, 2004). PratA consists of nine consecutive tetratricopeptide repeat (TPR) units, a motif that is known to mediate protein–protein interactions. Thereby, it could form a bridge connecting multiple proteins and serve as a scaffold factor for correct assembly of PSII

Ruxolitinib solubility dmso (Schottkowski et al., 2009a). PratA directly interacts with the C-terminus of the D1 reaction center protein of PSII, and its inactivation affects the C-terminal processing of D1, an early step of PSII biogenesis. This D1 maturation occurs in almost all photosynthetic organisms, and it is required for the subsequent docking of the subunits of the oxygen-evolving complex to the lumenal side of PSII. Most intriguingly, PratA was shown to be a soluble protein

located in the periplasm, which forms part of a ∼200 kDa complex of an as yet unknown composition and function (Fulda et al., 2000; Klinkert et al., 2004; Schottkowski et al., 2009a). However, a minor fraction (10–20%) of PratA was found to associate with membranes in a D1-dependent manner. Cellular fractionation experiments using two consecutive sucrose gradients revealed that the membrane-bound PratA is apparently not associated with either the PM or TMs, but co-sediments with an intermediate membrane subfraction, which was therefore named PratA-defined membrane (PDM) subfraction (Schottkowski et al., 2009a). Albeit the different density of PDMs as compared with that of PMs, it cannot be ruled out that PDMs might be identical to previously described specialized PM subregions, in which PSII subunits tend to accumulate (Srivastava et al., 2006). Membrane fractions resembling PDMs with regard www.selleckchem.com/products/AG-014699.html to their density have already been observed in earlier

studies, where they have been postulated to be linked to so-called thylakoid centers (Hinterstoisser et al., 1993). Based on electron microscopic analyses, thylakoid centers were initially described in some cyanobacteria as tubular structures found at the inner face of the Cediranib (AZD2171) PM, at points where thylakoids extend projections into the cytoplasm (Kunkel, 1982). Recently, this idea was revisited based on a more detailed cryo-electron tomography analysis in Synechocystis 6803 (van de Meene et al., 2006). Interestingly, PratA inactivation and, thus, defective PSII assembly leads to a significant accumulation of the pD1 precursor protein in PDM fractions (Schottkowski et al., 2009a). This suggests that PratA function is required for efficient membrane flow from PDMs to TMs, underlining the role of PDMs for PSII reaction-center assembly. Interestingly, related ‘biogenesis regions/centers’ have recently been observed in the eukaryotic green alga Chlamydomonas reinhardtii, where they are formed by membranes surrounding the pyrenoid structure of the chloroplast (Uniacke & Zerges, 2007). This might indicate an evolutionary conservation of the molecular principles that underlie TM biogenesis.

It is also used as part of combination formulations for rice (Singh et al., 2008; Saha & Rao, 2009). Chlorimuron-ethyl

http://www.selleckchem.com/products/cetuximab.html exerts carry-over effects on succeeding crops such as sugar beet, corn and cotton. It reduced the yield of sugar beet planted 1 year after its application (Renner & Powell, 1991). Chlorimuron-residue haremed corn (Curran et al., 1991), and also harmed sunflower, watermelon, cucumber and mustard when observed 16 weeks after application (Johnson & Talbert, 1993). Although its persistence is moderate in soil [half-life (T1/2) 30 days], like many other sulfonylurea herbicides, its persistence increases with increasing pH. The T1/2 of chlorimuron under acidic conditions (pH 5) is 17–25 days, whereas at higher pH this may increase to 70 days. The half-life of chlorimuron in a silt-loam soil was 7 days at pH 6.3 and 18 days at pH 7.8 (Brown, 1990). By using a root bioassay technique, Schroeder (1994) determined the half-life of chlorimuron in soils of different pH-ranges as 12–50 days. Bedmar et al. (2006) observed a wide range of half-life for chlorimuron in soil from 30 days at pH 5.9 to 69 days at pH 6.8. Chlorimuron-ethyl degrades in the agricultural environment primarily via pH- and temperature-dependent chemical hydrolysis (Beyer et al., 1988; Brown, 1990; Hay, 1990), as observed for many sulfonylurea herbicides, such as sulfometuron-methyl (Harvey et al., Trichostatin A mouse 1985),

