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Biomedical subjects

N Singh

Publications and source records attributed to N Singh.

At least 127 records · Page 7Linked to original sources
PubMed2001

Diverse macular dystrophy phenotype caused by a novel complex mutation in the ELOVL4 gene.

PURPOSE: A 5-bp deletion in ELOVL4, a photoreceptor-specific gene, has been associated with autosomal dominant (ad) macular dystrophy phenotypes in five related families, in which phenotypes range from Stargardt-like macular dystrophy (STGD3; Mendelian Inheritance in Man 600110) to pattern dystrophy. This has been the only mutation identified in ELOVL4 to date, which is associated with macular dystrophy phenotypes. In the current study, the potential involvement was investigated of an ELOVL4 gene variation in adSTGD-like and other macular dystrophy phenotypes segregating in a large unrelated pedigree from Utah (K4175). METHODS: The entire open reading frame of the ELOVL4 gene was analyzed by direct sequencing in a proband from the K4175 family. The combination of denaturing high-performance liquid chromatography (DHPLC) analysis and direct sequencing of all available family members was used to further assess segregation of identified ELOVL4 variants in the pedigree. RESULTS: A complex mutation, two 1-bp deletions separated by four nucleotides, was detected in all affected members of the family. The mutation results in a frameshift and the truncation of the ELOVL4 protein, similar to the effect of the previously described 5-bp deletion. CONCLUSIONS: The discovery of a second mutation in the ELOVL4 gene segregating with macular dystrophy phenotypes confirms the role of this gene in a subset of dominant macular dystrophies with a wide range of clinical expressions and suggests a role for modifying genes and/or environmental factors in the disease process.

Adolescent↗
PubMed2001

Treatment of a molasses based distillery effluent in a constructed wetland in central India.

A field-scale 4-celled, horizontal subsurface constructed wetland (CW) was installed to evaluate removal efficiencies of wastewater constituents in an industrial distillery effluent. Total and dissolved solids, NH4-N, TKN, P and COD were measured. This CW design provides four serial cells with synthetic liners and a river gravel base. The first two unplanted cells provide preliminary treatment. Specific gravel depths and ensuing biofilm growth provides anaerobic treatment in Cell 1 and anaerobic treatment in Cell 2. Cell 3 was planted with Typha latifolia with an inserted layer of brick rubble (for phosphorus removal). Locally grown reed, Phragmites karka was planted in Cell 4. COD was reduced from 8420 mg/l 3000 from Cell 1 to the outlet of Cell 4. Likewise other parameters: total and dissolved solids, ammonium and total nitrogen, and total P, indicated declining trends at the 4-celled CW effluent. This study reveals how high strength distillery wastewater strongly impacts morphology, aeration anatomy in the chiseled plant tissues, reed growth; and composition of the biofilm in the specialized substratum. The reliability of a CW for organic and nutrients reduction, in association with a poorly performing conventional system is discussed. There is an immense potential for appropriately designed constructed wetlands to improve high strength wastewaters in India.

Bacteria, Anaerobic↗
PubMed2001

Epidemiological applications: a case report of a village epidemic of gastroenteritis.

This is a case report of an epidemic of gastroenteritis which was investigated and controlled by epidemiological methods only, before laboratory investigations could be done to confirm the original epidemiological conclusions--from contaminated home made ice-cubes. The case and process are reported in order to encourage similar uses of epidemiology by field public health practitioners, especially within the district or primary health care systems and particularly in places where laboratory support are difficult to avail. The case is used also to discuss the equipments and facilities that ought to be part of the support system for every modern field public health practitioner. These should include computers, modern communication facilities and epidemiological support systems, especially senior epidemiologists; as such senior personnel are available to junior colleagues in the other areas of specialist medical practice.

Disease Outbreaks↗
PubMed2001

Teenage pregnancies in the Rewa medical sub-division, Fiji.

