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1.
J Perinatol ; 2019 Aug 08.
Artigo em Inglês | MEDLINE | ID: mdl-31395954

RESUMO

OBJECTIVE: To determine the proportion of infant deaths occurring in the setting of a confirmed genetic disorder. STUDY DESIGN: A retrospective analysis of the electronic medical records of infants born from 1 January, 2011 to 1 June, 2017, who died prior to 1 year of age. RESULTS: Five hundred and seventy three deceased infants were identified. One hundred and seventeen were confirmed to have a molecular or cytogenetic diagnosis in a clinical diagnostic laboratory and an additional seven were diagnosed by research testing for a total of 124/573 (22%) diagnosed infants. A total of 67/124 (54%) had chromosomal disorders and 58/124 (47%) had single gene disorders (one infant had both). The proportion of diagnoses made by sequencing technologies, such as exome sequencing, increased over the years. CONCLUSIONS: The prevalence of confirmed genetic disorders within our cohort of infant deaths is higher than that previously reported. Increased efforts are needed to further understand the mortality burden of genetic disorders in infancy.

2.
Skelet Muscle ; 8(1): 23, 2018 07 30.
Artigo em Inglês | MEDLINE | ID: mdl-30060766

RESUMO

BACKGROUND: Dystroglycanopathies are a clinically and genetically heterogeneous group of disorders that are typically characterised by limb-girdle muscle weakness. Mutations in 18 different genes have been associated with dystroglycanopathies, the encoded proteins of which typically modulate the binding of α-dystroglycan to extracellular matrix ligands by altering its glycosylation. This results in a disruption of the structural integrity of the myocyte, ultimately leading to muscle degeneration. METHODS: Deep phenotypic information was gathered using the PhenoTips online software for 1001 patients with unexplained limb-girdle muscle weakness from 43 different centres across 21 European and Middle Eastern countries. Whole-exome sequencing with at least 250 ng DNA was completed using an Illumina exome capture and a 38 Mb baited target. Genes known to be associated with dystroglycanopathies were analysed for disease-causing variants. RESULTS: Suspected pathogenic variants were detected in DPM3, ISPD, POMT1 and FKTN in one patient each, in POMK in two patients, in GMPPB in three patients, in FKRP in eight patients and in POMT2 in ten patients. This indicated a frequency of 2.7% for the disease group within the cohort of 1001 patients with unexplained limb-girdle muscle weakness. The phenotypes of the 27 patients were highly variable, yet with a fundamental presentation of proximal muscle weakness and elevated serum creatine kinase. CONCLUSIONS: Overall, we have identified 27 patients with suspected pathogenic variants in dystroglycanopathy-associated genes. We present evidence for the genetic and phenotypic diversity of the dystroglycanopathies as a disease group, while also highlighting the advantage of incorporating next-generation sequencing into the diagnostic pathway of rare diseases.


Assuntos
Variação Genética , Distrofia Muscular do Cíngulo dos Membros/genética , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Pré-Escolar , Distroglicanas/metabolismo , Feminino , Predisposição Genética para Doença , Glicosilação , Heterozigoto , Homozigoto , Humanos , Masculino , Pessoa de Meia-Idade , Proteínas Musculares/genética , Distrofia Muscular do Cíngulo dos Membros/metabolismo , Mutação , Fenótipo , Sequenciamento Completo do Exoma/métodos , Adulto Jovem
3.
Am J Hum Genet ; 101(2): 267-273, 2017 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-28777933

RESUMO

Ribosomal RNA (rRNA) is transcribed from rDNA by RNA polymerase I (Pol I) to produce the 45S precursor of the 28S, 5.8S, and 18S rRNA components of the ribosome. Two transcription factors have been defined for Pol I in mammals, the selectivity factor SL1, and the upstream binding transcription factor (UBF), which interacts with the upstream control element to facilitate the assembly of the transcription initiation complex including SL1 and Pol I. In seven unrelated affected individuals, all suffering from developmental regression starting at 2.5-7 years, we identified a heterozygous variant, c.628G>A in UBTF, encoding p.Glu210Lys in UBF, which occurred de novo in all cases. While the levels of UBF, Ser388 phosphorylated UBF, and other Pol I-related components (POLR1E, TAF1A, and TAF1C) remained unchanged in cells of an affected individual, the variant conferred gain of function to UBF, manifesting by markedly increased UBF binding to the rDNA promoter and to the 5'- external transcribed spacer. This was associated with significantly increased 18S expression, and enlarged nucleoli which were reduced in number per cell. The data link neurodegeneration in childhood with altered rDNA chromatin status and rRNA metabolism.


