Associations between diet composition, dietary pattern, and weight outcomes after bariatric surgery: a systematic review.

INTRODUCTION: Literature describing the impact of dietary intake on weight outcomes after bariatric surgery has not been synthesized. This study aimed to synthesize the evidence regarding any association between diet composition and weight outcomes post-bariatric surgery. METHODS: CINAHL, Cochrane, Embase, MEDLINE and Scopus were searched for adult studies up to June 2021 that assessed any association between dietary intakes (≥1-macronutrient, food group, or dietary pattern) and weight outcomes at 12-months or longer after bariatric surgery. Risk of bias and quality assessments were conducted using the Scottish Intercollegiate Guidelines Network checklists and the NHMRC's Level of Evidence and Grades for Recommendations. Study findings were presented according to the time of post-surgery dietary intake assessment (≤12months, between 12 and 24 months, ≥24months). RESULTS: 5923 articles were identified, 260 were retrieved for full text screening, and 36 were eligible for inclusion (9 interventional including five randomized-controlled trials, and 27 observational cohort studies; sample sizes: 20-1610; total sample: 5065; follow-up periods: 1 year-12 years; level of evidence: II to IV, risk of bias: low to high). Findings on the association between long-term weight outcomes and dietary composition up to 24-months were mixed. After 24-months, studies consistently suggested no significant associations between weight loss and macronutrient composition or core food group patterns, or between carbohydrate, protein or food group patterns and weight recurrence. A single cohort study reported a weak association between diet quality score and weight-recurrence after 24-months. CONCLUSION: There was no strong evidence to support significant associations between diet composition and weight outcomes post-bariatric surgery. The heterogeneity in study design and quality may reduce generalizability to external populations. Individualized dietary recommendations may be useful to support long-term post-surgery weight outcomes. More studies are needed to define and measure diet quality in this patient cohort. REGISTRATION: PROSPERO (CRD42021264120).

A self-determination theory analysis of reflective debrief themes about dietetic student placement experiences in hospital: implications for education.

BACKGROUND: Healthcare placements in dietetics education contribute significantly to student learning. Exploring students' self-conceptualisation of placement experiences may provide insights to better support learning. Self-determination theory (SDT) has been used to seek insight into clinical and educational settings but has not yet been applied to dietetic placement learning. The present study investigated dietetics students' reflections of key influences on placement learning experiences and their alignment with an SDT framework. METHODS: A post-placement two-stage critical incident debrief was conducted with seven successive cohorts (168 students) of dietetic undergraduate students on final placement. In debriefs, students' anonymous themes were collected and discussed, inductively analysed, and then mapped against an SDT framework of psychological and motivational constructs. RESULTS: Nine key themes were identified that impacted upon placement experiences. Four themes related to framework constructs: (1) Supervisor (and Peer) Autonomy Support; (2) Perceived Competence; (3) Relatedness; and (4) Autonomy and Intrinsic Motivation. Non-SDT themes were also present, including: (5) Learning Environment and Experience; as well as themes about professional behaviours and identity: (6) Teamwork and Interactions; (7) Managing Emotions and Self-Care; (8) Dietetic Communications and Behaviours; and (9) Developing a Professional Identity. CONCLUSIONS: Embedding a structured debrief in the curriculum and using a psychological motivational SDT framework to analyse themes arising can provide valuable information about the learning needs of students on placement with potential for wider application in dietetic learning and teaching and workforce employability. The current findings may have application in university curricula before and after professional placement.

Efficacy of a dietitian-led very low calorie diet (VLCD) based model of care to facilitate weight loss for obese patients prior to elective, non-bariatric surgery.

BACKGROUND: Elective surgery in obese adults carries a higher risk of post-operative infection and prolonged hospital stays, and surgeons may postpone surgery for patients with obesity until they lose weight. The present study aimed to determine the efficacy of a dietitian-led very low calorie diet (VLCD)-based model of care with respect to achieving weight loss for obese patients prior to surgery. METHODS: This mixed-methods study included a medical chart audit of patients referred to a VLCD-based model over 23 months, as well as a survey of recently treated patients and surgeons who utilised the model. Preoperative weight loss targets were set by surgeons, and the dietitian prescribed individualised VLCD-based treatment. Efficacy was determined as weight loss considered sufficient for surgery, clinical safety of VLCD-based treatment, feasibility, and stakeholder value. Pre/post-intervention differences in clinical measures were explored by paired t-test or Wilcoxon tests as appropriate. RESULTS: Data on seventy-eight eligible patients [mean (SD) 45 (13) years, 90% female, body mass index 44.3 (6.2) kg m-2 ] demonstrated significant mean (SD) weight loss of 7.4% (5.3%) body weight (P < 0.05). Most patients (70%, n = 50/71) achieved sufficient weight loss to proceed to surgery. Fifty-six per cent of patients reported mild side effects (n = 43/77) and none led to treatment cessation. Surgeons reported VLCD-based treatment made operations easier (83%, n = 10/12) and shorter (75%, n = 9/12) and all recommended the model of care. All surveyed patients (n = 24) reported satisfaction with their VLCD-based model experience. CONCLUSIONS: A dietitian-led VLCD-based model achieved sufficient weight loss to facilitate elective surgery for most patients. The approach was feasible, highly valued by patients and surgeons, and resulted in perceived surgical benefits.