To assess the magnitude of teenage pregnancies in the Rewa Medical Sub-division as well as the socio-demographic characteristics of the affected teenagers so as to provide a baseline for tackling the problem. The study was a 5 year retrospective study (1994-1998) of the medical records of the Nausori Maternity Unit, the only unit for these purposes in the entire Subdivision. Pregnancies that were intentionally terminated were not included, as no such data was available from these our public health services. An average of 11.1% of the 5319 obstetric patients attended to at the centre for the 5 years were teenagers. Their age range was 13 to 19 years. Proportionately more Fijians had such teenage pregnancies than their Indo-Fijian counterparts. The same was true of their being unmarried or being VDRL positive. A larger percentage of the Indian teenagers received assisted deliveries than the Fijians, but this was not statistically significant, being 6% and 4% respectively. Low birth weight was 19% among these teenagers (compared with 5.9% overall). Efforts are needed in the area of family life education to improve on aspects of teenage pregnancies. Since this is an area of education that has many conflicting values in the modern world, it is advocated that parents as well as many agencies as possible should be targets as well as join in this task in order meet the needs as due. Such education should cover and respect all the values concerned.

Adolescent↗
PubMed2000

The chaperone protein BiP binds to a mutant prion protein and mediates its degradation by the proteasome.

Familial prion diseases are thought to result from a change in structure of the mutant prion protein (PrP), which takes a pathogenic conformation. We have examined the role of molecular chaperones in the folding of normal and mutant PrP Q217R (PrP(217)) in transfected neuroblastoma cells. In a previous report we showed that, although most of the PrP(217) forms escape the endoplasmic reticulum quality control system and aggregate in post-Golgi compartments, a significant proportion of PrP(217) retains the C-terminal glycosylphosphatidyl inositol signal peptide (PrP32), and does not exit the endoplasmic reticulum (Singh, N., Zanusso, G., Chen, S. G., Fujioka, H., Richardson, S., Gambetti, P., and Petersen, R. B. (1997) J. Biol. Chem. 272, 28461-28470). We have now studied the folding and turnover of PrP32 to understand the mechanism by which abnormal PrP forms cause cellular toxicity in our cell culture model and in the human brain carrying the Gerstmann-Sträussler-Scheinker disease Q217R mutation. In this report, we show that PrP32 remains associated with the chaperone BiP for an abnormally prolonged period of time and is degraded by the proteasomal pathway. This study is the first demonstration that BiP is chaperoning the folding of PrP and plays a role in maintaining the quality control in the PrP maturation pathway. Our data provide new insight into the diverse pathways of mutant PrP metabolism and neurotoxicity.

Amino Acid Substitution↗
PubMed2000

Lymphocytes lacking I kappa B-alpha develop normally, but have selective defects in proliferation and function.

NF-kappaB has been implicated in the development, activation, and function of B and T lymphocytes. We have evaluated the in vivo effects of deletion of IkappaB-alpha, a major inhibitor of NF-kappaB, on lymphocyte development, proliferation, and function. To elucidate the long term role of IkappaB-alpha in lymphocytes, fetal liver cells of 14.5-day-old IkappaB-alpha(-/-) or wild-type embryos were transplanted into irradiated recombinase-activating gene-2-deficient mice. Within 4 wk, the IkappaB-alpha(-/-) fetal liver cells reconstitute mature B and T cell populations in the recipients comparable to those produced by wild-type fetal liver cells. However, the proliferative responses of IkappaB-alpha(-/-) B cells are enhanced, whereas those of IkappaB-alpha(-/-) T cells are reduced. The levels of IgG1, IgG2a, IgA, and IgE produced by IkappaB-alpha(-/-) B cells are elevated relative to those produced by IkappaB-alpha(+/+) or IkappaB-alpha(+/-). Moreover, the specific immune responses to OVA and the generation of germinal centers are impaired in recipients of IkappaB-alpha(-/-) fetal liver cells. These results indicate that IkappaB-alpha plays a vital role in signal transduction pathways regulating lymphocyte proliferation and also in the production of specific Ig isotypes.

Animals↗
PubMed2000

Interaction between chloroquine and diverse pharmacological agents in chloroquine resistant Plasmodium yoelii nigeriensis.

The effect of a number of pharmacological agents on the enhancement of antimalarial activity of chloroquine was evaluated against chloroquine resistant line of Plasmodium yoelii nigeriensis (N-67). The response after combination therapy was monitored on the basis of alteration in the course of parasitaemia, the extension of mean survival time and the percent cure rate in different groups. The study was designed to compare the in vivo efficacy of a number of resistance modulating agents found effective in several in vitro studies against chloroquine resistant P. falciparum isolates. Based on their efficacy in this rodent model, the response of combination of chloroquine with agents representing diverse chemical moieties has been categorised as curative, moderately active and inactive. Out of the 22 agents evaluated, only cyproheptadine-chloroquine combination produced curative response. Ketotifen, azatadine, pheniramine, amitriptyline, fluoxetine, verapamil, penfluridol and trifluoperazine demonstrated moderate activity while loratadine, terfenadine, promethazine, ranitidine, nifedipine, diltiazem, chlorpromazine, amiodarone, tamoxifen, dipyridamol, propranolol, acyclovir and amantidine were inactive. The study advocates the suitability of proposed rodent model to shortlist potential resistance reversal agents.

