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1.
Jpn J Infect Dis ; 76(2): 151-154, 2023 Mar 24.
Artigo em Inglês | MEDLINE | ID: mdl-36450570

RESUMO

Japanese encephalitis virus (JEV) is a mosquito-borne virus belonging to the JEV serocomplex within the genus Flavivirus, family Flaviviridae. It has 5 genotypes, G1-G5, based on the envelope (E) protein nucleotide sequence. JEV G3 circulated in Japan until the early 1990s when it was replaced by G1. JEV G3 was isolated from swine serum samples (sw/Kochi/1/2004) in the Kochi Prefecture, western Japan, in 2004. In addition, the 2018 isolates from pigs and cows (sw/Kochi/492/2018 and bo/Kochi/211/2018) in the same prefecture were identified as G3. The nucleotide sequencing results of the sw/Kochi/492/2018 and bo/Kochi/211/2018 polyprotein region differed from those of the sw/Kochi/1/2004 strain described in our previous report. Seven JEV isolates were identified as G1 in the same geographical area as that in this study. This result indicates that both JEV G1 and G3 are present in the Kochi area.


Assuntos
Vírus da Encefalite Japonesa (Espécie) , Encefalite Japonesa , Doenças dos Suínos , Feminino , Animais , Suínos , Bovinos , Encefalite Japonesa/epidemiologia , Encefalite Japonesa/veterinária , Japão/epidemiologia , Genótipo , Doenças dos Suínos/epidemiologia , Filogenia
2.
J Infect Dis ; 217(10): 1601-1611, 2018 04 23.
Artigo em Inglês | MEDLINE | ID: mdl-29409030

RESUMO

Background: Merkel cell polyomavirus (MCPyV) is a ubiquitous cutaneous virus that causes Merkel cell carcinoma, which develops preferentially in white populations from Europe and North America. However, the genomic variations of MCPyV among ethnic groups have not been well delineated, and even less is known regarding alterations in the noncoding control region (NCCR) in the general population. Methods: MCPyV strains recovered from skin swab specimens from 250 healthy participants with distinct ethnicities and geographic origins were subjected to sequencing analysis of the NCCR. Results: A 25-base pair tandem repeat caused by a 25-base pair insertion within the NCCR was found predominantly in Japanese and East Asian individuals. Based on the presence of 2 other insertions and a deletion, the NCCR could be classified further into 5 genotypes. This tandem repeat was also found exclusively in the NCCR from Japanese patients with Merkel cell carcinoma, while other genotypes were detected in white patients from Europe and North America. Conclusions: Our results suggest that the MCPyV NCCR varies according to ethnicity and that assessing the short NCCR sequence provides a rapid and simple means for identification of the Japanese and East Asian variant genotype. It remains to be established whether these NCCR variations are associated differentially with the pathogenesis of MCPyV-driven Merkel cell carcinoma between regions with varying endemicity.


Assuntos
Variação Genética/genética , Poliomavírus das Células de Merkel/genética , Infecções por Polyomavirus/virologia , Pele/virologia , Idoso , Povo Asiático/genética , Carcinoma de Célula de Merkel/virologia , DNA Viral/genética , Europa (Continente) , Feminino , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , América do Norte , Filogenia , Neoplasias Cutâneas/virologia , Infecções Tumorais por Vírus/virologia
3.
J Gen Virol ; 96(Pt 2): 288-293, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25351518

RESUMO

The dengue virus (DENV) envelope protein domain 3 (ED3) is the target of potent virus neutralizing antibodies. The DENV-2 ED3 contains adjacent type-specific and DENV complex-reactive antigenic sites that are composed of a small number of residues that were previously demonstrated to be critical for antibody binding. Site-directed mutagenesis of a DENV-2 16681 infectious clone was used to mutate critical residues in the DENV-2 type-specific (K305A and P384A) and DENV complex-reactive (K310A) antigenic sites. The K305A mutant virus multiplied like the parent virus in mosquito and mammalian cells, as did the P384A mutant virus, which required a compensatory mutation (G330D) for viability. However, the K310A mutant virus could not be recovered. The DENV-2 type-specific critical residue mutations K305A and P384A+G330D reduced the ability of DENV-2 type-specific, but not DENV complex-reactive, mAbs to neutralize virus infectivity and this was directly correlated with mAb binding affinity to the rED3 mutants.


