14, 95% CI 1.04–1.25) were more likely to achieve suppression than individuals residing in British Columbia. Individuals with a history of IDU were less likely to achieve suppression (HR 0.58, 95% CI 0.53–0.64).

Patients on initial antiretroviral regimens containing efavirenz (HR 1.30, 95% CI 1.16–1.47), lopinavir (HR 1.19, 95% CI 1.06–1.34) and atazanavir (HR 1.29, 95% CI 1.14–1.46) were more likely to achieve suppression NU7441 cell line than those whose first regimen contained nevirapine. Patients who initiated nelfinavir were less likely to achieve suppression (HR 0.66, 95% CI 0.56–0.78). Finally, patients with low baseline viral load measurements were more likely to achieve suppression (<4 log10 copies/mL, HR 1.49, 95% CI 1.29–1.65; 4–5 log10 copies/mL, HR 1.27, 95% CI 1.17–1.37) than patients with baseline viral load measures ≥5 log10 copies/mL. A life table was used to further explore the association of baseline viral load with suppression during follow-up. In Table 3, the probabilities of suppression at 6, 12, 18 and 24 months are listed by baseline viral load measure. Using a Bonferroni correction

for multiple comparisons Cobimetinib price (statistical significance level of P<0.0125, which is 0.05/4), it was found that, while baseline viral load was significantly associated with suppression at both 6 and 12 months of follow-up (P<0.001), by 18 and 24 months, baseline viral load was no longer a significant factor (P=0.050 and 0.223, respectively). In order to ascertain what effect baseline viral load had beyond 12 months, a subset of the data was analysed (n=832), which excluded PTK6 patients who achieved suppression earlier than 12 months as well as those with a follow-up time of less than 12 months. A Kaplan–Meier analysis showed that baseline viral load was not significantly associated with suppression for those followed for more than 12 months (log-rank P=0.118) (data not shown). Kaplan–Meier curves exploring provincial differences in time to suppression for subset populations indicated that provincial differences in suppression still existed when men, women, injecting drug users, non-injecting drug users

and those testing positive for hepatitis C were examined exclusively (Fig. 2). There were no provincial differences in suppression for those testing negative for hepatitis C (P=0.115). In this large multi-site Canadian cohort study we found that increased age, lower baseline viral load, having an AIDS diagnosis at baseline, male sex, non-IDU history and treatment in Ontario rather than British Columbia predicted increased likelihood of suppression. We also found that suppression was more likely with currently preferred regimens that include two NRTIs plus either an NNRTI or a ritonavir-boosted PI. Our finding of a 57% probability of suppression after 6 months of therapy is consistent with findings from other cohorts [17,18].

In our present study, PPIase was identified as one of the 12 gastric cancer-specific H. pylori genes. The result was supported by PCR-based screening of H. pylori strains, demonstrating that 50% of the H. pylori isolates obtained from gastric Metformin mw cancer patients were PPIase positive, whereas <24% of the H. pylori isolates from superficial gastritis patients were positive. PPIases catalyze the slow interconversion between cis and trans conformation of proline residues and affect protein folding and function (Kern et al., 1995). Thus, PPIases emerge as key

players in the control of fundamental proteins involved in cell proliferation and oncogenic transformation (Lu et al., 2007). Consistent with this, PPIases have been characterized as a virulence factor of L. pneumophila and T. cruzi (Fischer et al., 1992; Pereira et al., 2002). In addition, a novel pathogen-associated factor, HP0175, which contains PPIase core at its C-terminus, has been shown to induce gastric epithelial cell death through interaction with TLR4 (Pathak et al., 2006). Apoptosis contributes to the pathological outcome of the infection by disturbing the balance between the rate of new cell production and the rate of cell loss by apoptosis. Atrophic gastritis and gastric dysplasia after H. pylori

infection are associated with accelerated apoptosis of the gastric epithelium (Xia & Talley, 2001). PPIases may contribute to the pathology of gastric cancer by inducing hyperproliferation of gastric epithelium. Although PPIase is identified buy E7080 as a gastric cancer-specific H. pylori gene, our present result shows that fewer than a quarter of the superficial gastritis-associated H. pylori strains contain this gene. Given that PPIase plays an important role in cell growth, apoptosis and oncogenic transformation, we would predict that the PPIase-positive subpopulation of the superficial gastritis patients may

