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Pengembangan Vaksin Inaktif Tetelo Genotipe VII Isolat Lokal pada Kondisi Laboratorium. (DEVELOPMENT OF TETELO INACTIVATED VACCINE GENOTYPE VII LOCAL ISOLATE IN LABORATORY CONDITION) Risa Indriani; Ni Luh Putu Indi Dharmayanti
Jurnal Veteriner Vol 17 No 3 (2016)
Publisher : Faculty of Veterinary Medicine, Udayana University and Published in collaboration with the Indonesia Veterinarian Association

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Abstract

Tetelo/Newcastle disease (ND) inactive vaccine of genotipe VII virus local isolate have been developedin laboratory condition and compared with commercial ND vaccine. A total of 200 commercial layer chickenat 4 weeks age were divided into four groups, that were (1) vaccinated with ND genotype VII Indonesia/GTT/11, (2) vaccinated with commercial ND vaccine genotype VII, (3) vaccinated with commercial genotypeVI and (4) unvaccinated as control group. After two weeks post vaccination, 10 chicken from each groupwere sellected randomly and challenged with 105 EID50 per 0,1 mL of ND virus genotype VII Indonesian/GTT/11 by intramuscular. Chicken were observed, and swab were collected from oropharyngeal and cloacaat 2, 5, 7, 12 and 14 days post challenge. The result of this study showed inactived vaccine genotype VIIIndonesia/GTT/11 can induced a good antibody titer response to vaccinated chicken with mean titer 7.30log2 and CI 6.3 to 7.8, while commercial ND vaccine genotipe VII was 5.30 log2 with CI 3.8-6.7, andcommercial genotype VI was 4.8 log2 with CI 4.1-5.4. The level of protection which determined by noclinical signs, mortality and viral shedding showed 100% protection in chicken vaccinated with Indonesia/GTT/11 and commercial genotype VII were 100%, compared with control chicken, and vaccined commercialND vaccine genotype VII, compared with control chicken. While in chicken vaccinated commercial NDvaccine genotype VI showed viral shedding on day two post challenge, but there were no clinical sign andmortality. Based on this results, Indonesia/GTT/11 genotype VII ND vaccine could be used as an alternativeND vaccine to protect chicken from infection of ND virus genotype VII in the field.
Sirkulasi Virus Flu Burung Subtipe H5 pada Unggas di Jawa Barat, Banten, dan Jawa Timur Sepanjang Tahun 2008-2009 (CIRCULATION OF AVIAN INFLUENZA OF H5 SUBTYPE ON BIRDS IN WEST JAVA, BANTEN AND EAST JAVA DURING 2008-2009) Dyah Ayu Hewajuli; Ni Luh Putu Indi Dharmayanti
Jurnal Veteriner Vol 13 No 3 (2012)
Publisher : Faculty of Veterinary Medicine, Udayana University and Published in collaboration with the Indonesia Veterinarian Association

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Abstract

The epidemic of avian influenza (AI) in Indonesia initially occurred at the end of 2003 which caused100% death of the affected chickens. It was caused by avian influenza virus (AIV) subtype H5. Recent datashowed that highly pathogenic avian influenza (HPAI)-H5N1 virus is still endemic among bird populationin Indonesia. A study was therefore conducted to find out the distribution of AIV-H5N1 in several regionsin Indonesia. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the presenceof AI-H5 virus and hemagglutination inhibition (HI) test was used to detect the presence of anti-AIV-H5antibody. Results showed that anti-AIV-H5 antibody was detected in 36 % and was not detected in 64% oftested birds in West Java, Banten and East Java. The AIV-H5 antibody titer varied from low to high titer.The AIV-H5 was detected in samples from Cianjur (30%), Blitar (1.9&), Serang (12.5%) and pandeglang(17.5%). It was evident that AIV-H5 is still endemic in Indonesia.
Identifikasi Flu Burung H5N1 pada Unggas di Sekitar Kasus Flu Burung pada Manusia Tahun 2011 di Bekasi (AVIAN INFLUENZA H5N1 IDENTIFICATION IN AVIAN SPECIES SURROUNDING AVIAN INFLUENZA H5N1 HUMAN CASES IN BEKASI, WEST JAVA, 2011) Dyah Ayu Hewajuli; Ni Luh Putu Indi Dharmayanti
Jurnal Veteriner Vol 15 No 1 (2014)
Publisher : Faculty of Veterinary Medicine, Udayana University and Published in collaboration with the Indonesia Veterinarian Association