Assuntos
Vírus da Dengue/imunologia , Epitopos/imunologia , Proteínas do Envelope Viral/imunologia , Anticorpos Neutralizantes/imunologia , Anticorpos Antivirais/imunologia , Análise Mutacional de DNA , Vírus da Dengue/genética , Epitopos/genética , Viabilidade Microbiana , Modelos Moleculares , Mutagênese Sítio-Dirigida , Conformação Proteica , Proteínas do Envelope Viral/genética , Replicação Viral
4.
J Gen Virol ; 91(Pt 9): 2249-53, 2010 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-20444995

RESUMO

Dengue virus (DENV) is a mosquito-borne disease caused by four genetically and serologically related viruses termed DENV-1, -2, -3 and -4. The DENV envelope (E) protein ectodomain can be divided into three structural domains designated ED1, ED2 and ED3. The ED3 domain contains DENV type-specific and DENV complex-reactive antigenic sites. To date, nearly all antigenic studies on the E protein have focused on DENV-2. In this study, the epitope recognized by a DENV-3 type-specific monoclonal antibody (mAb 14A4-8) was mapped to the DENV-3 ED3 domain using a combination of physical and biological techniques. Epitope mapping revealed that amino acid residues V305, L306, K308, E309, V310, K325, A329, G381 and I387 were critical for the binding of mAb 14A4-8 and amino acid residues T303, K307, K386, W389 and R391 were peripheral residues for this epitope. The location of the mAb 14A4-8 epitope overlaps with the DENV complex-reactive antigenic site in the DENV-3 ED3 domain.


Assuntos
Antígenos Virais/química , Vírus da Dengue/imunologia , Proteínas do Envelope Viral/imunologia , Substituição de Aminoácidos , Animais , Anticorpos Monoclonais , Anticorpos Antivirais , Afinidade de Anticorpos , Reações Antígeno-Anticorpo , Antígenos Virais/genética , Sítios de Ligação/genética , Linhagem Celular , Vírus da Dengue/genética , Mapeamento de Epitopos , Epitopos/química , Epitopos/genética , Modelos Moleculares , Estrutura Terciária de Proteína , Proteínas do Envelope Viral/química , Proteínas do Envelope Viral/genética
5.
Virology ; 384(1): 16-20, 2009 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-19101005

RESUMO

The disease dengue (DEN) is caused by four genetically and serologically related viruses termed DENV-1, -2, -3, and -4. The DENV envelope (E) protein ectodomain can be divided into three structural domains designated ED1, ED2, and ED3. The ED3 contains the DENV type-specific and DENV complex-reactive (epitopes shared by DENV 1-4) antigenic sites. In this study the epitopes recognized by four DENV complex-reactive monoclonal antibodies (MAbs) with neutralizing activity were mapped on the DENV-3 ED3 using a combination of physical and biological techniques. Amino acid residues L306, K308, G381, I387, and W389 were critical for all four MAbs, with residues V305, E309, V310, K325, D382, A384, K386, and R391 being critical for various subsets of the MAbs. A previous study by our group (Gromowski, G.D., Barrett, N.D., Barrett, A.D., 2008. Characterization of dengue complex-specific neutralizing epitopes on the envelope protein domain III of dengue 2 virus. J. Virol 82, 8828-8837) characterized the same panel of MAbs with DENV-2. The location of the DENV complex-reactive antigenic site on the DENV-2 and DENV-3 ED3s is similar; however, the critical residues for binding are not identical. Overall, this indicates that the DENV complex-reactive antigenic site on ED3 may be similar in location, but the surprising result is that DENV 2 and 3 exhibit unique sets of residues defining the energetics of interaction to the same panel of MAbs. These results imply that the amino acid sequences of DENV define a unique interaction network among these residues in spite of the fact that all flavivirus ED3s to date assume the same structural fold.