Animals↗
PubMed2000

Differential gene expression in apoptosis: identification of ribosomal protein S29 as an apoptotic inducer.

To identify genes that are specifically involved in apoptosis, poly(A)(+) RNAs were isolated from untreated control rat thymocytes and from adriamycin-induced apoptotic thymocytes. Directionally cloned cDNA libraries were then constructed in UNIZAP-XR vectors followed by biotin-based subtractive hybridization. Three clones were confirmed to be differentially expressed by dot blotting. Sequence analysis revealed homology to two genes previously identified, whereas one clone was novel and did not have homology to any known sequence. One clone was identical to the ribosomal protein S29, and the other was homologous to L8 ribosomal protein. Northern blot analysis revealed a marked increase in the expression of mRNA encoding ribosomal protein S29 in the apoptotic thymocytes compared to the controls. Transfection studies revealed that enhanced S29 expression resulted in increased apoptosis in rat thymocytes and HeLa cells as assessed by various morphological and biochemical characteristics, including cell shrinkage, chromatin condensation, membrane blebbing, formation of apoptotic bodies, TUNEL, FACS, and internucleosomal DNA fragmentation. This was accompanied by upregulation of p53, Caspase 3, and bax, whereas bcl-2 was downregulated as revealed by Western blotting. The current findings provide the first hint of a role for ribosomal protein S29 in the apoptotic process.

Animals↗
PubMed2000

Type IV collagen of the glomerular basement membrane. Evidence that the chain specificity of network assembly is encoded by the noncollagenous NC1 domains.

The ultrafiltration function of the glomerular basement membrane (GBM) of the kidney is impaired in genetic and acquired diseases that affect type IV collagen. The GBM is composed of five (alpha1 to alpha5) of the six chains of type IV collagen, organized into an alpha1.alpha2(IV) and an alpha3.alpha4.alpha5(IV) network. In Alport syndrome, mutations in any of the genes encoding the alpha3(IV), alpha4(IV), and alpha5(IV) chains cause the absence of the alpha3. alpha4.alpha5 network, which leads to progressive renal failure. In the present study, the molecular mechanism underlying the network defect was explored by further characterization of the chain organization and elucidation of the discriminatory interactions that govern network assembly. The existence of the two networks was further established by analysis of the hexameric complex of the noncollagenous (NC1) domains, and the alpha5 chain was shown to be linked to the alpha3 and alpha4 chains by interaction through their respective NC1 domains. The potential recognition function of the NC1 domains in network assembly was investigated by comparing the composition of native NC1 hexamers with hexamers that were dissociated and reconstituted in vitro and with hexamers assembled in vitro from purified alpha1-alpha5(IV) NC1 monomers. The results showed that NC1 monomers associate to form native-like hexamers characterized by two distinct populations, an alpha1.alpha2 and alpha3.alpha4.alpha5 heterohexamer. These findings indicate that the NC1 monomers contain recognition sequences for selection of chains and protomers that are sufficient to encode the assembly of the alpha1.alpha2 and alpha3.alpha4.alpha5 networks of GBM. Moreover, hexamer formation from the alpha3, alpha4, and alpha5 NC1 monomers required co-assembly of all three monomers, suggesting that mutations in the NC1 domain in Alport syndrome may disrupt the assembly of the alpha3.alpha4.alpha5 network by interfering with the assembly of the alpha3.alpha4.alpha5 NC1 hexamer.

Animals↗
PubMed2000

Cytomegalovirus antigenemia directed pre-emptive prophylaxis with oral versus I.V. ganciclovir for the prevention of cytomegalovirus disease in liver transplant recipients: a randomized, controlled trial.