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Abstract

H5N1 subtype Avian Influenza (AI) virus is the causal agent  of AI disease in humans. In Indonesia,the first human AI occurred in Tangerang 2005.  Human AI in Indonesia has now spread into 12 provinces,including West Java, Jakarta, Banten, North Sumatra, East Java, Central Java, Lampung, South Sulawesi,West Sumatra, South Sumatra, Riau, and Bali. Until 2011, the total human AI cases were 182 cases  with150 deaths. This study was conducted to identify of H5N1 AI virus in birds in area surrounding a humanAI human case  in Bekasi city  in March 2011 and to investigate its role in the spread of AI to humans usingmethods of Hemaglutination Inhibition (HI ), and Reverse Transcriptase-Polymerase Chain Reaction(RT-PCR). The result showed that 80% of birds in the area surrounding AI  surrounding H5N1 AI humancase in Bekasi 2011 were antibody negative  against  H5N1-AI virus. Antibody against H5N1-AI viruswith the titer less than 4 log 2 was detected in 4.4%  of birds and  with antibody titer 04 4-7 log 2 in 15%of birds. By RT-PCR, H5N1 AI virus was not detected in 47.6% of bird samples. H5 positive and N1negative  AI virus was detected in  30.2% samples.  Only 11.2% samples showed positive for H5N1 AI virus.The results suggest that H5N1-AI virus affecting birds may have a positive role in transmitting to thevirus to human in Bekasi 2011.
Amantadine Resistant of Indonesian H5N1 Subtype Influenza Viruses During 2003-2008 NI LUH PUTU INDI DHARMAYANTI; FERA IBRAHIM; AMIN SOEBANDRIO
Microbiology Indonesia Vol. 4 No. 1 (2010): April 2010
Publisher : Indonesian Society for microbiology

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1101.851 KB) | DOI: 10.5454/mi.4.1.3

Abstract

The M2 protein of 146 avian influenza (AI) viruses data available in public database (NCBI), including 20 AI isolates used in this study, were sequenced at the M2 protein to find out the probability of mutation and the increase of resistance to amantadine after more than 5 years of their circulation in Indonesia. The results showed that during 2003-2008, around 62.58% (92/147) AI viruses in Indonesia have showed resistance to amantadine and 10 of them have dual mutations at V27A and S31N.
Molecular Analysis of H5N1 Avian Influenza Virus from Avian Species: Compared with Genbank Data of the Indonesian H5N1 Human Cases NI LUH PUTU INDI DHARMAYANTI
Microbiology Indonesia Vol. 3 No. 2 (2009): August 2009
Publisher : Indonesian Society for microbiology

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (3921.193 KB) | DOI: 10.5454/mi.3.2.6

Abstract

In Indonesia, the H5N1 avian influenza (AI) disease has been circulating for more than five years and has infected various types of avian species and human beings. Generally, avian influenza cases in human beings are suspected to be spread by chicken, birds or waterfowl previously infected by avian influenza. The data supporting this assumption were very limited, therefore the molecular characterization on four avian influenza genome segments such as hemagglutinin, neuraminidase, matrix and non structural that was isolated from the avian species surrounding the avian influenza cases in human was conducted. The analysis was conducted on these genes which were responsible for binding receptors, the pathogenicities, and the resistance to antiviral drugs, thus the virus changes can be detected by comparing the sequence data of GenBank from human cases related to the avian species. The four avian influenza viruses used in this study isolated from avian influenza cases surrounding the avian influenza cases in human in 2007. The results of genetic analysis showed that these four viruses and the available sequence data from the GenBank for of avian influenza virus in human and avian have the receptor a-2,3 of sialic acid which is the avian receptor. The A/Ck/West Java/Bks2/2007 virus is collected from the chicken surrounding the avian influenza cases in human that resembles the data of avian influenza virus from human, A/Indonesia/CDC1031/2007 from GenBank. The viruses conferred similarities amino acid sequence of hemagglutinin, neuraminidase, matrix and non structural protein. All viruses used have deletion at the position 80-84 of the NS1 protein and possessed the ESEV motif which may contribute to an increased virulence. The avian influenzaviruses examined in this study also show resistance to amantadine