Assuntos
Vírus da Dengue/genética , Proteínas do Envelope Viral/genética , Proteínas do Envelope Viral/imunologia , Substituição de Aminoácidos , Animais , Anticorpos Monoclonais , Antígenos Virais/imunologia , Culicidae/virologia , Dengue/genética , Dengue/transmissão , Vírus da Dengue/classificação , Vírus da Dengue/imunologia , Epitopos/genética , Epitopos/imunologia , Genoma Viral , Humanos , Modelos Moleculares , Mutagênese Sítio-Dirigida , Fases de Leitura Aberta , Conformação Proteica , Proteínas do Envelope Viral/química , Proteínas Virais/genética
6.
J Med Virol ; 80(6): 997-1003, 2008 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-18428122

RESUMO

A total of 189 conjunctival scrapings were collected from patients in Tokyo, Japan by monitoring adenovirus infection in community-based clinics during 2005 and 2006. Of the 189 samples, 155 (82%) had adenoviruses detected by polymerase chain reaction (PCR). The serotypes were determined by PCR-restriction fragment length polymorphism (PCR-RFLP) analysis, using a combination of endonucleases, such as HhaI, AluI, and HaeIII, and neutralization tests (NTs). PCR-RFLP identified five serotypes: serotype 3: 16.8%, serotype 4: 9.7%, serotype 8: 34.8%, serotype 11: 23.2%, and serotype 37: 15.5%. Adenovirus 8 was the most common serotype identified. A subset consisting of 25 isolates identified as adenovirus 8 from this study plus 25 isolates from Kawasaki were analyzed using PCR sequencing of the hexon gene. Compared with prototype adenovirus serotype 8 and serotype 9 derived in Tokyo and Kawasaki, these isolates shared 61.7-62.8% and 80.5-82.7% amino acid homology, respectively, suggesting that a variant adenovirus serotype 8 was involved in this outbreak, and is different from the prototype adenovirus 8 virus. This variant had not been detected in Japan prior to 1996 and appears to be the most common adenovirus type 8 involved in cases of epidemic keratoconjunctivitis in Japan at present.


Assuntos
Infecções por Adenoviridae/virologia , Adenoviridae/genética , Adenoviridae/isolamento & purificação , Túnica Conjuntiva/virologia , Conjuntivite Viral/virologia , Adenoviridae/classificação , Infecções por Adenoviridae/epidemiologia , Adolescente , Adulto , Idoso , Sequência de Aminoácidos , Sequência de Bases , Proteínas do Capsídeo/química , Proteínas do Capsídeo/genética , Criança , Pré-Escolar , Conjuntivite Viral/epidemiologia , DNA Viral/análise , DNA Viral/genética , Genes Virais/genética , Humanos , Japão/epidemiologia , Pessoa de Meia-Idade , Dados de Sequência Molecular , Alinhamento de Sequência , Análise de Sequência de DNA
7.
J Med Virol ; 79(2): 200-5, 2007 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-17177307

RESUMO

Over a 2-year period between 2001 and 2003, a total of 115 conjunctival scrapings were collected from patients with keratoconjuctivitis from several hospitals in Yokohama, Japan. Out of 115, 94 (82.4%) cases of adenoviruses were detected by polymerase chain reaction (PCR); 60 (52.1%) by cell culture isolation; and 16 (14.0%) by enzyme-linked immunosorbent assay (ELISA). The serotypes were determined by PCR- restriction fragment length polymorphism analysis (PCR-RFLP) and by the neutralization test (NT). PCR-RFLP was performed using a combination of endonucleases such as HhaI, AluI, and HaeIII. Of the 94 PCR-positive samples, the serotypes of 91 (96.8%) were identified by PCR-RFLP analysis (adenovirus 3: 50%, 4: 11%, and 8: 32%). Out of the 115 samples, 60 samples were identified by the neutralization (adenovirus 3, 4, 7, and 8). When both PCR-RFLP and the neutralization techniques were used, 53.2%, 11.7%, 1.1%, and 34% of the samples were identified as adenovirus 3, 4, 7, and 8, respectively. In contrast to the results of a nationwide surveillance report, adenovirus 3 was found as a major cause of keratoconjunctivitis in the Yokohama area. The nationwide surveillance report did not reflect accurately the epidemiological situation in the local area. In order to obtain surveillance data that would be useful for the prevention of an adenovirus conjunctivitis epidemic, it seems that local epidemiology is more important than that nationwide surveillance.


