RESUMO
Distinguishing between aplastic anemia (AA) and hypoblastic myelodysplastic syndrome (hMDS) with a low percentage of bone marrow (BM) blasts (<5%) can be difficult due to the overlap in clonality and a spectrum of genetic alternations between the two subtypes of diseases. However, due to recent advances in DNA sequencing technology, both spectrum and frequency of mutations can be accurately determined and monitored by next-generation sequencing (NGS) at initial diagnosis and during immunosuppressive therapy (IST) in patients with AA or hMDS. This improvement in acquiring a patient's genetic status and clonal evolution can provide more proper, precise, and on-time information to guide disease management, which is especially helpful in the absence of traditional morphologic/cytogenetic evidence.
Assuntos
Anemia Aplástica/diagnóstico , Anemia Aplástica/genética , Leucemia/genética , Mutação/genética , Síndromes Mielodisplásicas/diagnóstico , Síndromes Mielodisplásicas/genética , Idoso , Feminino , Sequenciamento de Nucleotídeos em Larga Escala/métodos , HumanosAssuntos
Betacoronavirus , Infecções por Coronavirus/complicações , Taxa de Filtração Glomerular , Túbulos Renais Proximais/fisiopatologia , Pneumonia Viral/complicações , Adulto , Idoso , Idoso de 80 Anos ou mais , COVID-19 , Feminino , Glicosúria/epidemiologia , Hospitalização , Humanos , Hiponatremia/epidemiologia , Masculino , Pessoa de Meia-Idade , Pandemias , Estudos Retrospectivos , SARS-CoV-2RESUMO
Recently, a novel bunyavirus, severe fever with thrombocytopenia syndrome virus (SFTSV), was isolated in central China. The virus can cause multi-clinical symptoms: severe fever, thrombocytopenia, leukocytopenia, with a mortality rate of ~10%. Several studies show that SFTSV could undergo rapid evolution via gene mutation and homologous recombination. However, as an important evolutionary force for segmented-genome viruses, reassortment has not been reported in SFTSV. In this study, we identified two SFTSV strains of which the S segment has different origin from M and L, suggesting that reassortment might be potential force driving rapid change of SFTSV. This result might shed new light on the evolutionary behavior of the novel virus.