have the potential to develop severe gastric diseases such as atrophic gastritis, gastric dysplasia and gastric cancer. Thus, it would be worthwhile to clinically follow-up these superficial gastritis patients infected Montelukast Sodium with PPIase-positive H. pylori. PPIase may represent a novel marker for gastric cancer and a potential therapeutic target. This work was supported by grants from the National Basic Research Development Program of China (973 Program Award No.2010CB529304), National Natural Science Foundation of China (Award No.3100074) and the Foundation of the Key Laboratory of Cancer Intervention in Liaoning Province (Award No. 2009S106). “
“The cold stress response of Pseudomonas putida KT2440 was investigated by genomewide deep cDNA sequencing and gel-free MS-based protein profiling. Transcriptome and proteome profiles were assessed at 30 °C and 2 h after a downshift from 30 to 10 °C.

, 1998), by means of homologous recombination, which yielded a strain designated tet-RAM2. Using this strain, the effect of RAM2 repression on growth was investigated at several time points. The Epigenetics Compound Library manufacturer number of viable tet-RAM2 cells treated with 20 mg L−1 doxycycline showed a drastic decline 6 h after doxycycline addition (Fig.

2a). Similarly, the number of viable tet-RAM2 cells recovered from mice kidneys was also significantly lower in mice treated with doxycycline compared with untreated mice (Table 3). There was a similar reduction of viable cells obtained from kidneys of doxycycline-treated mice in a control strain, in which the essential TEF3 gene was placed under a tet-regulatable promoter (data not shown) (Nakayama et al., 1998). These

experiments demonstrate that RAM2 expression is required for viability not only in vitro but also in the organs of infected mice. To assess the importance of the ERG20 gene (Genolevures ID: CAGL0L00319g) for in vitro and in vivo growth, we generated tet-ERG20, in which the ERG20 gene was also placed under the control of the tet-regulatable promoter, 97t. Similar to tet-RAM2 cells, severe growth defects were observed in the ERG20-depleted cells cultured in vitro (Fig. 2b). Interestingly, there was no significant difference between doxycycline-treated mice and doxycycline-non-treated mice when viable tet-ERG20 Alectinib mouse cells were recovered from mice kidneys at 14 days after infections (Table 3). In addition, the growth profile of tet-ERG20 cells in doxycycline-treated mice was almost the same as that of wild-type CBS138 cells obtained from mice kidneys (Table 3). Using the Mann–Whitney U-test with respect to CBS138 and tet-ERG20 recovered cells, or doxycycline-treated and doxycycline-non-treated cells of each strain, the P value was >0.05,

indicating no significant difference. These results suggest that the ERG20 gene is essential for growth in vitro, but is not required for Loperamide in vivo growth in mice. Serum containing cholesterol can rescue the growth of C. glabrata cells in which a sterol defect has occurred (Nakayama et al., 2000; Bard et al., 2005). Because FPP is also utilized for sterol biosynthesis, we investigated whether serum sterol might ameliorate some of the growth defects resulting from repressing ERG20 gene expression as observed in ERG9-depleted cells (Nakayama et al., 2000). All tested strains showed normal growth in the tested media when no doxycycline was added. When the ERG20 gene was repressed by doxycycline, the growth of tet-ERG20 cells was rescued when the concentration of human serum was >2.5%. In contrast, the tet-RAM2 cells showed doxycycline-generated growth defects in the presence of all serum concentrations as observed for 99TEF3 (Fig. 3 and data not shown). These results indicate that adding serum would reverse the growth inhibition due to decreased FPP synthesis in C. glabrata.

, 2009). We believe that the beneficial effects on colonic microbiota observed in this work were produced by fermentation of the nonglycaemic carbohydrates, mainly pectin, present in almond skins. Previous studies have demonstrated the prebiotic potential of pectic oligosaccharides generated from bergamot and orange peel ABT-199 mouse (Manderson et al., 2005; Mandalari et al., 2007). Costabile et al. (2008) have recently shown

that ingestion of a whole grain breakfast cereal was more bifidogenic compared with an equivalent amount of wheat bran-based breakfast period after a 21-day feeding period. In the present study, we have shown a significant increase in Bifidobacterium spp. and to a lesser extent of Lactobacillus/Enterococcus spp. after incubation with almond skins (Table 2). The PI was calculated using the equation presented by Palframan et al. (2003, Fig. 2), although a more recent