Assuntos
Adenovírus Humanos/classificação , Adenovírus Humanos/isolamento & purificação , Túnica Conjuntiva/virologia , Conjuntivite Viral/epidemiologia , Conjuntivite Viral/virologia , Manejo de Espécimes/métodos , Infecções por Adenovirus Humanos/epidemiologia , Infecções por Adenovirus Humanos/virologia , Adenovírus Humanos/genética , DNA Viral/análise , DNA Viral/isolamento & purificação , Ensaio de Imunoadsorção Enzimática , Células HeLa , Humanos , Japão/epidemiologia , Ceratoconjuntivite/epidemiologia , Ceratoconjuntivite/virologia , Testes de Neutralização , Reação em Cadeia da Polimerase , Polimorfismo de Fragmento de Restrição , Sorotipagem , Cultura de Vírus
8.
Virology ; 354(1): 48-57, 2006 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-16945400

RESUMO

We evaluated the immunogenicity and protective activity of plasmid DNA vaccines encoding the influenza virus NP gene (pNP) alone or in combination with the herpes simplex virus type 1 protein 22 gene (pVP22). Optimal immune responses were observed in BALB/c mice immunized with the combination of pVP22 plus pNP, as assessed by enzyme-linked immunosorbent assay (ELISA), enzyme-linked immunospot (ELISPOT) and intracellular cytokine staining (ICCS). These mice also showed maximal resistance following challenge with the A/PR/8/34 (H1N1) and A/Udron/72 (H3N2) strains of influenza virus. The susceptibility of immunized mice to virus infection was significantly increased following depletion of either CD4+ or CD8+ T cells. These results indicate that a plasmid DNA vaccine encoding pVP22 plus NP induces a high level of cross-protective immunity against influenza virus subtypes.


Assuntos
Vírus da Influenza A/imunologia , Vacinas contra Influenza/imunologia , Influenza Humana/prevenção & controle , Nucleoproteínas/imunologia , Proteínas de Ligação a RNA/imunologia , Vacinas de DNA/imunologia , Proteínas do Core Viral/imunologia , Proteínas Estruturais Virais/imunologia , Animais , Anticorpos Antivirais/sangue , Fusão Gênica Artificial , Peso Corporal , Citocinas/biossíntese , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Vetores Genéticos , Humanos , Vacinas contra Influenza/genética , Influenza Humana/imunologia , Depleção Linfocítica , Subpopulações de Linfócitos/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Proteínas do Nucleocapsídeo , Nucleoproteínas/genética , Plasmídeos/genética , Proteínas de Ligação a RNA/genética , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/imunologia , Linfócitos T/imunologia , Vacinas de DNA/genética , Proteínas do Core Viral/genética , Proteínas Estruturais Virais/genética
9.
J Virol ; 80(13): 6218-24, 2006 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-16775309