Quality of development and reporting of dietetic intervention studies in primary care: a systematic review of randomised controlled trials.

BACKGROUND: High-quality research methodologies and clear reporting of studies are essential to facilitate confidence in research findings. The aim of the present study was to conduct an in-depth examination of the methodological quality and reporting of studies included in a recent systematic review of dietitians' effectiveness at providing individualised nutrition care to adult patients. METHODS: The methodological quality and reporting of 27 Randomised Controlled Trials (RCTs) were appraised using the UK Medical Research Council (MRC) Guidelines for complex interventions and the CONSORT checklist for reporting RCTs. A quality appraisal checklist was developed for each guideline/assessment tool aiming to evaluate the extent to which each study met the designated criteria. Excerpts from studies that best addressed criteria were collated to provide exemplary accounts of how criteria may be achieved in future studies. RESULTS: None of the reviewed studies met more than half of the MRC Guidance criteria, indicating that there is clear room for improvement in reporting the methodological underpinnings of these studies. Similarly, no studies met all criteria of the CONSORT checklist, suggesting that there is also room for improvement in the design and reporting of studies in this field. CONCLUSIONS: Dietitians, researchers and journal editors are encouraged to use the results and exemplary accounts from this review to identify key aspects of studies that could be improved in future research. Improving future research will enhance the quality of the evidence-base that investigates the outcomes of dietary interventions involving dietitians.

Is it possible to enhance the confidence of student dietitians prior to professional placements? A design-based research model.

BACKGROUND: Student confidence is an important contributor to a successful professional placement experience. The present study aimed to evaluate a placement preparation program for student dietitians and to assess the impact on self-rated confidence with respect to commencing placements. METHODS: The present study is part of a design-based research approach that involves students in a cyclic enquiry to evaluate and improve curricula. Nutrition and Dietetics students at an Australian university participated in a 1-week mandatory workshop - Pre-Placement week (PrePW), N = 98 students: in 2015 (n = 54) and 2016 (n = 44). An online survey was conducted before and after PrePW using a five-point Likert scale (1 = not confident; 5 = very confident) to assess self-rated confidence to commence placements. Mean (SD) scores were calculated. Paired and independent t-tests evaluated within- and between-group differences, respectively. RESULTS: Before PrePW, the mean (SD) for student confidence to commence placements overall (in all areas of practise) was 'somewhat confident' [2.9 (0.6) in 2015 and 3.0 (0.7) in 2016]. Students were least confident to commence Clinical Practice [2015: 2.5 (0.6); 2016: 2.8 (0.6)] compared to Food Service Management (FSM) [2015: 3.2 (0.9); 2016: 3.1 (0.9)] and Community and Public Health Nutrition (CPHN) [2015: 3.3 (0.9); 2016: 3.2 (0.8)]. Student feedback from PrePW 2015 was used to change the curriculum and PrePW program. The 2016 students reported significantly greater confidence within all areas of practice: Clinical Practice [3.4 (0.6)], FSM [3.7 (0.6)] and CPHN [3.8 (0.6)], including confidence to commence placements overall [3.6 (0.6)] (P < 0.05). CONCLUSIONS: Design-based research provides a useful framework for improvement to curricula and, in this case, was successful in enhancing student confidence in preparation for professional placement.

Pressure ulcer healing with an intensive nutrition intervention in an acute setting: a pilot randomised controlled trial.