definition of PI proposed ‘the increase in the absolute number of bifidobacteria expressed divided by the daily dose of prebiotic ingested’ (Roberfroid, 2007). Dietary carbohydrates, specifically resistant starches and fibres, are known to produce selleck chemicals SCFAs, such as acetic, propionic and butyric acids, through fermentation (Wong et al., 2006). In the present work, fermentation of almond skins increased the concentration of mainly acetate and propionate (Table 3). Bifidobacteria are acetate/lactate producers; therefore, an increase in the percentage of these organic acids was expected

with an increase in the activity or the numbers of this bacterial group. Fermentation of FOS resulted in the highest production of lactate, acetate and butyrate after 8- and 24-h incubations, whereas similar amounts of propionate were detected after addition of FOS and almond skins: these observations indicate the different types of bacterial fermentation Thiamet G occurring on the substrates. An additional physiological effect of dietary fibre is related to the role played by the antioxidant compounds linked to the polysaccharides, such as ferulic acid (Napolitano et al., 2009). Several cell wall-bound phenolics, mainly p-hydroxybenzoic acid, vanillic acid and t-ferulic acid, have been found in almond skins and their concentration did not significantly change post in vitro gastric plus duodenal digestion. It is known that colonic microbiota esterases can facilitate a slow, but continuous absorption of phenolic compounds through the colon by cleaving the ester bonds (Vardakou et al., 2008). Therefore, the beneficial effects associated with gut microbiota might also be associated with the antioxidant moiety present in the fibre. The conversion of polyphenols to phenolic acids by the colonic microbiota is known to increase the occurrence of phenolic acids as one of the major group of phenolic metabolites (Lafay & Gil-Izquierdo, 2008).

PHIS is a detailed comparative database that gives participating hospitals an opportunity to assess epidemiology trends, resource utilization, and other data that can be used to assess performance and outcomes.15 Cases were obtained from the PHIS database, using a query of ICD-9 codes 0.840-0.849 for primary diagnoses of malaria listed for inpatients treated at PHIS hospitals between January 2003 and June 2008. De-identified patient data included demographics, location, type of malaria, procedures performed,

hospital charges, and All Patient Refined Diagnosis Related Groups (APR-DRG) severity index. The APR-DRG severity index is an automated scoring derived from standardized clinical parameters (3M Health Information Systems), and provides a unified method of comparing severity http://www.selleckchem.com/products/MK-1775.html across Daporinad research buy institutions but does not necessarily correlate with the specific diagnostic criteria of severe malaria by CDC criteria. Using total admissions to PHIS hospitals as the denominators, cumulative incidences (CI) were generated for the PHIS hospitals across the United States in aggregate, each region, and at CNMC. Chi-square and t-tests were used for comparisons. Logistic regression was used to compare CI and generate odds ratios. Multivariate

analysis of variance was employed to ascertain mean hospital charges. This research study was reviewed and approved by the CNMC institutional review board and the PHIS. Ninety-eight cases (inpatient

and outpatient) of malaria were treated at CNMC during the study period, and detailed case records were available in 93. Sixty-two percent (n = 61) of patients were admitted to the hospital and 31% of that group (n = 19) were treated Silibinin in the intensive care unit for severe malaria. Patient epidemiology and clinical parameters are reported in Table 1. Time until diagnosis, by malaria species, in terms of time in the United States and number of days sick prior to diagnosis is reported in Table 2. Forty-six percent (n = 45) of patients were long-term U.S. residents who visited friends or relatives in their country of origin, 37% (n = 36) were recent immigrants, and travel purpose status was not recorded in 17% of cases. GIS mapping of these cases relative to sub-Saharan population density is shown in Figure 1. The vast majority of cases originated with an exposure in sub-Saharan Africa (95%). Seventy-nine cases (85%) were exposed in West Africa, with Nigeria the most common country of exposure, 37% of all cases. The peak incidence was in August. Ninety case files commented on prophylaxis use. Prophylaxis was not used by 70% of patients and either an ineffective regimen or an improperly used “effective” regimen was reported in 24%. Only 6% of cases reported proper adherence to an effective regimen.