RESUMO

Toll-like receptors (TLRs) recognize microbial components and trigger the signaling cascade that activates the innate and adaptive immunity. TLR adaptor molecules play a central role in this cascade; thus, we hypothesized that overexpression of TLR adaptor molecules could mimic infection without any microbial components. Dual-promoter plasmids that carry an antigen and a TLR adaptor molecule such as the Toll-interleukin-1 receptor domain-containing adaptor-inducing beta interferon (TRIF) or myeloid differentiation factor 88 (MyD88) were constructed and administered to mice to determine if these molecules can act as an adjuvant. A DNA vaccine incorporated with the MyD88 genetic adjuvant enhanced antigen-specific humoral immune responses, whereas that with the TRIF genetic adjuvant enhanced cellular immune responses. Incorporating the TRIF genetic adjuvant in a DNA vaccine targeting the influenza HA antigen or the tumor-associated antigen E7 conferred superior protection. These results indicate that TLR adaptor molecules can bridge innate and adaptive immunity and potentiate the effects of DNA vaccines against virus infection and tumors.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/imunologia , Proteínas Adaptadoras de Transporte Vesicular/imunologia , Adjuvantes Imunológicos , Vacinas Anticâncer/imunologia , Imunidade Inata , Vacinas contra Influenza/imunologia , Vacinas de DNA/imunologia , Proteínas Adaptadoras de Transdução de Sinal/genética , Proteínas Adaptadoras de Transporte Vesicular/genética , Adjuvantes Imunológicos/genética , Animais , Antígenos Virais/genética , Antígenos Virais/imunologia , Vacinas Anticâncer/genética , Feminino , Humanos , Imunidade Inata/genética , Imunização , Vacinas contra Influenza/genética , Influenza Humana/genética , Influenza Humana/imunologia , Influenza Humana/prevenção & controle , Camundongos , Camundongos Endogâmicos BALB C , Fator 88 de Diferenciação Mieloide , Neoplasias/genética , Neoplasias/imunologia , Neoplasias/terapia , Proteínas E7 de Papillomavirus/genética , Proteínas E7 de Papillomavirus/imunologia , Plasmídeos/genética , Plasmídeos/imunologia , Regiões Promotoras Genéticas/genética , Regiões Promotoras Genéticas/imunologia , Vacinas de DNA/genética
10.
Neurobiol Dis ; 20(2): 541-9, 2005 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-15908227

RESUMO

This work examines whether administering the F(ab' )2 fragment of an IgG1 monoclonal antibody (mAb) targeting the N-terminal 1-13 amino acids of the beta-amyloid peptide (Abeta mAb) reduces amyloid deposition in Alzheimer's disease (AD). The F(ab')2 fragment was injected intraperitoneally or intracranially into Tg2576 mice, a murine model of human AD. Both routes of administration significantly reduced Abeta plaque formation in the brain, as determined immunohistochemically and by monitoring levels of Abeta1-40 and Abeta1-42 peptide. Use of the F(ab')2 fragment significantly reduced phagocytic infiltration in the CNS when compared to intact mAb. Since IgG1 Abs do not fix complement, these findings suggest that effective in vivo clearance of amyloid deposits can be achieved without stimulation of FcR-reactive phagocytes or activation of the complement cascade.


Assuntos
Doença de Alzheimer/tratamento farmacológico , Peptídeos beta-Amiloides/antagonistas & inibidores , Anticorpos Monoclonais/farmacologia , Fragmentos Fab das Imunoglobulinas/farmacologia , Placa Amiloide/efeitos dos fármacos , Doença de Alzheimer/imunologia , Doença de Alzheimer/fisiopatologia , Peptídeos beta-Amiloides/química , Peptídeos beta-Amiloides/imunologia , Animais , Anticorpos Monoclonais/imunologia , Anticorpos Monoclonais/uso terapêutico , Encéfalo/efeitos dos fármacos , Encéfalo/imunologia , Encéfalo/fisiopatologia , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Movimento Celular/fisiologia , Proteínas do Sistema Complemento/efeitos dos fármacos , Proteínas do Sistema Complemento/imunologia , Proteínas do Sistema Complemento/metabolismo , Modelos Animais de Doenças , Encefalite/tratamento farmacológico , Encefalite/imunologia , Encefalite/prevenção & controle , Fragmentos Fab das Imunoglobulinas/imunologia , Fragmentos Fab das Imunoglobulinas/uso terapêutico , Injeções Intraperitoneais , Injeções Intraventriculares , Camundongos , Camundongos Transgênicos , Fragmentos de Peptídeos/antagonistas & inibidores , Fragmentos de Peptídeos/química , Fragmentos de Peptídeos/imunologia , Fagócitos/efeitos dos fármacos , Fagócitos/fisiologia , Placa Amiloide/imunologia , Placa Amiloide/metabolismo , Estrutura Terciária de Proteína/efeitos dos fármacos , Estrutura Terciária de Proteína/fisiologia
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