Assuntos
Encefalopatias/genética , Nucléolo Celular/patologia , Doenças Neurodegenerativas/genética , Proteínas Pol1 do Complexo de Iniciação de Transcrição/genética , RNA Ribossômico 18S/biossíntese , Adolescente , Adulto , Atrofia/genética , Encéfalo/patologia , Encefalopatias/patologia , Criança , Cromatina/metabolismo , Proteínas de Ligação a DNA/genética , Feminino , Humanos , Masculino , Doenças Neurodegenerativas/patologia , Polimorfismo de Nucleotídeo Único/genética , Regiões Promotoras Genéticas/genética , Adulto Jovem
4.
Eur J Hum Genet ; 25(4): 509-511, 2017 04.
Artigo em Inglês | MEDLINE | ID: mdl-28098151

RESUMO

Gain-of-function variants in some RAS-MAPK pathway genes, including PTPN11 and NRAS, are associated with RASopathies and/or acquired hematological malignancies, most notably juvenile myelomonocytic leukemia (JMML). With rare exceptions, the spectrum of germline variants causing RASopathies does not overlap with the somatic variants identified in isolated JMML. Studies comparing these variants suggest a stronger gain-of-function activity in the JMML variants. As JMML variants have not been identified as germline defects and have a greater impact on protein function, it has been speculated that they would be embryonic lethal. Here we identified three variants, which have previously only been identified in isolated somatic JMML and other sporadic cancers, in four cases with a severe pre- or neo-natal lethal presentation of Noonan syndrome. These cases support the hypothesis that these stronger gain-of-function variants are rarely compatible with life.


Assuntos
GTP Fosfo-Hidrolases/genética , Mutação em Linhagem Germinativa , Leucemia Mielomonocítica Juvenil/genética , Proteínas de Membrana/genética , Síndrome de Noonan/genética , Proteína Tirosina Fosfatase não Receptora Tipo 11/genética , Feminino , Humanos , Recém-Nascido , Síndrome de Noonan/diagnóstico , Gravidez
5.
PLoS One ; 9(2): e89673, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24586954

RESUMO

mRNA synthesis, processing, and destruction involve a complex series of molecular steps that are incompletely understood. Because the RNA intermediates in each of these steps have finite lifetimes, extensive mechanistic and dynamical information is encoded in total cellular RNA. Here we report the development of SnapShot-Seq, a set of computational methods that allow the determination of in vivo rates of pre-mRNA synthesis, splicing, intron degradation, and mRNA decay from a single RNA-Seq snapshot of total cellular RNA. SnapShot-Seq can detect in vivo changes in the rates of specific steps of splicing, and it provides genome-wide estimates of pre-mRNA synthesis rates comparable to those obtained via labeling of newly synthesized RNA. We used SnapShot-Seq to investigate the origins of the intrinsic bimodality of metazoan gene expression levels, and our results suggest that this bimodality is partly due to spillover of transcriptional activation from highly expressed genes to their poorly expressed neighbors. SnapShot-Seq dramatically expands the information obtainable from a standard RNA-Seq experiment.