The association of GFP-labeled S. Enteritidis with WBC was determined by flow cytometry 60 min after infection. Four independent labelings were performed. In the first one, mouse monoclonal antibodies against CD172α [formerly SWC3, clone DH59B from Veterinary Medical Research and Development Inc., Pullman, WA, immunoglobulin Sunitinib chemical structure G1 (IgG1)] and SWC8 (clone MIL-3, gift from Dr Joan Lunney, Animal Parasitology Institute, Beltsville, MD, IgM) were added to the infected WBC. Thereafter, bound monoclonal antibodies were detected by polyclonal goat anti-mouse antibodies against IgG1 and IgM conjugated with Alexa Fluor 647 (Molecular Probes) or phycoerythrin (Southern Biotechnology), respectively.

Together with flow cytometer light scattering, this analysis allowed the differentiation of granulocytes (CD172α+ and SWC8+), monocytes (CD172α+ and Y-27632 solubility dmso SWC8−) and lymphocytes (CD172α− and SWC8−). In an additional two analyses, WBC were labeled separately with mouse anti-IgM (clone K52 1C3 from Serotec,

IgG1) and mouse anti-CD3 (clone 8E6 from VMRD, IgG1) monoclonal antibodies, followed by secondary antibodies as above. This allowed the determination of B- and T-lymphocytes, respectively. The analyses were performed using a FACSCalibur™ (Becton Dickinson) equipped with a 488 nm argon-ion laser and a 633 nm diode laser and cellquest™pro software (Becton Dickinson). One hour after the infection of WBC, the cells were pelleted filipin by centrifugation at 2000 g for 10 min and resuspended in 30 μL of 4% gelatine warmed to 45 °C. After solidification, each sample was cut into 1–3 mm3 blocks, fixed with 3% glutaraldehyde

and postfixed with 1% osmium tetroxide for 1 h. Samples were dehydrated with acetone and embedded in Epon 812 (Serva). Embedded samples were heat polymerized at 60 °C for 4 days and 100-nm ultrathin sections were prepared using an LKB ultramicrotome. Finally, the ultrathin sections were stained with uranyl acetate and lead citrate and observed using a Philips EM 208 transmission electron microscope under an acceleration of 90 kV. At least 300 different cells were viewed and the percentage of infected WBC was determined. Data were evaluated using the nonparametric Mann–Whitney test comparing the WBC infected by different mutants with the WBC infected by the wild-type S. Enteritidis. All the statistical calculations were performed using prism statistical software (Graph Pad Software). The purified porcine WBC consisted of T-lymphocytes (56% of all WBC, average from four animals), followed by granulocytes (33%), B-lymphocytes (8%) and monocytes (3%). The viability of the cells was over 90% and this did not change throughout the experiment, as determined by both propidium iodide staining and LDH release (not shown). In the presence of serum, granulocytes exhibited the highest affinity for S.

3 per 1000 person-years, with almost half of those who developed renal stones having eGFR <60 at the time of ATV initiation [34]. The nephrotoxic potential

of both TDF and ATV is low in patients with normal renal function. However, in patients with CKD and impaired renal function (eGFR <75 mL/min/1.73m2), alternative ARVs should be considered. In patients undergoing renal transplantation, PIs give rise to challenging DDIs with calcineurin inhibitors (http://www.hiv-druginteractions.org). Post-transplantation, acute allograft rejection and impaired renal function are common [35]. We suggest TDF and ATV are avoided in patients who are waiting or who have undergone, renal transplantation, and that specialist advice is sought regarding selleck chemicals choice and appropriate dose of ARVs. NNRTIs, Veliparib supplier INIs, ABC and 3TC have not been associated with CKD and can be used in HIV-positive patients with CKD. In patients with impaired renal function, specific ARV drugs (all NRTIs except ABC) may need to be dose-adjusted [36]. Impaired survival has been reported with ART prescription errors in patients undergoing dialysis [37]. We recommend dose adjustment of renally cleared ARVs in patients with renal failure but caution against the risk of overinterpreting estimates of renal function for this purpose as true measures of renal function may be substantially higher in patients with mild–moderate renal impairment. Specific