BACKGROUND: The efficacy of pre-emptively administered oral ganciclovir in preventing cytomegalovirus (CMV) disease has not been documented in liver transplant recipients. We sought to compare the efficacy of pre-emptive oral ganciclovir with that of i.v. ganciclovir for the prevention of CMV disease after liver transplantation, and to determine whether withholding prophylaxis in the absence of CMV antigenemia, reliably identified patients in whom no prophylaxis was necessary. METHODS: Surveillance cultures for CMV pp65 antigenemia were performed in all patients at weeks 2, 4, 6, 8, 12, and 16. Patients with CMV antigenemia were randomized into two study groups. The experimental group received oral ganciclovir for 6 weeks (2 g t.i.d. for 2 weeks, then 1 g t.i.d. for 4 weeks), and the control group received i.v. ganciclovir (5 mg/kg q 12 hr) for 7 days. RESULTS: Of 72 consecutive liver transplant recipients studied, CMV antigenemia occurred in 31% (22 of 72). Twenty-two patients with asymptomatic antigenemia were randomized to two study groups. CMV disease (viral syndrome) occurred in 9% (1 of 11) of the patients in the i.v. ganciclovir group and in 0% (0 of 11) of the patients in the oral ganciclovir group. None of the study patients developed tissue invasive CMV disease. The median reduction in antigenemia level with oral ganciclovir was 55% at week 1, and 100% at week 2. Overall, 64% of the patients by week 1, 93% by week 2, and 100% by week 4 had antigenemia levels below the baseline after oral ganciclovir. Of 50 patients without CMV antigenemia, none developed CMV disease. CONCLUSIONS: Pre-emptive prophylaxis based on CMV antigenemia can effectively target the patients for CMV prophylaxis; 69% of the patients never received antiviral prophylaxis and did not develop CMV disease. Antiviral therapy instituted upon detection of antigenemia prevented tissue invasive CMV in both ganciclovir groups. Pre-emptively administered oral ganciclovir was effective as prophylaxis for CMV disease after liver transplantation.

Administration, Oral↗
PubMed2000

Aminotroponiminates as ligands for potential metal-based nitric oxide sensors.

A family of new fluorescently labeled ligands, HRDATI, was prepared to develop transition-metal-based NO sensing strategies. The ligands are composed of aminotroponiminates (ATIs) with a dansyl fluorophore on one of the imine nitrogen atoms and an alkyl substituent, either i-Pr (8), t-Bu (9), or Bz (10), on the other. Bis(chelate) Co2+ ([Co(i-PrDATI)2] (12), [Co(t-BuDATI)2] (14), [Co(BzDATI)2] (15)) and Zn2+ ([Zn(i-PrDATI)2] (13)) complexes were prepared and characterized by X-ray crystallography. The bis(ATI) complex [Co(i-Pr2ATI)2] (11) was also prepared and its X-ray crystal structure determined. Cyclic voltammetry reveals reversible redox waves at -2.57 and -0.045 V (vs Cp2Fe/Cp2Fe+) in THF for the Co2+/Co+ and Co3+/Co2+ couples, respectively, of 11. Only a Co2+/Co+ wave at -2.09 V is observed for 12. When excited at 350 nm, the HRDATI ligands and the diamagnetic Zn2+ complex 13 fluoresce around 500 nm, whereas the paramagnetic Co2+ complexes quench the fluorescence. These air-stable cobalt compounds react with nitric oxide to dissociate a DATI ligand and form neutral dinitrosyl complexes, [Co(NO)2(RDATI)]. The release of the fluorophore-containing ligand is accompanied by an increase in fluorescence intensity, thus providing a strategy for fluorescent NO sensing. Linking two DATI moieties via a tetramethylene chain affords the ligand H2DATI-4 (18). The Co2+ complex [Co(DATI-4)] (19) reacts more readily with NO than the bis(DATI) compounds and also displays an increase in fluorescence intensity upon NO binding.

Journal Article↗
PubMed2000

Modulation of halofantrine resistance after coadministration of halofantrine with diverse pharmacological agents in a rodent malaria model.

The declining efficacy of antimalarial drugs against Plasmodium falciparum strains has been reported from several endemic regions of the world. Strategic evaluation of several pharmacological agents in combination with chloroquine to enhance the sensitivity of the latter against resistant parasites has been documented in several studies. However no attempts have been directed to monitor the efficacy of such biological response modifiers for reversing the resistance to halofantrine. In the present study the comparative efficacy of a total of 22 pharmacological agents representing diverse categories including antihistamines, antidepressants, calcium channel blockers, neuroleptics etc. has been determined in combination with halofantrine against halofantrine resistant Plasmodium yoelii nigeriensis. Results show significant potentiation of the efficacy of halofantrine when administered concurrently with histamine H1 receptor antagonists cyproheptadine and ketotifen. Combination with pheniramine, amitriptyline, verapamil and penfluridol also produced moderate degree of potentiation which was well marked during the early phase of progression of parasitaemia.