chlorsulfuron (Sabadie, 1990), metsulfuron-methyl (Sabadie, 1991), rimsulfuron (Schneiders et al., 1993), nicosulfuron (Sabadie, 2002) and flazasulfuron (Bertrand et al., 2003). The phototransformation of chlorimuron by sunlight also takes place on the soil HA 1077 surface (Choudhury & Dureja, 1996a) and in water (Venkatesh et al., 1993; Choudhury & Dureja, 1996b). Within the surface soil chlorimuron is also considered to serve as a source of carbon, nitrogen and sulfur for microorganisms. There are reports on the utilization of sulfonylurea herbicides by microorganisms. The metabolic pathways for the degradation of chlorsulfuron and metsulfuron-methyl

by Streptomyces griseolus (Joshi et al., 1985; Reiser & Steiglitz, 1990), and trisulfuron by S. griseolus in artificial media (Dietrich et al., 1995) have been established. At low pH the degradation of trisulfuron-methyl takes place by chemical hydrolysis, whereas in neutral to alkaline soil, microorganisms play the dominant role in its degradation (Peeples et al., 1991), and the major degradation route is cleavage of the sulfonylurea bridge (Vega et al., 2000). Streptomyces griseolus can also de-esterify and O-dealkylate the chlorimuron-ethyl molecule (Reiser & Steiglitz, 1990). A bacterium, Pseudomonas sp., isolated from chlorimuron-ethyl-contaminated soil degrades the herbicide by cleaving the sulfonylurea bridge (Ma et al., 2009), and a yeast strain, Sporobolomyces sp., was isolated as a chlorimuron-degrading organism (Xiaoli et al., 2009).

DNA was isolated using a French pressure cell press (Thermo Spectronic, Rochester, NY) and purified by chromatography on hydroxyapatite (Cashion et al., 1977). The analytical protocol was according to De Ley et al. (1970) as modified by Huss et al. (1983), using a model Cary 100 Bio UV/VIS-spectrophotometer equipped with a Peltier-thermostatted 6 × 6 multicell changer and a temperature controller with an in situ temperature

probe (Varian, Palo Alto, CA). Testing with the API 20NE system was performed following the manufacturer’s specifications (bioMérieux Italia, Bagno a Ripoli, Italy). Substrate assimilations were checked after 24 and 48 h. Growth tests carried out in the presence of different PAHs demonstrated that Burkholderia sp. DBT1 is able to grow on both Tanespimycin ic50 phenanthrene and DBT as the sole sources of carbon and energy, although the growth on this latter substrate proceeds with a lower H 89 in vitro yield (Fig. 1). Moreover, DBT1 is also capable of utilizing naphthalene and fluorene provided after a 3-day induction on phenanthrene (Fig. 1) or DBT (data not shown). When strain DBT1 was grown on YMA plates added with crystals of different PAHs, a change in the colour of the colonies was detected. Briefly, DBT1 colonies became red in the presence of DBT, yellow when treated with fluorene and orange/pink and

weakly yellow when phenanthrene and naphthalene were added to Petri dishes, respectively (Fig. 2). This change in colour may be attributed to PAH cleavage.

In particular, DBT1 colonies became red when treated with DBT, owing to the Protein kinase N1 transformation of DBT to oxidized intermediates (Kodama et al., 1970, 1973). When fluorene crystals were added to Petri dishes, DBT1 colonies acquired a yellow colour, as already observed by Casellas et al. (1997) and Seo et al. (2009). On the other hand, when grown in the presence of phenanthrene, the strain DBT1 produced an orange/pink pigment. This phenotype has also been reported in Alcaligenes faecalis AFK2, which degrades phenanthrene via o-phthalate by a protocatechuate pathway (Kiyohara et al., 1982). Finally, with the addition of naphthalene crystals, DBT1 colonies became weakly yellow, as already observed in a Pseudomonas strain (Kiyohara & Nagao, 1977). These results suggest that the strain DBT1 may rely on a broad substrate specificity towards different PAHs. Interestingly, enzymes for the degradation of naphthalene and fluorene can be induced by either phenanthrene or DBT. This indicates that these compounds, chiefly phenathrene, may act as major substrates for Burkholderia sp. DBT1. API 20NE tests were carried out on the following strains: Burkholderia sp. DBT1, B. fungorum LMG 16225T and B. cepacia LMG 1222T. Burkholderia fungorum and B.