ARVs that require dose adjustment in patients with reduced renal function include 3TC, FTC, TDF, DDI, ZDV and MVC (depending on PI use). For further information and advice, the reader should refer to the summary of product characteristics for each ARV. CVD is a leading cause of non-AIDS Gemcitabine chemical structure morbidity and mortality among HIV-positive individuals [1, 2] and an increased risk of CVD events has been observed when compared with HIV-negative populations [3-8]. This has been attributed to the increased prevalence of surrogate markers of CVD (such as dyslipidaemia) and the proinflammatory

state associated with HIV infection. However, because ART may not mitigate (or indeed may exacerbate) these effects, caution is required in extrapolating from these makers to effects on overall mortality. The following recommendations apply to patients with, or at high risk, of CVD. For the purposes of these guidelines, patients with an elevated CVD risk are as defined in the JBS2 guidelines [9] and include: People with any form of established atherosclerotic CVD. Asymptomatic people who have an estimated multifactorial CVD risk >20% over 10 years. People with diabetes mellitus (type 1 or 2). People with elevated blood pressure >160 mmHg systolic or >100 mmHg diastolic, or lesser degrees of blood pressure elevation with target organ damage. People with elevated total cholesterol to high-density lipoprotein cholesterol ratio >6.0. People with familial dyslipidaemia. NICE does not recommend a specific CVD risk calculation for the UK population [10].

3 per 1000 person-years, with almost half of those who developed renal stones having eGFR <60 at the time of ATV initiation [34]. The nephrotoxic potential

of both TDF and ATV is low in patients with normal renal function. However, in patients with CKD and impaired renal function (eGFR <75 mL/min/1.73m2), alternative ARVs should be considered. In patients undergoing renal transplantation, PIs give rise to challenging DDIs with calcineurin inhibitors (http://www.hiv-druginteractions.org). Post-transplantation, acute allograft rejection and impaired renal function are common [35]. We suggest TDF and ATV are avoided in patients who are waiting or who have undergone, renal transplantation, and that specialist advice is sought regarding www.selleckchem.com/screening/apoptosis-library.html choice and appropriate dose of ARVs. NNRTIs, selleck chemicals llc INIs, ABC and 3TC have not been associated with CKD and can be used in HIV-positive patients with CKD. In patients with impaired renal function, specific ARV drugs (all NRTIs except ABC) may need to be dose-adjusted [36]. Impaired survival has been reported with ART prescription errors in patients undergoing dialysis [37]. We recommend dose adjustment of renally cleared ARVs in patients with renal failure but caution against the risk of overinterpreting estimates of renal function for this purpose as true measures of renal function may be substantially higher in patients with mild–moderate renal impairment. Specific

ARVs that require dose adjustment in patients with reduced renal function include 3TC, FTC, TDF, DDI, ZDV and MVC (depending on PI use). For further information and advice, the reader should refer to the summary of product characteristics for each ARV. CVD is a leading cause of non-AIDS O-methylated flavonoid morbidity and mortality among HIV-positive individuals [1, 2] and an increased risk of CVD events has been observed when compared with HIV-negative populations [3-8]. This has been attributed to the increased prevalence of surrogate markers of CVD (such as dyslipidaemia) and the proinflammatory

state associated with HIV infection. However, because ART may not mitigate (or indeed may exacerbate) these effects, caution is required in extrapolating from these makers to effects on overall mortality. The following recommendations apply to patients with, or at high risk, of CVD. For the purposes of these guidelines, patients with an elevated CVD risk are as defined in the JBS2 guidelines [9] and include: People with any form of established atherosclerotic CVD. Asymptomatic people who have an estimated multifactorial CVD risk >20% over 10 years. People with diabetes mellitus (type 1 or 2). People with elevated blood pressure >160 mmHg systolic or >100 mmHg diastolic, or lesser degrees of blood pressure elevation with target organ damage. People with elevated total cholesterol to high-density lipoprotein cholesterol ratio >6.0. People with familial dyslipidaemia. NICE does not recommend a specific CVD risk calculation for the UK population [10].

Supplementation of the growth medium with 100 μg mL−1 of exogenous leucine did not affect the expression of any of the analyzed LEE gene (Fig. 1b). To analyze whether the effect of Lrp on the expression of LEE genes was direct or indirect