OBJECTIVE: To investigate the feasibility of recruitment, retention, intervention delivery and outcome measurement in a nutritional intervention to promote pressure ulcer healing in an acute setting. METHOD: Some 50 tertiary hospital patients with stage II or greater pressure ulcer were randomised to receive either individualised nutritional care by a dietitian, including prescription of wound healing supplements; or standard nutritional care. Relevant nutritional and pressure ulcer (PU) parameters were collected at day 5, 10, 15, 22 and then weekly or until discharge. RESULTS: The median length of hospital stay was 14 days (1-70) with 29 patients discharged by day 15. There were 24 patients discharged before their PU fully healed. Per cent change in valid PU area and score measures from baseline to day 15 were chosen for outcome data analysis to account for varying initial size and severity of the wound and length of stay. There was a larger percentage reduction in PU measures in the intervention group, but this was not statistically significant. Little difference was found in nutritional intake between the control and intervention groups indicating a requirement to focus on effective delivery of the intervention in future studies. Future studies in the acute setting need to account for length of stay and ideally follow patients until full healing. CONCLUSION: Results indicate a positive association with nutrition intervention and PU healing and that a rigorously designed and adequately powered study is feasible. DECLARATION OF INTEREST: This research was supported by a grant from the Queensland Health, Health Practitioner Research Scheme. The authors have no conflicts of interest to declare.

Replication profile of PCDH11X and PCDH11Y, a gene pair located in the non-pseudoautosomal homologous region Xq21.3/Yp11.2.

In order to investigate the replication timing properties of PCDH11X and PCDH11Y, a pair of protocadherin genes located in the hominid-specific non-pseudoautosomal homologous region Xq21.3/Yp11.2, we conducted a FISH-based comparative study in different human and non-human primate (Gorilla gorilla) cell types. The replication profiles of three genes from different regions of chromosome X (ZFX, XIST and ATRX) were used as terms of reference. Particular emphasis was given to the evaluation of allelic replication asynchrony in relation to the inactivation status of each gene. The human cell types analysed include neuronal cells and ICF syndrome cells, considered to be a model system for the study of X inactivation. PCDH11 appeared to be generally characterized by replication asynchrony in both male and female cells, and no significant differences were observed between human and gorilla, in which this gene lacks X-Y homologous status. However, in differentiated human neuroblastoma and cerebral cortical cells PCDH11X replication profile showed a significant shift towards allelic synchrony. Our data are relevant to the complex relationship between X-inactivation, as a chromosome-wide phenomenon, and asynchrony of replication and expression status of single genes on chromosome X.

PCDH11 is X/Y homologous in Homo sapiens but not in Gorilla gorilla and Pan troglodytes.

Protocadherin X (PCDHX) and Protocadherin Y (PCDHY) are cell-surface adhesion molecules expressed predominantly in brain. The human PCDH11X/Y gene pair is located in the non-pseudoautosomal X-Y homologous region (Xq21.3/Yp11.2). The possible existence of PCDH11 gene dosage differences between human and non-human primates is of evolutionary significance with respect to species differences and escape from X inactivation, and has been repeatedly debated. Previous investigations on the X/Y homologous status of PCDH11 and adjacent sequences in non-human primates have highlighted the complexity of the molecular pattern and evolutionary history of this genomic region. This paper provides for the first time direct evidence for the absence of the PCDH11 genefrom the Y chromosome of chimpanzee (Pan troglodytes) as well as gorilla (Gorilla gorilla). By confirmingthe suspected lack of X-Y homologous status for PCDH11 in non-human primates, our results reinforce the hypothesis of a hominid-specific role for this gene in brain development.

A new 2-carbamoyl pteridine that inhibits mycobacterial FtsZ.

The preparation of a new 2-carbamoyl pteridine, its activity data against FtsZ from M. tuberculosis (Mtb), and in vitro antibacterial data against Mtb strain H37Ra are presented.

Crystallization of the Mycobacterium tuberculosis cell-division protein FtsZ.

Mycobacterium tuberculosis FtsZ (MtbFtsZ), an essential protein in bacterial cell division, has been crystallized in the presence of a new inhibitor of MtbFtsZ polymerization and GTPase activity, ethyl (6-amino-2,3-dihydro-4-phenyl-1H-pyrido[4,3-b][1, 4]diazepin-8-yl)carbamate (SRI-7614). Crystals of the MtbFtsZ-SRI-7614 complex (form I, 30% polyethylene glycol 4000, 0.1 M sodium citrate pH 5.6, 0.2 M NH(4)OAc, 293 K) belong to space group P6(1) or P6(5), with unit-cell parameters a = 88.78, c = 178. 02 A, and diffract to 2.3 A resolution. A second crystal form, of the GDP complex, grows in the presence or absence of Mg(2+) from PEG 4000 at 277 K or from (NH(4))(2)SO(4) at 293 K, respectively (form II, space group P6(2)22 or P6(4)22, with unit-cell parameters a = 135.02, c = 328.97 A or a = 129.30, c = 327.97 A, respectively). Complete data sets to approximately 7 A resolution have been collected from both. Exceptional form II crystals diffract to at least 4.5 A resolution. Determination of the MtbFtsZ structure may advance the design of improved inhibitors of FtsZ polymerization.