Assuntos
RNA Mensageiro/metabolismo , Processamento Alternativo , Biflavonoides/farmacologia , Células HeLa/metabolismo , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Íntrons , Modelos Teóricos , Método de Monte Carlo , RNA/genética , Precursores de RNA , Processamento de RNA , Estabilidade de RNA , RNA Mensageiro/genética , Análise de Sequência de RNA/métodos , Transcrição Genética
6.
Am J Med Genet A ; 158A(8): 1909-17, 2012 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-22786811

RESUMO

Norrie disease (ND) is an X-linked recessive disorder characterized by congenital blindness, progressive sensorineural hearing loss and cognitive impairment. The ocular phenotype has been well described, while the extraocular manifestations of the disorder are not well understood. We present the data from the Norrie Disease Registry, which consists of 56 patients with detailed clinical histories and genotype data. This study represents the largest, detailed investigation into the phenotypic spectrum of ND to date and more importantly expands knowledge of the extraocular clinical manifestations. We identify several novel aspects of the syndrome that will improve the management of these patients. In particular, we expand our understanding of the neurologic manifestations in ND and identify a chronic seizure disorder in approximately 10% of all patients. In addition, details of the hearing phenotype are described including the median age of onset (12 years of age) and how genotype affects onset. Moreover, we find vascular disease to be a significant component of ND; and vascular health should be, in the future, a component of patient clinical care. In summary, the results expand our understanding of the phenotypic variability and genotypic heterogeneity in ND patients.


Assuntos
Cegueira/congênito , Doenças do Sistema Nervoso/patologia , Espasmos Infantis/patologia , Cegueira/genética , Cegueira/patologia , Doenças Genéticas Ligadas ao Cromossomo X , Genótipo , Humanos , Masculino , Doenças do Sistema Nervoso/genética , Testes Neuropsicológicos , Fenótipo , Degeneração Retiniana , Espasmos Infantis/genética , Inquéritos e Questionários
7.
Amyotroph Lateral Scler ; 13(2): 217-22, 2012 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-22292843

RESUMO

SOD1, ANG, TARDBP and FUS mutations have been associated with amyotrophic lateral sclerosis (ALS). Our goal was to extend molecular genetic analysis to newly identified ALS genetic loci and to determine the frequency of mutations, distribution of disease genes, and variant spectrum of these genes in a large United States ALS-phenotype cohort. We screened 1220 probands with an ALS phenotype, referred originally for SOD1 molecular genetic analysis. 1128 SOD1-negative probands were screened for ANG, and 277 and 223 SOD1- and ANG-negative samples were screened for TARDBP and FUS, respectively. One hundred additional probands were specifically screened only for FUS exon 15. We identified a total of 36 different SOD1 mutations, including three novel mutations, in 92 probands. ANG screening identified three mutations, including two novel mutations, and TARDBP screening identified two previously reported TARDBP mutations. We also identified four mutations in FUS, including the reported FUS in-frame deletion, c.430_447del, p.Gly144_Tyr149del, in a patient with inclusion body myositis, and two known FUS missense mutations. From this study, we estimate frequencies for SOD1, ANG, TARDBP and FUS mutations, in this United States cohort, to be 7.5%, 0.71%, 0.72% and 1.9%, respectively. In conclusion, we identify novel variants in SOD1, ANG, TARDBP and FUS, and expand the FUS-associated clinicopathologic phenotype.


Assuntos
Esclerose Amiotrófica Lateral/genética , Técnicas de Laboratório Clínico , Proteínas de Ligação a DNA/genética , Proteína FUS de Ligação a RNA/genética , Ribonuclease Pancreático/genética , Superóxido Dismutase/genética , Esclerose Amiotrófica Lateral/fisiopatologia , Predisposição Genética para Doença , Testes Genéticos , Humanos , Mutação , Fenótipo , Superóxido Dismutase-1 , Estados Unidos
8.
RNA ; 15(3): 459-72, 2009 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-19155325

RESUMO

Histone mRNAs are the only eukaryotic cellular mRNAs that are not polyadenylated. Synthesis of mature histone mRNA requires only a single processing reaction: an endonucleolytic cleavage between a conserved stem-loop and a purine-rich downstream element to form the 3' end. The stem-loop binding protein (SLBP) is required for processing, and following processing, histone mRNA is transported to the cytoplasm, where SLBP participates in translation of the histone mRNA and is also involved in regulation of histone mRNA degradation. Here we present an analysis of histone mRNA metabolism in cells with highly reduced levels of SLBP using RNA interference. Knocking down SLBP in U2OS cells results in a reduction in the rate of cell growth and an accumulation of cells in S-phase. Surprisingly, there is only a modest (twofold) decrease in histone mRNA levels. Much of histone mRNA in the SLBP knockdown cells is properly processed but is retained in the nucleus. The processed histone mRNA in SLBP knockdown cells is not rapidly degraded when DNA replication is inhibited. These results suggest a previously undescribed role for SLBP in histone mRNA export.