(e.g. through the action of an intermediate, Lrp-dependent transcription factor), we performed an EMSA with the Selleckchem Daporinad purified Lrp protein of C. rodentium and the promoter region of the Lrp-dependent LEE genes. DNA regions containing the transcriptional and translational signals and extending approximately 400 bp upstream of the first codon of the LEE1–LEE5 and grlRA operons were PCR amplified and cloned into pGEM-Teasy vectors, as described in ‘Materials and methods’. Restriction fragments PLX4032 mw containing the amplified regions were then extracted, gel purified, radioactively labeled, and used in EMSA experiments. To check that the His-tagged version of Lrp was able to specifically bind an Lrp-box,

we performed a preliminary experiment using a 400-bp DNA fragment carrying the lrp promoter region of C. rodentium, because it is known that Lrp controls the expression of its own structural gene in many Lrp-containing organisms (Ernsting et al., 1992; Napoli et al., 1999; Cordone et al., 2005). As shown in Fig. 2a, specific binding to the lrp promoter region of C. rodentium was observed, thus indicating that also in this organism Lrp controls its own expression and that the presence of the His-tag at the N-terminal end of Lrp does not interfere with the DNA-binding activity of the protein. Lrp was then used in a series of mobility-shift experiments with the promoter region of LEE1, LEE2, LEE3, LEE4, LEE5, and grlRA. Thiamet G Specific binding was only observed when the promoter region of LEE1 was used as a probe (Fig. 2b), whereas with all the other LEE operons, no interactions were observed (Fig. 2c and data not shown). In all cases, the specificity of the interaction was tested by the addition

of specific competitor DNA as a probe. Analysis of the nucleotide sequence of the various promoter regions analyzed by EMSA allowed us to identify a potential Lrp-box only upstream of the LEE1 and lrp promoters (Fig. 3a). Based on the consensus sequence previously proposed for Lrp (Cui et al., 1995), the identified sequences match in 10 of 15 positions of the consensus (Fig. 3b). Although EMSA data do not conclusively exclude the possibility that Lrp failed to interact with the promoter region of LEE genes other than LEE1 because of a peculiar structure/conformation of the target DNA fragments, they clearly indicate that Lrp directly contacts LEE1 promoter. The promoter-proximal gene of the LEE1 operon encodes the transcriptional regulator Ler, known to positively regulate several LEE genes.

These results contrast with an earlier study from Cote d’Ivoire that reported more than half of the participants declaring sexual abstinence and those who were sexually active having a Alpelisib datasheet low frequency

of sexual intercourse (once a month or less) [30]. A major finding of the current study is that South Indian patients with higher viral loads were more likely to transmit HIV to their seronegative partners, and during the 12 months of follow-up, patients in seroconverting relationships continued to have significantly higher viral loads than patients in serodiscordant relationships. Although studies from other regions have documented that PVL is a marker for HIV transmission [10–12,14], the findings of the current study differ from an earlier study from Zambia in which PVL was only weakly predictive of male-to-female transmission within couples and rates of male-to-female and female-to-male transmission were similar [16]. In an earlier study at our centre, men with PVLs >100 000 were more likely to be in concordant relationships [31]. Although the

most important justification for expanding access to ART in resource-limited settings has been to prolong the life of HIV-infected patients, a secondary outcome could also be a reduction in the risk of HIV transmission because Gemcitabine nmr ART dramatically suppresses peripheral blood levels of HIV-1 RNA [32]. The incidence of HIV infection among the initially seronegative partners was 6.52 per 100 person-years. An earlier study from Western India documented a lower incidence rate of seroconversion (1.22 per 100 person-years) among serodiscordant couples, which was attributed to high rates of condom use, low rates of STIs and high CD4 T lymphocyte counts [21]. However, a study from Zambia documented a similar transmission rate between couples (7.7 per 100 person-years) [16]. The Rakai study reported an even higher incidence of 11.8 Fossariinae per 100

person-years [9]. These varying incidences of HIV transmission in different settings are likely to reflect different numbers of partners, varying duration of relationships, availability of ART, coital frequency, availability of clinical care and the structures of various sexual networks [33]. Herpes simplex virus type-2 (HSV-2) co-infection has been identified as a key risk factor for the heterosexual transmission of HIV [13,34], and HSV-2 infection reactivation in HIV-infected individuals can lead to a rise in HIV viral load and increased rates of HIV seroconversion [8,35]. In the current study, a substantial number of patients presented with genital HSV-2 at enrolment and patients in relationships that seroconverted between 6 and 12 months of follow-up had a higher period prevalence of genital HSV-2. Acyclovir suppressive therapy can suppress genital and plasma HIV RNA levels [36], and could be used as prophylactic therapy in populations with high HSV-2 burdens to reduce the transmission of HIV.