Slow polymerization of Mycobacterium tuberculosis FtsZ.

The essential cell division protein, FtsZ, from Mycobacterium tuberculosis has been expressed in Escherichia coli and purified. The recombinant protein has GTPase activity typical of tubulin and other FtsZs. FtsZ polymerization was studied using 90 degrees light scattering. The mycobacterial protein reaches maximum polymerization much more slowly ( approximately 10 min) than E. coli FtsZ. Depolymerization also occurs slowly, taking 1 h or longer under most conditions. Polymerization requires both Mg(2+) and GTP. The minimum concentration of FtsZ needed for polymerization is 3 microM. Electron microscopy shows that polymerized M. tuberculosis FtsZ consists of strands that associate to form ordered aggregates of parallel protofilaments. Ethyl 6-amino-2, 3-dihydro-4-phenyl-1H-pyrido[4,3-b][1,4]diazepin-8-ylcarbamate+ ++ (SRI 7614), an inhibitor of tubulin polymerization synthesized at Southern Research Institute, inhibits M. tuberculosis FtsZ polymerization, inhibits GTP hydrolysis, and reduces the number and sizes of FtsZ polymers.

The two toxoplasma gondii hypoxanthine-guanine phosphoribosyltransferase isozymes form heterotetramers.

Two isozymes of the purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT) of the apicomplexan protozoan Toxoplasma gondii are encoded by the single HGPRT gene as a result of differential splicing. Western blotting of total T. gondii protein shows that both isozymes I and II, which differ by 49 amino acids, are expressed. Both form enzymatically active homotetramers when overexpressed in Escherichia coli. The specific activity of HGPRT-I is five times that of HGPRT-II. When both isozymes are co-expressed in E. coli, HGPRT-I.HGPRT-II heterotetramers form. The predominant heterotetramer has enzymatic activity similar to HGPRT-II, and gel filtration chromatography demonstrates that its size is intermediate between the sizes of HGPRT-I and HGPRT-II. Mass spectrometric analysis of cross-linked homo- and heterotetramers reveals species of distinct molecular mass for HGPRT-I, HGPRT-II, and HGPRT-I.HGPRT-II and suggests that the predominant heterotetramer consists of one HGPRT-I subunit and three HGPRT-II subunits. The implications of this finding are discussed.

Substrate deformation in a hypoxanthine-guanine phosphoribosyltransferase ternary complex: the structural basis for catalysis.

BACKGROUND: Hypoxanthine-guanine phosphoribosyltransferases (HGPRTs) are well-recognized antiparasitic drug targets. HGPRT is also a paradigmatic representative of the phosphoribosyltransferase family of enzymes, which includes other important biosynthetic and salvage enzymes and drug targets. To better understand the reaction mechanism of this enzyme, we have crystallized HGPRT from the apicomplexan protozoan Toxoplasma gondii as a ternary complex with a substrate and a substrate analog. RESULTS: The crystal structure of T. gondii HGPRT with the substrate Mg2+-PRPP and a nonreactive substrate analog, 9-deazaguanine, bound in the active site has been determined at 1.05 A resolution and refined to a free R factor of 15.4%. This structure constitutes the first atomic-resolution structure of both a phosphoribosyltransferase and the central metabolic substrate PRPP. This pre-transition state complex provides a clearer understanding of the structural basis for catalysis by HGPRT. CONCLUSIONS: Three types of substrate deformation, chief among them an unexpected C2'-endo pucker adopted by the PRPP ribose ring, raise the energy of the ground state. A cation-pi interaction between Tyr-118 and the developing oxocarbenium ion in the ribose ring helps to stabilize the transition state. Enforced substrate propinquity coupled with optimal reactive geometry for both the substrates and the active site residues with which they interact contributes to catalysis as well.

Crystal structures of the Toxoplasma gondii hypoxanthine-guanine phosphoribosyltransferase-GMP and -IMP complexes: comparison of purine binding interactions with the XMP complex.