Assuntos
Transporte Ativo do Núcleo Celular , Histonas/metabolismo , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , RNA Mensageiro/metabolismo , Fatores de Poliadenilação e Clivagem de mRNA/genética , Fatores de Poliadenilação e Clivagem de mRNA/metabolismo , Sequência de Bases , Ciclo Celular , Núcleo Celular/metabolismo , Técnicas de Silenciamento de Genes , Histonas/química , Histonas/genética , Humanos , Dados de Sequência Molecular
9.
Genes Dev ; 22(1): 50-65, 2008 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-18172165

RESUMO

Histone mRNAs are rapidly degraded at the end of S phase or when DNA replication is inhibited. Histone mRNAs end in a conserved stem-loop rather than a poly(A) tail. Degradation of histone mRNAs requires the stem-loop sequence, which binds the stem-loop-binding protein (SLBP), active translation of the histone mRNA, and the location of the stem-loop close to the termination codon. We report that the initial step in histone mRNA degradation is the addition of uridines to the 3' end of the histone mRNA, both after inhibition of DNA replication and at the end of S phase. Lsm1 is required for histone mRNA degradation and is present in a complex containing SLBP on the 3' end of histone mRNA after inhibition of DNA replication. We cloned degradation intermediates that had been partially degraded from both the 5' and the 3' ends. RNAi experiments demonstrate that both the exosome and 5'-to-3' decay pathway components are required for degradation, and individual histone mRNAs are then degraded simultaneously 5' to 3' and 3' to 5'.


Assuntos
Histonas/genética , Oligorribonucleotídeos/metabolismo , Processamento Pós-Transcricional do RNA , Estabilidade de RNA/fisiologia , RNA Mensageiro/metabolismo , Nucleotídeos de Uracila/metabolismo , Sequência de Bases , Citoplasma/metabolismo , Células HeLa , Histonas/metabolismo , Humanos , Modelos Genéticos , Dados de Sequência Molecular , RNA Mensageiro/química , Fase S
10.
Methods Enzymol ; 449: 23-45, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-19215752

RESUMO

Replication-dependent histone mRNAs are coordinately regulated in parallel with DNA replication. Histone mRNAs accumulate to high levels only in S-phase cells and are degraded rapidly at the end of S phase or when DNA replication is inhibited in S-phase cells. The unique 3' end on histone mRNAs is the cis element responsible for the regulation of histone mRNA degradation. This chapter describes the approaches used to demonstrate the connection between translation of histone mRNA and its degradation as well as the pathway of histone mRNA degradation in mammalian cells. In particular, the initial step in histone mRNA degradation is attachment of an oligo(U) tail to the 3' end of histone mRNA, providing a platform for binding factors that trigger mRNA degradation.


Assuntos
Ciclo Celular/genética , Ciclo Celular/fisiologia , Histonas/genética , Estabilidade de RNA/genética , RNA Mensageiro/metabolismo , Células HeLa , Humanos , Modelos Biológicos , Hibridização de Ácido Nucleico , Biossíntese de Proteínas/fisiologia , RNA Mensageiro/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa
11.
Cell Cycle ; 6(8): 972-81, 2007 Apr 15.
Artigo em Inglês | MEDLINE | ID: mdl-17404513

RESUMO

The changes in global gene expression in response to DNA damage may derive from either direct induction or repression by transcriptional regulation or indirectly by synchronization of cells to specific cell cycle phases, such as G1 or G2. We developed a model that successfully estimated the expression levels of >400 cell cycle-regulated genes in normal human fibroblasts based on the proportions of cells in each phase of the cell cycle. By isolating effects on the gene expression associated with the cell cycle phase redistribution after genotoxin treatment, the direct transcriptional target genes were distinguished from genes for which expression changed secondary to cell synchronization. Application of this model to ionizing radiation (IR)-treated normal human fibroblasts identified 150 of 406 cycle-regulated genes as putative direct transcriptional targets of IR-induced DNA damage. Changes in expression of these genes after IR treatment derived from both direct transcriptional regulation and cell cycle synchronization.