DNA was isolated using a French pressure cell press (Thermo Spectronic, Rochester, NY) and purified by chromatography on hydroxyapatite (Cashion et al., 1977). The analytical protocol was according to De Ley et al. (1970) as modified by Huss et al. (1983), using a model Cary 100 Bio UV/VIS-spectrophotometer equipped with a Peltier-thermostatted 6 × 6 multicell changer and a temperature controller with an in situ temperature

probe (Varian, Palo Alto, CA). Testing with the API 20NE system was performed following the manufacturer’s specifications (bioMérieux Italia, Bagno a Ripoli, Italy). Substrate assimilations were checked after 24 and 48 h. Growth tests carried out in the presence of different PAHs demonstrated that Burkholderia sp. DBT1 is able to grow on both Ion Channel Ligand Library purchase phenanthrene and DBT as the sole sources of carbon and energy, although the growth on this latter substrate proceeds with a lower AZD6738 research buy yield (Fig. 1). Moreover, DBT1 is also capable of utilizing naphthalene and fluorene provided after a 3-day induction on phenanthrene (Fig. 1) or DBT (data not shown). When strain DBT1 was grown on YMA plates added with crystals of different PAHs, a change in the colour of the colonies was detected. Briefly, DBT1 colonies became red in the presence of DBT, yellow when treated with fluorene and orange/pink and

weakly yellow when phenanthrene and naphthalene were added to Petri dishes, respectively (Fig. 2). This change in colour may be attributed to PAH cleavage.

In particular, DBT1 colonies became red when treated with DBT, owing to the Sorafenib manufacturer transformation of DBT to oxidized intermediates (Kodama et al., 1970, 1973). When fluorene crystals were added to Petri dishes, DBT1 colonies acquired a yellow colour, as already observed by Casellas et al. (1997) and Seo et al. (2009). On the other hand, when grown in the presence of phenanthrene, the strain DBT1 produced an orange/pink pigment. This phenotype has also been reported in Alcaligenes faecalis AFK2, which degrades phenanthrene via o-phthalate by a protocatechuate pathway (Kiyohara et al., 1982). Finally, with the addition of naphthalene crystals, DBT1 colonies became weakly yellow, as already observed in a Pseudomonas strain (Kiyohara & Nagao, 1977). These results suggest that the strain DBT1 may rely on a broad substrate specificity towards different PAHs. Interestingly, enzymes for the degradation of naphthalene and fluorene can be induced by either phenanthrene or DBT. This indicates that these compounds, chiefly phenathrene, may act as major substrates for Burkholderia sp. DBT1. API 20NE tests were carried out on the following strains: Burkholderia sp. DBT1, B. fungorum LMG 16225T and B. cepacia LMG 1222T. Burkholderia fungorum and B.

Each monkey sat in a testing room, unrestrained, in a wheeled transport cage placed 20 cm from a touch-sensitive monitor (38 cm wide × 28 cm high) on which pairs of visual stimuli could be presented (eight-bit colour clipart bitmap images, 128 × 128 pixels) and responses recorded. Rewards (190-mg Noyes pellets) were delivered from a dispenser (MED Associates, St Albans, Vermont) into a food well immediately to the right of the touch screen. A large metal food box, situated to the left below the touch screen, contained each individual’s daily food allowance

(given in addition to the reward pellets) consisting of proprietary monkey food, fruit, peanuts and seeds, delivered immediately after testing each day. This was supplemented by a forage mix of seeds and grains given ∼6 h prior to testing in the home cage. Stimulus presentation, experimental contingencies, reward Epacadostat ic50 selleckchem delivery and food box opening was controlled by a computer using in-house software. The mOFC animals were tested pre- and postoperatively on

a simple two-choice task. Before the start of testing, all macaques had received extensive training with touch screens and knew that touching a stimulus on the screen could lead to food reward. Each day, macaques were presented with two novel stimuli on the touch screen at the same time in a left/right configuration. Each stimulus’ side of presentation varied from trial to trial. On each trial, selecting one stimulus caused the other to extinguish and reward to be delivered according to the reward schedule. Auditory tones were used to cue the animal to the presentation of the stimuli, to the selection of a stimulus and to the potential delivery of a reward. Each stimulus was associated with a different Pregnenolone outcome probability,

one stimulus always being rewarded more than the other. At the start of testing, each stimulus was randomly assigned one of two reward probabilities (Fig. 6A). The ratios of reward associated with the two stimuli were either 75 : 25 (in other words one stimulus had a 0.75 probability of reward while the other had a 0.25 probability of reward) or 50 : 18. Each schedule was performed twice and in an interleaved manner. Monkeys’ touches registered their stimulus selections. Upon a decision being made rewards were delivered according to a specific schedule (75 : 25 and 50 : 18) with a fixed probability with a reward matching contingency in place (Herrnstein, 1997; Sugrue et al., 2004; Kennerley et al., 2006; Rudebeck et al., 2008b). This meant that rewards once allocated to a stimulus remained available until that stimulus was chosen. Further details can be found in Rudebeck et al. (2008b).