Animals↗
PubMed2000

The alloreactive and self-restricted CD4+ T cell response directed against a single MHC class II/peptide combination.

The cellular basis for allograft rejection derives from the strong T cell response to cells bearing foreign MHC. While it was originally assumed that alloreactive T cells focus their recognition on the polymorphic residues that differ between syngeneic and allogeneic MHC molecules, studies with MHC class I-restricted CTL have shown that MHC-bound peptides play a critical role in allorecognition. It has been suggested that alloreactive T cells depend more strongly on interactions with the MHC molecule than with the associated peptide, but there is little evidence to support this idea. Here we have studied the alloreactive and self-restricted response directed against the class II H2-Ab molecule bound with a single peptide, Ep, derived from the H2-Ealpha chain. This MHC class II-peptide combination was a poor target and stimulator of alloreactive CD4+ T cell responses, indicating that MHC-bound peptides are as important for alloreactive CD4+ T cells as they are for alloreactive CTL. We also generated alloreactive T cells with exquisite specificity for the Ab/Ep complex, and compared their reactivity with self-restricted T cells specific for the same Ab/Ep complex. Our results showed that peptide-specific alloreactive T cells, as compared with self-restricted T cells, were more sensitive to peptide stimulation, but equally sensitive to amino acid substitutions in the peptide. These findings indicate that alloreactive and self-restricted T cells interact similarly with their MHC/peptide ligand.

Amino Acid Sequence↗
PubMed2000

Adherence to protease inhibitor therapy and outcomes in patients with HIV infection.

BACKGROUND: Combination antiretroviral therapy with protease inhibitors has transformed HIV infection from a terminal condition into one that is manageable. However, the complexity of regimens makes adherence to therapy difficult. OBJECTIVE: To assess the effects of different levels of adherence to therapy on virologic, immunologic, and clinical outcome; to determine modifiable conditions associated with suboptimal adherence; and to determine how well clinicians predict patient adherence. DESIGN: Prospective, observational study. SETTING: HIV clinics in a Veterans Affairs medical center and a university medical center. PATIENTS: 99 HIV-infected patients who were prescribed a protease inhibitor and who neither used a medication organizer nor received their medications in an observed setting (such as a jail or nursing home). MEASUREMENTS: Adherence was measured by using a microelectronic monitoring system. The adherence rate was calculated as the number of doses taken divided by the number prescribed. Patients were followed for a median of 6 months (range, 3 to 15 months). RESULTS: During the study period, 45,397 doses of protease inhibitor were monitored in 81 evaluable patients. Adherence was significantly associated with successful virologic outcome (P < 0.001) and increase in CD4 lymphocyte count (P = 0.006). Virologic failure was documented in 22% of patients with adherence of 95% or greater, 61% of those with 80% to 94.9% adherence, and 80% of those with less than 80% adherence. Patients with adherence of 95% or greater had fewer days in the hospital (2.6 days per 1000 days of follow-up) than those with less than 95% adherence (12.9 days per 1000 days of follow-up; P = 0.001). No opportunistic infections or deaths occurred in patients with 95% or greater adherence. Active psychiatric illness was an independent risk factor for adherence less than 95% (P = 0.04). Physicians predicted adherence incorrectly for 41% of patients, and clinic nurses predicted it incorrectly for 30% of patients. CONCLUSIONS: Adherence to protease inhibitor therapy of 95% or greater optimized virologic outcome for patients with HIV infection. Diagnosis and treatment of psychiatric illness should be further investigated as a means to improve adherence to therapy.

Adult↗
PubMed2000

Allele-specific expression patterns of interleukin-2 and Pax-5 revealed by a sensitive single-cell RT-PCR analysis.