Assuntos
Ciclo Celular/genética , Dano ao DNA/genética , Regulação da Expressão Gênica , Transcrição Genética/genética , Ciclo Celular/efeitos da radiação , Células Cultivadas , DNA/biossíntese , DNA/efeitos da radiação , Perfilação da Expressão Gênica , Humanos , Telomerase/genética , Transfecção
12.
Environ Health Perspect ; 114(4): 553-9, 2006 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-16581545

RESUMO

Cell cycle arrest and stereotypic transcriptional responses to DNA damage induced by ionizing radiation (IR) were quantified in telomerase-expressing human diploid fibroblasts. Analysis of cytotoxicity demonstrated that 1.5 Gy IR inactivated colony formation by 40-45% in three fibroblast lines; this dose was used in all subsequent analyses. Fibroblasts exhibited > 90% arrest of progression from G2 to M at 2 hr post-IR and a similarly severe arrest of progression from G1 to S at 6 and 12 hr post-IR. Normal rates of DNA synthesis and mitosis 6 and 12 hr post-IR caused the S and M compartments to empty by > 70% at 24 hr. Global gene expression was analyzed in IR-treated cells. A microarray analysis algorithm, EPIG, identified nine IR-responsive patterns of gene expression that were common to the three fibroblast lines, including a dominant p53-dependent G1 checkpoint response. Many p53 target genes, such as CDKN1A, GADD45, BTG2, and PLK3, were significantly up-regulated at 2 hr post-IR. Many genes whose expression is regulated by E2F family transcription factors, including CDK2, CCNE1, CDC6, CDC2, MCM2, were significantly down-regulated at 24 hr post-IR. Numerous genes that participate in DNA metabolism were also markedly repressed in arrested fibroblasts apparently as a result of cell synchronization behind the G1 checkpoint. However, cluster and principal component analyses of gene expression revealed a profile 24 hr post-IR with similarity to that of G0 growth quiescence. The results reveal a highly stereotypic pattern of response to IR in human diploid fibroblasts that reflects primarily synchronization behind the G1 checkpoint but with prominent induction of additional markers of G0 quiescence such as GAS1.


Assuntos
Fibroblastos/efeitos da radiação , Fase G1 , Perfilação da Expressão Gênica , Radiação Ionizante , Fase de Repouso do Ciclo Celular , Linhagem Celular , Dano ao DNA , Diploide , Relação Dose-Resposta à Radiação , Fibroblastos/citologia , Humanos , Análise de Sequência com Séries de Oligonucleotídeos
13.
Mol Cell Biol ; 25(8): 3109-16, 2005 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15798197

RESUMO

The Timeless protein is essential for circadian rhythm in Drosophila. The Timeless orthologue in mice is essential for viability and appears to be required for the maintenance of a robust circadian rhythm as well. We have found that the human Timeless protein interacts with both the circadian clock protein cryptochrome 2 and with the cell cycle checkpoint proteins Chk1 and the ATR-ATRIP complex and plays an important role in the DNA damage checkpoint response. Down-regulation of Timeless in human cells seriously compromises replication and intra-S checkpoints, indicating an intimate connection between the circadian cycle and the DNA damage checkpoints that is in part mediated by the Timeless protein.


Assuntos
Ciclo Celular/fisiologia , Ritmo Circadiano/fisiologia , Dano ao DNA , Fatores de Transcrição/fisiologia , Proteínas Adaptadoras de Transdução de Sinal , Proteínas Mutadas de Ataxia Telangiectasia , Proteínas de Ciclo Celular/metabolismo , Linhagem Celular , Quinase 1 do Ponto de Checagem , Montagem e Desmontagem da Cromatina/fisiologia , Criptocromos , Replicação do DNA/efeitos dos fármacos , Replicação do DNA/fisiologia , Proteínas de Ligação a DNA , Regulação para Baixo/efeitos dos fármacos , Exodesoxirribonucleases/metabolismo , Flavoproteínas/metabolismo , Humanos , Hidroxiureia/farmacologia , Peptídeos e Proteínas de Sinalização Intracelular , Fosfoproteínas/metabolismo , Proteínas Quinases/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/farmacologia , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo
14.
J Eukaryot Microbiol ; 50(3): 224-32, 2003 May-Jun.
Artigo em Inglês | MEDLINE | ID: mdl-12836881