, 1998). Enteric septicemia of catfish

(ESC), caused by the bacterium E. ictaluri, is responsible for approximately 50% of economic losses to catfish farmers in the mTOR inhibitor United States (Klesius, 1993; Shoemaker et al., 2009). Edwardsiella ictaluri is a gram-negative enteric pathogen in catfish, and outbreaks of ESC are seasonal, occurring mainly in spring and fall with a temperature range of 22–28 °C (Tucker & Robinson, 1990). Ichthyophthiriasis is a major parasitic disease of freshwater fish worldwide, caused by a ciliated protozoan Ich. The parasite life cycle consists of an infective theront, a parasitic trophont, and a reproductive tomont (Hines & Spira, 1974; Matthews, 2005; Dickerson, 2006). Mature tomonts leave the fish host, attach to a substrate, and undergo multiple divisions to produce hundreds to thousands of infective theronts. Theronts swim actively in water in search of new fish hosts (Dickerson, 2006). The temperature ranges of ESC outbreaks overlap the optimum temperature window of Ich infection at 22–24 °C (Matthews, 2005; Dickerson, 2006). In 2002, 50.5% and 44.3% of all catfish operations (approximately 1000 total in the USA) had losses caused by ESC and by Ich (white spot), respectively (Hanson et al., 2008). The ability of parasites to enhance mortality because of bacterial diseases is presently receiving attention in aquaculture

Bumetanide research. However, there is limited information on whether Selleck Rapamycin parasites act as vectors to transmit pathogenic bacteria in fish. To prevent and manage bacterial diseases in aquaculture, it is

important to understand the potential of parasites to vector bacteria in fish. Parasites may easily transmit pathogenic bacteria from one fish to another within high-density fish populations on farms. In this trial, we used Ich–E. ictaluri as a model to study the interaction between the parasite, the bacteria, and the fish host. This study tested the hypothesis that Ich can vector E. ictaluri into channel catfish, Ictalurus punctatus. We further established that the bacteria were associated with the surface of the parasite. The bacteria multiplied and were transferred as the parasite divided. Channel catfish (industry pool strain) were obtained from disease-free stock from the USDA-ARS Catfish Genetic Research Unit, Stoneville, MS, and reared to the experimental size in indoor tanks at the USDA, Aquatic Animal Health Research Unit, Auburn, AL. I. multifiliis (ARS 10-1 strain) originally isolated from infected tropical pet fish was maintained by serial transmission on channel catfish held in 50-L glass aquaria, and theronts were cultured as described by Xu et al. (2000). Edwardsiella ictaluri AL-93-58 was transformed with the pZsGreen vector (Clontech, Mountain View, CA) by Russo et al. (2009).

, 1998). Enteric septicemia of catfish

(ESC), caused by the bacterium E. ictaluri, is responsible for approximately 50% of economic losses to catfish farmers in the Doramapimod clinical trial United States (Klesius, 1993; Shoemaker et al., 2009). Edwardsiella ictaluri is a gram-negative enteric pathogen in catfish, and outbreaks of ESC are seasonal, occurring mainly in spring and fall with a temperature range of 22–28 °C (Tucker & Robinson, 1990). Ichthyophthiriasis is a major parasitic disease of freshwater fish worldwide, caused by a ciliated protozoan Ich. The parasite life cycle consists of an infective theront, a parasitic trophont, and a reproductive tomont (Hines & Spira, 1974; Matthews, 2005; Dickerson, 2006). Mature tomonts leave the fish host, attach to a substrate, and undergo multiple divisions to produce hundreds to thousands of infective theronts. Theronts swim actively in water in search of new fish hosts (Dickerson, 2006). The temperature ranges of ESC outbreaks overlap the optimum temperature window of Ich infection at 22–24 °C (Matthews, 2005; Dickerson, 2006). In 2002, 50.5% and 44.3% of all catfish operations (approximately 1000 total in the USA) had losses caused by ESC and by Ich (white spot), respectively (Hanson et al., 2008). The ability of parasites to enhance mortality because of bacterial diseases is presently receiving attention in aquaculture

