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Suda Louisirirotchanakul, Pornparn Rojanasang, Kleophant Thakerngpol, Naree Choosrichom, Kridsda Chaichoune, Phisanu Pooruk, Aphinya Namsai, Robert Webster and Pilaipan Puthavathana

Abstract

Background: An outbreak of highly pathogenic avian influenza (HPAI) H5N1 virus in Thailand was first reported in 2004. To date, electron micrographs demonstrating the morphology of HPAI H5N1 virus particle are quite limited.

Objective: To demonstrate the morphology of HPAI H5N1 virus particles, avian influenza viruses with low pathogenicity, seasonal influenza viruses, and H5N1 structural components in infected cells. The M amino acid residues that might affect the viral morphology were also analyzed.

Methods: Electron micrographs of negatively-stained virus particles and positively-stained thin sections of the HPAI H5N1 virus infected cells were visualized under a transmission electron microscope. M amino acid sequences of the study viruses were retrieved from the GenBank database and aligned with those of reference strains with known morphology and residues that are unique for the morphological type of the virus particles.

Results: Morphologically, three forms of influenza virus particles, spherical, regular, and irregular rods, and long filamentous particles, were demonstrated. However, the spherical form was the most predominant morphological type and accounted for more than 80% of the virus populations examined. In addition, the viral entry and exit steps including incomplete particles in infected Madin-Darby canine kidney cells were visualized. Our analyses did not find any M amino acid residues that might influence the viral morphology.

Conclusion: Of all virus isolates studied, we demonstrated that the spherical particles were the major population observed regardless of virus subtype, host of origin, virus virulence, or passage history. Our study suggested that the morphology of influenza virus particles released, might not be strongly influenced by M gene polymorphism.

Open access

Magdalena Fidecka-Skwarzynska, Marek Juda, Lucyna Maziarczyk and Anna Malm

References 1. Alberici I. et al.: Pathogens causing urinary tract infections in infants: A European overview by the ESCAPE study group. Eur. J. Pediatr., 2014. 2. Bien J. et al.: Role of uropathogenic Escherichia coli virulence factors in development of urinary tract infection and kidney damage. Int. J. Nephrol., 2012, Article ID 681473, 2012. doi: 10.1155/2012/681473 3. Firoozeh F. et al.: Detection of virulence genes in Escherichia coli isolated from patients with cystitis and pyelonephritis. Int. J. Infect

Open access

Zhong-ying Bao, Xiao Ming, Xiao-dong Yuan and Shu-hong Duan

References 1. Huang YL. Clinical Infectious Diseases. Beijing: People’s Medical Publishing House, 1990:246-253. 2. Peng WW. Epidemiology fifth edition. Beijing: People’s Health Publishing House, 2002:156-157. 3. Harris JB, LaRocque RC, Qadri F, Ryan ET, Calderwood SB. Cholera. Lancet 2012;379(9835):2466-2476. 4. Jiang LJ, Wang R, Qiao Y, Wang BR. O1 group O139 and non-O1 Vibrio cholerae virulence comparative study. Adv Microbial Immunol 1995; 23:1-11. 5. Duan YQ, Yang B, Cui JD

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Mongkol Pongsuchart, Amornpun Sereemaspun and Kiat Ruxrungtham

detection of infectious spleen and kidney necrosis virus by loop-mediated isothermal amplification combined with a lateral flow dipstick. Archives of Virology. 2010; 155:385-9. 7. Odenthal KJ, Gooding JJ. An introduction to electrochemical DNAbiosensors. Analyst. 2007; 132: 603-10. 8. Noguera P, Posthuma-Trumpie G, van Tuil M, van der Wal F, de Boer A, Moers A, et al. Carbon nanoparticles in lateral flow methods to detect genes encoding virulence factors of Shiga toxin-producing Escherichia coli. Analytical and Bioanalytical Chemistry. 2011

Open access

Andika C. Putra, Keiji Tanimoto, Elisna Syahruddin, Sita Andarini, Yoshio Hosoi and Keiko Hiyama