RESUMO

Phylogenetic analysis of small-subunit ribosomal RNA gene sequences for gymnamoebae of the families Vexilliferidae, Paramoebidae, and Vannellidae identified two distinct lineages that are supported by gross morphological characters. This analysis indicates that paramoebids and vexilliferids are part of one lineage and that vannellids belong to another. A shared morphological character unique to the paramoebid/vexilliferid lineage members is the presence of dactylopodiate subpseudopodia. However, cell surface structures, normally used for taxonomic discrimination, range from simple hair-like filaments without any apparent organization (Neoparamoeba), to hexagonal glycostyles (Vexillifera) or more elaborate surface scales (Korotnevella). Taxa within the vannellid lineage all lack subpseudopodia and appear flabellate, spatulate or linguiform while in locomotion. Cell surface structures of taxa within the vannellid lineage range from filaments organized into hexagonal arrays (Lingulamoeba, Platyamoeba) to pentagonal glycostyles (Clydonella, Vannella). Vannellid lineage members of the genera Clydonella and Lingulamoeba were studied at the level of electron microscopy. Unique cell surface features validate these as genera distinct from Vannella and Platyamoeba. Genetic and ultrastructural data are used to discuss the phylogenetic interrelationships for the taxa studied.


Assuntos
Genes de Protozoários , Genes de RNAr , Lobosea/classificação , Animais , DNA de Protozoário/genética , DNA de Protozoário/isolamento & purificação , DNA Ribossômico/genética , Lobosea/citologia , Lobosea/genética , Lobosea/ultraestrutura , Locomoção , Microscopia Eletrônica , Filogenia , RNA de Protozoário/genética , RNA Ribossômico/genética , Alinhamento de Sequência , Análise de Sequência de DNA , Especificidade da Espécie
15.
AIDS Res Hum Retroviruses ; 19(3): 235-43, 2003 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-12689416

RESUMO

Semen HIV is separate and distinct from blood HIV and work has revealed that seminal plasma HIV particles do not arise from infected cells in semen. These findings indicate that semen-producing organs contain multiple, separate populations of HIV host cells. To test this hypothesis, we have examined leukocytes in semen-producing organs of male mice. Cells expressing F4/80 (tissue-specific macrophage marker) were abundant in testicular interstitium and as dendritic-like cells in the lumenal epithelium of the epididymis, especially the initial segment. Cells expressing CD45 (panleukocyte marker) were found rarely in the testicular interstitium, commonly in epididymal epithelium, were most abundant in the interstitium of the epididymis, and were more readily released from minced tissues than were F4/80(+) cells. Unlike the testis and epididymis, F4/80(+) cells in seminal vesicles also appeared to be CD45(+). Seminal vesicle leukocytes were restricted to the epithelium surrounding the lumen and were not released by mincing. CD11b (monocyte/B cell marker) was detected in testicular and seminal vesicle interstitium, but not in the epididymis. Hemicastration and vasectomy caused a limited redistribution of the leukocytes. These findings confirm the existence of tissue-specific populations of leukocytes in semen-producing organs and indicate that some populations are highly tissue adherent. The regionalized, tissue-adherent macrophages in the testicular interstitium, the initial segment of the caput epididymis, and the seminal vesicle epithelium suggest the existence of reservoirs of HIV-infected cells in humans that could contribute virus particles, but not infected cells, to semen and possibly blood.


Assuntos
Soropositividade para HIV/transmissão , Leucócitos Mononucleares/fisiologia , Camundongos/cirurgia , Orquiectomia , Animais , Biomarcadores , Epididimo/imunologia , HIV-1/isolamento & purificação , Leucócitos Mononucleares/virologia , Masculino , Sêmen/metabolismo , Sêmen/virologia , Glândulas Seminais , Vasectomia
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