VAV2 research. However, there is limited information on whether selleck inhibitor parasites act as vectors to transmit pathogenic bacteria in fish. To prevent and manage bacterial diseases in aquaculture, it is

important to understand the potential of parasites to vector bacteria in fish. Parasites may easily transmit pathogenic bacteria from one fish to another within high-density fish populations on farms. In this trial, we used Ich–E. ictaluri as a model to study the interaction between the parasite, the bacteria, and the fish host. This study tested the hypothesis that Ich can vector E. ictaluri into channel catfish, Ictalurus punctatus. We further established that the bacteria were associated with the surface of the parasite. The bacteria multiplied and were transferred as the parasite divided. Channel catfish (industry pool strain) were obtained from disease-free stock from the USDA-ARS Catfish Genetic Research Unit, Stoneville, MS, and reared to the experimental size in indoor tanks at the USDA, Aquatic Animal Health Research Unit, Auburn, AL. I. multifiliis (ARS 10-1 strain) originally isolated from infected tropical pet fish was maintained by serial transmission on channel catfish held in 50-L glass aquaria, and theronts were cultured as described by Xu et al. (2000). Edwardsiella ictaluri AL-93-58 was transformed with the pZsGreen vector (Clontech, Mountain View, CA) by Russo et al. (2009).

Both protozoan and bacterial strain, as well as their particular combinations, significantly influenced the outcome of their interactions (Table 1). Pseudomonas fluorescens CHA0 was especially harmful (Figs 1 and 2, Table 1). This strain efficiently restrains growth of various plant-pathogenic fungi, inhibits egg hatch and cause mortality of plant-pathogenic nematode juveniles, (Keel et al., 1992; Siddiqui et al., 2006) and inhibits several nontarget fungi (Winding et al., 2004). Jousset et al. (2006) found that only mutants STA-9090 molecular weight completely devoid of metabolite production (GacA/GacS-negative)

supported protozoan growth, which suggests that the high toxicity of CHA0 is linked to the production of a broad

range of different secondary Epacadostat cost metabolites. We observed that the strains producing extracellular metabolites, i.e. CHA0 and DSS73, were more harmful to protozoa than strains that mainly produce membrane-bound metabolites, i.e. DR54 and MA342 (Fig. 1). To analyze this matter further, we arranged our Pseudomonas strains into three groups: those without secondary metabolites, those that produce membrane-bound secondary metabolites, and a group of bacteria producing extracellular secondary metabolites. We then correlated growth rates of each of these three groups to the growth rates of E. aerogenes. We found a very high correlation between the growth rates of E. aerogenes and the supposedly harmless Pseudomonas (r2=0.85, P=0.0002); we obtained no correlation at all between 4��8C E. aerogenes and the Pseudomonas with extracellular metabolites (r2=0.02, P=0.36), whereas Pseudomonas with membrane-bound metabolites correlated better and almost significantly (r2=0.26, P=0.08). We suggest that the relatively increased ability to cope with membrane-bound toxins in organisms with higher growth rates can be attributed to egestion of harmful remnants enclosed in the food vacuole (membrane parts) whereas

extracellular metabolites are in contact with the cell surface and are difficult to avoid. This is in accordance with the mechanism discussed by Deines et al. (2009). They elegantly showed that volume-specific clearance rate correlated positively with toxin tolerance; probably because organisms with a relative higher clearance rate use their food less efficiently, and egest cell remnants that contain harmful substances. Everything else being equal, volume-specific clearance rate and intrinsic growth rate will correlate. Hence, we suggest that egestion of harmful remnants can explain the higher tolerance. The ability of protozoa to grow on specific bacteria did not correlate particularly well with low-level taxonomic group (Table 1). For example, the two strains of B. designis reacted quite differently to the presented bacteria.