. Novel CFTR mutations in a Korean infant with cystic fibrosis and pancreatic insufficiency. J Korean Med Sci. 2010; 25:163-5. 6. Collins F. Genetics terminology for respiratory physicians. Paediatr Respir Rev. 2009; 10:124-33. 7. Fu J, Festen EA, Wijmenga C. Multi-ethnic studies in complex traits. Hum Mol Genet. 2011; 20:R206-13. 8. Ober C, Hoffjan S. Asthma genetics 2006: the long and winding road to gene discovery. Genes Immun. 2006; 7:95-100. 9. Moffatt MF, Kabesch M, Liang L, Dixon AL, Strachan D

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Warisa Amornrit, Veerachat Muangsombut, Tanapol Wangteeraprasert and Sunee Korbsrisate

expression in Caco-2 human intestinal cells. J Nutr. 2001; 131:1452-8. 8. Bullen JJ, Ward CG, Wallis SN. Virulence and the role of iron in Pseudomonas aeruginosa infection. Infect Immun. 1974; 10:443-50. 9. Wuthiekanun V, Smith MD, Dance DA, White NJ. Isolation of Pseudomonas pseudomallei from soil in north-eastern Thailand. Trans R Soc Trop Med Hyg. 1995; 89:41-3. 10. Schaible UE, Kaufmann SH. Iron and microbial infection. Nat Rev Microbiol. 2004; 2:946-53. 11. Loprasert S, Sallabhan R, Whangsuk W, Mongkolsuk

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Wichit Thaveekarn, Sunchai Payungporn, Narumol Pakmanee, Sunutcha Suntrarachun, Suchitra Khunsap and Suthidee Petsong

PE-PGRS family protein. PE-PGRS is a large family of typical proteins of pathogenic mycobacteria whose members are characterized by an N-terminal PE domain followed by a large Gly-Ala repeat-rich C-terminal domain [ 18 ]. The genes of the PE-PGRS family proteins are most often clustered in a region of the genome, often as overlapping genes. The proline- glutamic acid (PE) domain is responsible for the cellular localization of these proteins on bacterial cells [ 19 ]. The hypothetical proteins found 3 positions shown in Table 1 might be involved in virulence

Open access

Mayyada F. Darweesh

.: Comparison of biochemical tests, Api system, Vitek 2 system and PCR of the enteropathogenic bacteria isolated from children with persistent diarrhea. And the occurrence of virulence factors and antibiotic resistance in the isolates. Master Thesis. Faculty of Science, University of Kufa 2014. 5. Al-Hissnawy, D.; AL-Thahab, A.A.; Al-Jubori,S.A.: Evaluation of Citrobacter freundii isolated in Najaf governorate as an enterotoxin producer. Medical J. Babylon. 9(1): 1-5, 2012. 6. Tuwaij, N.S.: Molecular Study of Quinolone Resistance in Klebsiella

Open access

Jin Zhang

.1016/j.molimm.2015.01.009 Golshani M. Rafati S. Dashti A. Gholami E. Siadat S.D. Oloomi M. Vaccination with recombinant L7/L12-truncated Omp31 protein induces protection against Brucella infection in BALB/c mice Mol. Immunol. 2015 65 2 287 292 [2] Tian M., Qu J., Bao Y., Gao J., Liu J., Wang S., et al., Construction of pTM series plasmids for gene expression in Brucella species, J. Microbiol. Methods, 2016, 123, 18-23. Tian M. Qu J. Bao Y. Gao J. Liu J. Wang S. Construction of pTM series plasmids for gene expression in Brucella species J. Microbiol. Methods

Open access

Yuan Liu

References 1 Jiang J, Duo L. Study on the Correlation between Psoriasis Vulgaris and HLADRB1*07 allele in Xinjiang Uygur Autonomous Region. Journal of Medical Postgraduates, 2012, 25 (1): 54-57. 2 Hort W, Mayser P. Malassezia virulence determinants. Curr Opin Infect Dis, 2011, 24(2): 100-105. 3 Rup E, Skora M, Krzysciak P, et al . Distribution of Malassezia species in patients with psoriasis-quality assessment. Postep Dermatol Alergol, 2010, 27(4): 264-268. 4 Gaitanis G, Magiatia P, Hantschke M, et al . The Malassezia genus in skin