides in univariate analyses (Table 2). Other covariates that were significantly associated with these outcomes included older male,

earlier start year of HAART, NNRTI-containing regimen and PI-containing regimen. Higher weight was significantly associated with development of elevated total:HDL cholesterol ratio and triglycerides (Table 2). Multivariable logistic regression models revealed that both HIV/HCV and HIV/HBV coinfections were associated with a decreased risk of developing 3-mercaptopyruvate sulfurtransferase elevated total cholesterol levels and total:HDL cholesterol ratio but that only HIV/HCV coinfection was associated with a decreased risk of developing elevated LDL cholesterol or triglycerides (Table 3). All models revealed that older age and male gender increased the risk of elevated lipids while initiation of HAART after 1998 was associated with a lower risk compared with initiation of HAART in 1997 or earlier (Table 3). Sensitivity analyses were conducted after classifying participants as HCV- or HBV-coinfected only if positive laboratory test results were available. Using these criteria, 186 participants were classified as HCV-coinfected and 116 as HBV-coinfected.

We observed a decline in the incidence of all CNS opportunistic infections except for PML. Different studies performed in France, Spain and Denmark have also shown a stabilization in the incidence of PML despite the widespread use of HAART [17, 23, 24]. This may be partly Selleck Talazoparib explained by the appearance of new cases of PML after the introduction of HAART associated with unmasking IRIS, as previously noted [25]. Different studies have shown a higher survival rate for CNS infections after the introduction of HAART [26, 27]. Indeed, patients with PML, which

is considered the most devastating CNS disorder associated with HIV, have shown improved prognoses [27-29]. Before the introduction of HAART, the median survival time for PML was 8–15 weeks [30], in contrast to the 44.5 months of estimated survival in our cohort. These data are similar to those obtained in other cohort studies performed in the HAART era [17, 24, 26, 27, 31, 32]. However, despite the improvement in survival and the reduction in the incidence, it is important to point out that overall prognosis Ku-0059436 cost of patients with CNS opportunistic infections is still

poor and most patients experience mild to severe neurological impairment and require long-term care [24, 25, 31, 32]. In our cohort, 31% of patients died and 29% were lost to follow-up. During the first 3 months after diagnosis of the CNS infection, the condition of 14 patients worsened and 24 died or were lost to follow-up. Finally, the estimated probability of survival was only 48% at 3 years. Taken together, these data indicate the necessity of early diagnosis of HIV infection and HAART in order to avoid the possibility of developing a CNS opportunistic infection. The incidence of IRIS in our cohort was 16.4%. This observation agrees with those in other cohorts, where between 17 and 25% of patients developed one or more manifestations as a consequence of the inflammatory syndrome after starting HAART [8, 33, 34]. A prospective study performed in South Africa showed an incidence Interleukin-3 receptor of 10% for patients initiating ART, including both unmasking and paradoxical forms of IRIS [35]. In our series, IRIS

presented as paradoxical IRIS in 55.5% of cases and the remaining 44.5% had unmasking IRIS. This finding is consistent with data from a multicentre cohort in which each type of IRIS represented 50% of cases [34]. Regarding the different neurological infections, two prospective studies reported that 13–17% of HIV-infected patients with cryptoccocal meningitis developed paradoxical IRIS after initiation of HAART [9, 36]. Of the 44 cases of IRIS described by Murdoch et al., 6.8% corresponded to cryptoccocal meninigitis, all of them unmasking IRIS [35]. Concerning PML, which has been the disease most commonly related to the development of IRIS, 25% of our cases met the criteria of IRIS, similar to the 18–23% described in previous observational studies [17, 27]. In our cohort, five of 40 (12.

The clinical and virological characteristics of the 76 genotype 1 HIV/HCV-coinfected patients are presented in Table 1. Patients’ characteristics did not differ between the group of six HIV/HCV-coinfected

patients harbouring HCV protease mutations and those without known HCV PI resistance mutations (Table 2). All of the sequences from HIV/HCV genotype 4-coinfected patients and those retrieved from the GenBank database had amino acid changes at position 36 (V36L) shown to confer decreased susceptibility to telaprevir. Finally, the NS3 catalytic triad (H57, D81 and S139) was highly conserved among the 120 sequences from HIV/HCV-coinfected this website patients. We found no significant difference in natural polymorphisms at positions associated with

HCV PI resistance between HCV-monoinfected and HIV/HCV-coinfected patients. Our results are in accordance with those of a study by Halfon et al. in a small group of patients. They did not find any difference in observed mutation rates between HCV-monoinfected and HIV/HCV-coinfected patients (19% and 18%, respectively) at positions associated with HCV PI resistance [9]. In contrast, Morsica et al. found a higher prevalence of HCV PI resistance mutations in 37 sequences obtained from coinfected patients in comparison with 250 sequences from HCV-monoinfected patients retrieved from the GenBank database (16.2% and 0.8%, respectively) [8]. In our study, which included a large number of patients, previous HCV treatment did not seem to influence the prevalence of HCV PI resistance mutations. No patient showed substitutions

at position A156, which are known to confer the highest level of resistance Dabrafenib to telaprevir or boceprevir. The role of other mutations is difficult to predict, but the possibility that they may have an impact on the virological response to treatment cannot be excluded and needs to be investigated. Indeed, HCV strains with naturally occurring mutations that may confer resistance to HCV PIs show reduced fitness and are generally sensitive to interferon and/or interferon plus ribavirin therapy regimens. The role of these mutations in long-term therapy buy Fludarabine and the likelihood of viral breakthroughs are still to be determined, in particular in patients who are nonresponders to previous interferon-based therapy or relapsers on this therapy. The preservation of the NS3 catalytic triad, as observed in our study, is probably attributable to functional constraints on the protease. Its structural and chemical integrity is required to process the HCV polyprotein. All sequences from genotype 4-infected patients contained mutation V36L, which is known to confer decreased susceptibility to telaprevir [11]. Large clinical trials to better document the efficacy of STAT-C in patients infected with genotype 4 are required. Our study on sequences from 120 HIV/HCV-coinfected patients suggests that the natural prevalence of strains resistant to HCV PIs does not differ between HCV-monoinfected and HIV/HCV-coinfected patients.