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1.
Virusdisease ; 34(1): 92-96, 2023 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-37009259

RESUMEN

To eliminate the rubella virus (RV), genetic characterization is vital for its detection, identification of endemic transmission, and diagnosis of imported cases. The 739-nucleotide region in the E1 gene has primarily been used for genotyping for epidemiological analysis. However, in the 2018-2019 RV outbreak, identical sequences were observed in patients who were not epidemiologically linked. Additionally, the 739 nt sequences from the outbreak in Tokyo in 2018-2019 were identical to RV identified in China in 2019. This suggests that this region may be insufficient to identify the detected RV strains as endemic or imported. In 62.4% of the specimens, the E1 gene sequences of the 1E RV genotype were identical. Additionally, the observed discordance of sequences from the mainly detected identical sequence in the 739-nt sequence of the E1 gene were one (31.0%), two (3.5%), three (2.6%), and four (0.23%). Moreover, a comparison of the complete structural protein-coding region suggests that the E2 gene is more diverse than the E1 and the capsid gene. Thus, conventional polymerase chain reaction (PCR) primers were developed to detect the E2 gene and improve epidemiological analysis. A comparison of the sequences identified during the RV outbreak in Tokyo revealed genetic differences in the sequences (15 of the 18 specimens). These results suggest that additional information could be obtained by simultaneously analyzing the E2 and the E1 region. The identified sequences can potentially aid in evaluating the RV strains detected during epidemiological analysis.

2.
Jpn J Infect Dis ; 76(4): 259-262, 2023 Jul 24.
Artículo en Inglés | MEDLINE | ID: mdl-37005274

RESUMEN

Mpox, caused by the mpox virus (MPXV), produces symptoms similar to those of smallpox when transmitted to humans. Since 1970, this disease has been endemic, particularly in Africa. However, since May 2022, the number of patients without a history of travel to endemic areas has increased rapidly globally. Under these circumstances, in July 2022, two different real-time PCR methods were used on specimens brought to the Tokyo Metropolitan Institute of Public Health. MPXV was detected in the skin samples, and it was inferred that the virus was a West African strain. Furthermore, a more detailed analysis of the genetic characteristics of the detected MPXV using next-generation sequencing revealed that the MPXV detected in Tokyo was strain B.1, which corresponds to the same strain that is prevalent in Europe and the USA. This suggests that mpox reported for the first time in Japan was imported and related to outbreaks in Europe and the USA. Therefore, it is necessary to continue monitoring outbreaks in Japan in conjunction with global epidemics.


Asunto(s)
Epidemias , Mpox , Humanos , Japón/epidemiología , Tokio/epidemiología , Brotes de Enfermedades
3.
Jpn J Infect Dis ; 76(1): 87-90, 2023 Jan 24.
Artículo en Inglés | MEDLINE | ID: mdl-36184395

RESUMEN

During the COVID-19 pandemic in 2021, Japan experienced an outbreak of respiratory syncytial virus (RSV) infection. A total of 51 RSV cases were detected in infant specimens, including 38 rhinorrhea and 13 nasopharyngeal swabs, collected at the Tokyo Metropolitan Institute of Public Health. Of the 51 cases, 12 were RSV-A and 39 were RSV-B. The G protein gene sequence of RSV-A belonged to the ON1 genotype, whereas RSV-B belonged to the BA9 genotype; thus, different types of RSV were detected during the same period, suggesting that the unusual 2021 RSV season was not due to a single strain or genotype. Of all RSV-positive cases, the proportion of patients aged ≥2 years was 56.8% in 2021, higher than the 31.2% reported in the past 5 years. This indicates that infants aged <1 year who were originally susceptible to RSV infection were less likely to be infected with RSV because of the COVID-19 control measures. The 2021 epidemic peaked in the 28th week, 9 weeks earlier than the average from 2016 to 2020. Therefore, it seems necessary to accumulate and analyze further data, such as factors that led to the outbreak and the characteristics of the detected viruses in 2021.


Asunto(s)
COVID-19 , Infecciones por Virus Sincitial Respiratorio , Virus Sincitial Respiratorio Humano , Lactante , Humanos , Japón/epidemiología , Tokio/epidemiología , Pandemias , COVID-19/epidemiología , Filogenia , Virus Sincitial Respiratorio Humano/genética , Infecciones por Virus Sincitial Respiratorio/epidemiología , Genotipo
4.
Antiviral Res ; 126: 1-7, 2016 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-26675666

RESUMEN

Although feline coronavirus (FCoV) causes feline infectious peritonitis (FIP), which is a fatal infectious disease, there are no effective therapeutic medicines or vaccines. Previously, in vitro studies have shown that cyclosporin (CsA) and FK506 inhibit virus replication in diverse coronaviruses. CsA and FK506 are targets of clinically relevant immunosuppressive drugs and bind to cellular cyclophilins (Cyps) or FK506 binding proteins (FKBPs), respectively. Both Cyp and FKBP have peptidyl-prolyl cis-trans isomerase (PPIase) activity. However, protein interacting with NIMA (Pin1), a member of the parvulin subfamily of PPIases that differs from Cyps and FKBPs, is essential for various signaling pathways. Here we demonstrated that genetic silencing or knockout of Pin1 resulted in decreased FCoV replication in vitro. Dipentamethylene thiuram monosulfide, a specific inhibitor of Pin1, inhibited FCoV replication. These data indicate that Pin1 modulates FCoV propagation.


Asunto(s)
Coronavirus Felino/enzimología , Peptidilprolil Isomerasa de Interacción con NIMA/metabolismo , Replicación Viral/fisiología , Secuencia de Aminoácidos , Animales , Gatos , Línea Celular , Coronavirus Felino/efectos de los fármacos , Coronavirus Felino/genética , Coronavirus Felino/fisiología , Ciclofilinas/efectos de los fármacos , Ciclosporina/farmacología , Replicación del ADN/efectos de los fármacos , Descubrimiento de Drogas , Peritonitis Infecciosa Felina/virología , Técnicas de Inactivación de Genes , Inmunosupresores/farmacología , Peptidilprolil Isomerasa de Interacción con NIMA/antagonistas & inhibidores , Peptidilprolil Isomerasa de Interacción con NIMA/biosíntesis , Peptidilprolil Isomerasa de Interacción con NIMA/genética , Piperidinas/farmacología , Interferencia de ARN , ARN Interferente Pequeño/genética , Proteínas de Unión a Tacrolimus/farmacología , Tiram/análogos & derivados , Tiram/farmacología , Replicación Viral/efectos de los fármacos
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