Both protozoan and bacterial strain, as well as their particular combinations, significantly influenced the outcome of their interactions (Table 1). Pseudomonas fluorescens CHA0 was especially harmful (Figs 1 and 2, Table 1). This strain efficiently restrains growth of various plant-pathogenic fungi, inhibits egg hatch and cause mortality of plant-pathogenic nematode juveniles, (Keel et al., 1992; Siddiqui et al., 2006) and inhibits several nontarget fungi (Winding et al., 2004). Jousset et al. (2006) found that only mutants Bleomycin completely devoid of metabolite production (GacA/GacS-negative)

supported protozoan growth, which suggests that the high toxicity of CHA0 is linked to the production of a broad

range of different secondary AZD6738 solubility dmso metabolites. We observed that the strains producing extracellular metabolites, i.e. CHA0 and DSS73, were more harmful to protozoa than strains that mainly produce membrane-bound metabolites, i.e. DR54 and MA342 (Fig. 1). To analyze this matter further, we arranged our Pseudomonas strains into three groups: those without secondary metabolites, those that produce membrane-bound secondary metabolites, and a group of bacteria producing extracellular secondary metabolites. We then correlated growth rates of each of these three groups to the growth rates of E. aerogenes. We found a very high correlation between the growth rates of E. aerogenes and the supposedly harmless Pseudomonas (r2=0.85, P=0.0002); we obtained no correlation at all between Sorafenib nmr E. aerogenes and the Pseudomonas with extracellular metabolites (r2=0.02, P=0.36), whereas Pseudomonas with membrane-bound metabolites correlated better and almost significantly (r2=0.26, P=0.08). We suggest that the relatively increased ability to cope with membrane-bound toxins in organisms with higher growth rates can be attributed to egestion of harmful remnants enclosed in the food vacuole (membrane parts) whereas

extracellular metabolites are in contact with the cell surface and are difficult to avoid. This is in accordance with the mechanism discussed by Deines et al. (2009). They elegantly showed that volume-specific clearance rate correlated positively with toxin tolerance; probably because organisms with a relative higher clearance rate use their food less efficiently, and egest cell remnants that contain harmful substances. Everything else being equal, volume-specific clearance rate and intrinsic growth rate will correlate. Hence, we suggest that egestion of harmful remnants can explain the higher tolerance. The ability of protozoa to grow on specific bacteria did not correlate particularly well with low-level taxonomic group (Table 1). For example, the two strains of B. designis reacted quite differently to the presented bacteria.

Without HAART, KS is associated with severe morbidity, high mortality and a life expectancy of < 6 months [5-7]. However, HAART has changed the natural history of AIDS-associated KS in industrialized countries since its introduction more than a decade ago. For HIV-infected individuals with KS in industrialized countries, HAART results in the regression of the size and number of existing lesions [8, 9]. At the population level, the use of HAART has been associated with a decreased proportion of new

AIDS-related cancers, with a 30–50% reduction in KS incidence in both the USA and Europe [10]. Most studies examining the clinical effects Selleckchem Trametinib of HAART on KS have come from high-income countries and from clinic cohorts where protease inhibitor (PI)-based regimens predominated The clinical effects of HAART on AIDS-associated KS in African countries, where programmes primarily use nonnucleoside reverse transcriptase inhibitor (NNRTI)-based therapy, is not known. To address this question we analysed data collected from individuals with HIV infection receiving NNRTI-based antiretroviral therapy in rural

Uganda as part of a randomized clinical trial [11]. We examined factors associated with the diagnosis of KS at baseline and during follow-up and determined which factors were associated with mortality among patients with KS. The Home-Based AIDS Care see more (HBAC) programme was a clinical trial of three different monitoring strategies for patients receiving HAART in rural Uganda. Clients of The AIDS Support Organization, a local HIV/AIDS care and support organization in the Tororo and Busia districts, were invited for assessment of HAART eligibility. Individuals with a CD4 T lymphocyte cell count ≤ 250 cells/μL or World Health Organization (WHO) stage III or IV disease (excluding isolated pulmonary tuberculosis) were provided with antiretroviral therapy. Participants were randomly assigned to one of three

monitoring arms: (1) quarterly CD4 cell count and viral load (VL) testing, with weekly home visits by a trained lay person for clinical monitoring using a standard symptom questionnaire; (2) quarterly CD4 cell count Vasopressin Receptor testing and clinical monitoring with weekly home visits; or (3) clinical monitoring with weekly home visits only. Participants also received cotrimoxazole prophylaxis, HIV prevention education and treatment for tuberculosis (TB) and other infectious illnesses as warranted. The first-line HAART regimen was stavudine, lamivudine and either nevirapine or efavirenz. Treatment guidelines allowed patients to be switched to a second-line regimen if immunological, virological or clinical signs of failure occurred, as appropriate to their assigned HAART monitoring arm. The study was approved by the Science and Ethics Committee of the Uganda Virus Research Institute and the Institutional Review Board of the United States Centers for Disease Control and Prevention.