The crystal structures of the guanosine 5'-monophosphate (GMP) and inosine 5'-monophosphate (IMP) complexes of Toxoplasma gondii hypoxanthine-guanine phosphoribosyltransferase (HGPRT) have been determined at 1.65 and 1.90 A resolution. These complexes, which crystallize in space groups P2(1) (a = 65.45 A, b = 90.84 A, c = 80. 26 A, and beta = 92.53 degrees ) and P2(1)2(1)2(1) (a = 84.54 A, b = 102.44 A, and c = 108.83 A), each comprise a tetramer in the crystallographic asymmetric unit. All active sites in the tetramers are fully occupied by the nucleotide. Comparison of these structures with that of the xanthosine 5'-monophosphate (XMP)-pyrophosphate-Mg(2+) ternary complex reported in the following article [Héroux, A., et al. (1999) Biochemistry 38, 14495-14506] shows how T. gondii HGPRT is able to recognize guanine, hypoxanthine, and xanthine as substrates, and suggests why the human enzyme cannot use xanthine efficiently. Comparison with the apoenzyme reveals the structural changes that occur upon binding of purines and ribose 5'-phosphate to HGPRT. Two structural features important to the HGPRT mechanism, a previously unrecognized active site loop (loop III', residues 180-184) and an active site peptide bond (Leu78-Lys79) that adopts both the cis and the trans configurations, are presented.

Crystal structure of Toxoplasma gondii hypoxanthine-guanine phosphoribosyltransferase with XMP, pyrophosphate, and two Mg(2+) ions bound: insights into the catalytic mechanism.

The crystal structure of the Toxoplasma gondii hypoxanthine-guanine phosphoribosyltransferase (HGPRT)-xanthosine 5'-monophosphate (XMP)-pyrophosphate-Mg(2+) ternary complex has been determined at 1. 60 A resolution. This biproduct, post-transition state structure is of a T. gondii HGPRT mutant (Asp150Ala or D150A). The D150A mutant has reduced activity (k(cat) lower by 11-, 296-, and 8.6-fold for hypoxanthine, guanine, and xanthine, respectively) compared to wild-type T. gondii HGPRT. The Michaelis constants for purine bases are altered only slightly, whereas those for alpha-D-5-phosphoribosyl 1-pyrophosphate (PRPP) are lower by approximately 6.5-fold. The ternary complex crystallizes in space group C222(1) (a = 55.21 A, b = 112.25 A, and c = 144.28 A) with two subunits in the asymmetric unit; the HGPRT tetramer is completed by the application of 2-fold crystallographic symmetry. All active sites contain XMP ¿bound in a fashion similar to that of the guanosine 5'-monophosphate (GMP) and inosine 5'-monophosphate (IMP) complexes reported in the preceding article [Héroux, A., et al. (1999) Biochemistry 38, 14485-14494]¿, pyrophosphate, and two Mg(2+) ions. Each Mg(2+) ion is octahedrally coordinated by two terminal pyrophosphate oxygen atoms and several ordered water molecules. This structure shows how HGPRT uses two Mg(2+) ions to orient and activate the pyrophosphate moiety of PRPP for attack by a purine base, and why mutation in humans of the residue corresponding to Asp206, the only HGPRT amino acid that directly contacts the Mg(2+) ions, causes Lesch-Nyhan syndrome (HGPRT(Kinston), D193N). The Leu78-Lys79 peptide bond in the active site adopts the cis configuration, which it must to bind PRPP or pyrophosphate. The contribution of cis-trans isomerization of this peptide bond to the energetics of substrate binding and product release is discussed. A comprehensive description of the HGPRT reaction mechanism is also proposed.

Screening of potential cancer preventing chemicals as aromatase inhibitors in an in vitro assay.

The inhibition of human placental aromatase was used to rank a series of compounds, with the objective of selecting compounds for further evaluation as chemopreventive agents. (+/-)-p-Aminoglutethimide, introduced over two decades ago as a treatment for breast cancer, had an IC50 of 6.5 microM. Five compounds were more potent than aminoglutethimide in this assay: (+)- vorozole, 4-hydroxyandrostenedione, miconazole nitrate, plomestane, and 4-methoxy-androst-4-ene-3,17-dione. Other compounds with known chemoprevention activity, such as curcumin and genistein, were inactive. This assay for aromatase inhibitors is a rapid, economical way of ranking compounds for further development as chemoprevention agents.

Antioxidant activity of michellamine alkaloids.