Autosomal genes that are subject to random allelic inactivation (RAI), like imprinted genes [1] and genes subject to X-inactivation [2], require mechanisms that dictate the differential transcriptional regulation of two sequence-identical alleles. RAI genes include olfactory receptor genes [3], and the various genes encoding antigen receptors on lymphocytes (immunoglobulin genes, T cell receptor genes and NK receptor genes [4] [5] [6] [7]). These observations raise the possibility that other genes might be similarly regulated. Moreover, an interesting possibility is that certain genes might be monoallelically expressed in some cells and biallelically expressed in others. Recently, reports of monoallelic expression of interleukin-2 (IL-2) [8] [9] and IL-4 [10] [11] have raised the possibility that the cytokine gene family may be subject to monoallelic expression. Another report suggests that the gene encoding the transcription factor Pax-5, which is involved in B-cell (and cerebellar) development [12] [13], is also subject to monoallelic expression [14]. Using a novel single-cell reverse transcription-polymerase chain reaction (RT-PCR) approach, we have analyzed the IL-2 and Pax-5 genes in mice. We found that IL-2 is monoallelically transcribed in some T cells and biallelically transcribed in others, raising interesting questions regarding cytokine gene regulation. Additionally, our analyses suggest that Pax-5 is consistently biallelically transcribed. Thus, the IL-2 gene and other cytokine genes may be regulated in a stochastic manner that results in 0, 1 or 2 alleles of a given cytokine gene expressed in each T cell. This type of regulation could account for the wide variety of different combinations of cytokine genes expressed in individual T cells and therefore plays a role in the generation of T cells with a range of different effector functions.

Alleles↗
PubMed2000

Encephalitis caused by human herpesvirus-6 in transplant recipients: relevance of a novel neurotropic virus.

BACKGROUND: Human herpesvirus-6 (HHV-6) is a neurotropic virus. Encephalitis is a significant clinical manifestation of HHV-6; however, sparse data on this entity exist in transplant recipients. METHODS: Cases of HHV-6 encephalitis reported in the literature (13 bone marrow transplant recipients and 1 liver transplant recipient) were reviewed. The diagnosis was established in all by viral isolation and/or detection of HHV-6 DNA in the cerebrospinal fluid by polymerase chain reaction or histopathologic method. RESULTS: HHV-6 encephalitis occurred a median of 45 days (range 10 days to 15 months) after transplantation. Mental status changes, ranging from confusion to coma (92%), seizures (25%), and headache (25%) were the predominant clinical presentations. Focal neurologic findings occurred in only 17% of the patients. Twenty-five percent of the patients had fever; however, the height of fever (< or =40 degrees C) in febrile patients was striking. Cerebrospinal fluid pleocytosis was generally lacking. Abnormal neuroimaging findings, characterized by low-attenuation lesions in the posterior cerebral lobes, were present only in 17% of the patients. Overall mortality in patients with HHV-6 encephalitis was 58% (7 of 12); 42% (5 of 12) of the deaths were caused by HHV-6. Cure was documented in 7 of 8 patients who received ganciclovir or foscarnet for > or =7 days, compared with 0% (0 of 4) in those who did not receive these drugs or received them for < 7 days (P=.01). CONCLUSIONS: HHV-6 may be associated with encephalitis after transplantation and warrants consideration in transplant recipients with encephalitis of unidentifiable etiology.

Adolescent↗
PubMed2000

Human herpesvirus-6 in liver transplant recipients: role in pathogenesis of fungal infections, neurologic complications, and outcome.

BACKGROUND: The clinical impact and relevance of human herpesvirus-6 (HHV-6) infection in liver transplant recipients, has not been fully discerned. METHODS: A prospective study of 80 consecutive liver transplant recipients was performed using surveillance cultures for HHV-6 at weeks 2, 3, 4, and 6 after transplantation. Viral isolation was used for the detection of HHV-6. RESULTS: HHV-6 infection occurred in 39% (31 of 80) of the patients. Patients with HHV-6 infection were more likely to have hepatocellular carcinoma as underlying liver disease (P=.09). Mental status changes of unidentifiable etiology were significantly more likely to occur in patients with HHV-6 compared with those without (26%, 9 of 31 vs. 6%, 3 of 49, P=.008). HHV-6 infection was an independent predictor of invasive fungal infections (odds ratio 8.3, 95% confidence interval, 1.2-58.0, P=.03). A significant association between HHV-6 infection and CMV infection after transplantation, CMV recipient and donor serostatus, rejection, or fever of unknown origin, could not be documented. Mortality at last follow-up in patients with HHV-6 infection (29%, 9 of 31) was significantly greater than those without HHV-6 (6%, 3 of 49, P=.008). CONCLUSIONS: Central nervous system complications of unknown etiology after liver transplantation may be related to HHV-6 infection. HHV-6 viremia was an independently significant predictor of invasive fungal infections and was associated with late mortality in liver transplantation recipients.

Adult↗