The alkaloids michellamines A, B, and C are natural products isolated from a Central African tropical plant Ancistrocladus korupensis. We have investigated the radical scavenging ability of these compounds. The alkaloids inhibited the azo-induced oxidation of beta-phycoerythrin with IC50 values in the 0.5- to 0.8-microM range. Michellamine B also protected rat liver mitochondria against lipid peroxidation induced by adenosine diphosphate and Fe2+. The alkaloids were more potent antioxidants in these assays than several compounds being considered clinically as chemoprevention agents.

Michellamine alkaloids inhibit protein kinase C.

Michellamines A, B, and C have shown antiviral activity against HIV-1 and HIV-2 in cell culture. They act in a complex manner by at least two reported antiviral mechanisms, inhibition of HIV reverse transcriptase and inhibition of HIV-induced cellular fusion. On the basis of their structural similarity to other protein kinase C (PKC) inhibitors, we have investigated another possible mechanism-inhibition of PKC. The michellamines were found to inhibit rat brain PKC with IC50 values in the 15-35 microM range. Michellamine B was a noncompetitive PKC inhibitor with respect to ATP with a Ki value of 4-6 microM, whereas mixed-type inhibition was observed when the peptide concentration was varied. Michellamine B inhibited the kinase domain of PKC similarly. These results indicate that the michellamines bind to the PKC kinase domain and not its regulatory domain. Molecular modeling showed that all three michellamines can bind in the active site cleft of the PKC kinase domain, to block both the ATP and the peptide substrate subsites.

PMTI, a broadly active unusual single-stranded polyribonucleotide, inhibits human immunodeficiency virus replication by multiple mechanisms.

Poly(1-methyl-6-thioinosinic acid), or PMTI, is a single-stranded polyribonucleotide and is the first homopolyribonucleotide devoid of Watson-Crick hydrogen bonding sites to show potent human immunodeficiency virus (HIV) inhibition. PMTI was found to be active when evaluated against a variety of low passage clinical HIV isolates in fresh human peripheral blood cells, including T cell-tropic and monocyte-macrophage-tropic viruses, syncytium-inducing and non-syncytium-inducing viruses and viruses representative of the various HIV-1 clades (A through F). The compound was active against HIV-2, all nucleoside and non-nucleoside reverse transcriptase (RT) inhibitor drug-resistant virus isolates tested and interacted with AZT or ddl to synergistically inhibit HIV infection. In biochemical inhibition assays, PMTI was determined to be a potent inhibitor of HIV-1 and HIV-2 RT, including RTs with mutations that engender resistance to nucleoside and non-nucleoside RT inhibitors. PMTI inhibited both the polymerase and RNase H activities of HIV RT. PMTI did not inhibit HIV-1 protease or integrase. Cell-based mechanism of action assays indicated that PMTI also interfered with early events in the entry of HIV into target cells. Furthermore, PMTI inhibited the fusion of gp120-expressing and CD4-expressing cells, but at concentrations approximately 1 log10 greater than those that inhibited virus entry. These results suggest that the homopolyribonucleotide PMTI blocks HIV replication in human cells at its earliest stages by multiple mechanisms, inhibition of virus entry and inhibition of RT.

Glycoprotein gD of MDV lacks functions typical for alpha-herpesvirus gD homologues.

Glycoprotein D (gD) belongs to family of conserved structural proteins of alpha-herpesviruses. During productive infection of cells by herpes simplex virus 1 (HSV-1) gD has several important functions, is involved in virus penetration to and release from infected cells and is one of main targets of neutralizing antibodies. Similar functions are shared also by other alpha-herpesvirus gD homologues. Surprisingly, in previous studies it was found that MDV gD expression could not be detected during infection in vitro using immunological methods. In this study we have analyzed expression of MDV gD and its biological consequences. In vitro expression using rabbit reticulocyte lysate and/or overexpression in transfected cells showed that the second ATG codon is required for synthesis of mature, glycosylated gD. In addition, it was found that gD overexpression is neither toxic for transfected cells nor is involved in membrane fusion. After MDV infection of a proprietary cell line stably transfected with plasmid overexpressing MDV gD, no viral particles could be found in culture. On the other hand, cells overexpressing the MDV gD were sensitive to MDV infection in similar way as parental, non-transfected cells. From our study and results of other authors we propound the following conclusions: (i) MDV gD expression is blocked during in vitro infection at transcription level; (ii) MDV gD is lacking many important functions characteristic for other alpha-herpesvirus gD homologues; (iii) overexpression of single MDV gD does not result in production of mature infectious MDV particles.