Growth Of Newcastle Disease Virus Research Articles

BotCl, the First Chlorotoxin-like Peptide Inhibiting Newcastle Disease Virus: The Emergence of a New Scorpion Venom AMPs Family.

Newcastle disease virus (NDV) is one of the most serious contagions affecting domestic poultry and other avian species. It causes high morbidity and mortality, resulting in huge economic losses to the poultry industry worldwide. Despite vaccination, NDV outbreaks increase the need for alternative prevention and control means. In this study, we have screened fractions of Buthus occitanus tunetanus (Bot) scorpion venom and isolated the first scorpion peptide inhibiting the NDV multiplication. It showed a dose dependent effect on NDV growth in vitro, with an IC50 of 0.69 µM, and a low cytotoxicity on cultured Vero cells (CC50 > 55 µM). Furthermore, tests carried out in specific pathogen-free embryonated chicken eggs demonstrated that the isolated peptide has a protective effect on chicken embryos against NDV, and reduced by 73% the virus titer in allantoic fluid. The N-terminal sequence, as well as the number of cysteine residues of the isolated peptide, showed that it belongs to the scorpion venom Chlorotoxin-like peptides family, which led us to designate it "BotCl". Interestingly, at 10 µg/mL, BotCl showed an inhibiting effect three times higher than its analogue AaCtx, from Androctonus australis (Aa) scorpion venom, on NDV development. Altogether, our results highlight the chlorotoxin-like peptides as a new scorpion venom AMPs family.

Quantitative evaluation of viral interference among Egyptian isolates of highly pathogenic avian influenza viruses (H5N1 and H5N8) with the lentogenic and velogenic Newcastle disease virus genotype VII in specific pathogen-free embryonated chicken eggs model

Background and Aim:Mixed infections of the highly pathogenic avian influenza virus (HPAIV) and Newcastle disease virus (NDV) are considered the most distressing problem of the poultry industry. The problem arises due to the influence of a hidden virus on the replication of another suspected virus. Consequently, misdiagnosis of the real cause of disease may become a source of infection for other healthy stock by transmission and dissemination of the hidden virus. This study aimed to determine the impact of HPAIV and NDV on each other in a specific pathogen-free embryonated chicken egg (SPF-ECE) model.Materials and Methods:HPAIVs (H5N1 and H5N8) and NDVs [avirulent NDV [avNDV] and velogenic NDV [vNDV]) were inoculated into the allantois cavity of SPF-ECE with graded titers (2, 3, and 4 log10 EID50) at 24 and 48 h of incubation, followed by the collection of allantoic fluid. A quantitative reverse transcription real-time polymerase chain reaction was used to determine the viral RNA copies of both viruses.Results:Obvious interference was reported on the growth of NDVs when co-inoculated with AIVs. NDV RNA titers reduction ranged from <3 to 5 log10 to complete suppression, but slight interference with the growth of AIVs occurred. H5N1 RNA titers showed <1-2 log10 reduction when co-inoculated with vNDV compared with the H5N1 control. The interference impact of H5N8 was more powerful than that of H5N1, while vNDV showed more resistance for interference than the avNDV strain. On the other hand, interference of AIVs was not observed except when vNDV was inoculated before H5N1. The interfering impact was increased after 48 h of inoculation, whereas no titer of avNDV was detectable.Conclusion:AIV strains had a powerful effect on NDV growth, regardless of which infection occurred first.

MiR-375 Has Contrasting Effects on Newcastle Disease Virus Growth Depending on the Target Gene.

MicroRNAs regulate post-transcriptional gene expression via either translational repression or mRNA degradation. They have important roles in both viral infection and host anti-infection processes. We discovered that the miR-375 is significantly upregulated in Newcastle disease virus (NDV)-infected chicken embryonic visceral tissues using a small RNA sequencing approach. Further research revealed that the overexpression of miR-375 markedly decreases the replication of the velogenic NDV F48E9 and the lentogenic NDV La Sota by targeting the M gene of NDV in DF-1 cells. Interestingly, miR-375 has another target, ELAVL4, which regulates chicken fibrocyte cell cycle progression and decreases NDV proliferation. In addition, miR-375 can influence bystander cells by its secretion in culture medium. Our results indicated that miR-375 is an inhibitor of NDV, but can also enhance NDV growth by reducing the expression of its target ELAVL4. These results emphasize the complex roles of microRNAs in the regulation of viral infections.

6-Gingerol prevents free transition metal Ion [Fe (Ii)] Induced free radicals mediated alterations by In vitro and Ndv growth in chicken eggs by In ovo

Background: The study of free radicals and their reactions is implicated in the pathogenesis of various human diseases. Therefore, antioxidants treatment plays a pivotal role in preventing the free radical-induced diseases. Objective: The objectives of this study were to examine the protective role of 6-gingerol from free transition metal ion-induced alterations by in vitro and Newcastle disease virus (NDV) in chicken eggs by in ovo . Materials and Methods: In this study, lipid peroxidation, DNA sugar oxidation, chelation of ferrous ions, DNA fragmentation, Cytochrome c-oxidation, ferric ion reducing activities and DPPH, superoxide and hydroxyl radicals scavenging activity by ESR studies were examined with 6-gingerol by in vitro . Furthermore, antiviral activity was screened with 6-gingerol by in ovo . Results: In vitro results showed that 254 μM/ml of 6-gingerol firmly inhibited erythrocyte membrane lipid peroxidation by 85.28% and DNA sugar oxidation by 91.26% when compared with butylated hydroxyanisole 74.42% (554 μM/ml) and 78.30% (824 μM/ml), respectively. Whereas, chelating activity of 6-gingerol was 80.2% which nearly similar to the EDTA activity (50 μg/ml) shown 83.93%. In addition, 6-gingerol (254μM/ml) scavenged the superoxide, hydroxyl, DPPH radicals by 84.96%, 90.45%, and 94.63% respectively and the same was strongly supported with ESR studies. Further, 254 μM/ml of 6-gingerol inhibited the DNA fragmentation, Cytochrome c-oxidation and reducing the ferric ion by in vitro and antiviral activity shown on NDV at 100 μg/ml. Conclusion: This study could enlighten that the 6-gingerol has a good metal sequester property and it could prevent the free radicals by in vitro and NDV growth in chicken eggs by in ovo . Abbreviations used: NDV: Newcastle Disease Virus; ESR: Electron Spin resonance; SOD: Super oxide Dismutase; HA: Hemagglutination.

The screening and evaluation of herbs and identification of herbal combinations with anti-viral effects on Newcastle disease virus

A total of 25 “heat-clearing and detoxifying” herbs used in Chinese medicine were investigated for their cytopathic effects on the growth of Newcastle Disease virus (NDV) in a chicken fibroblast cell line.The 5 herbs with the highest virus inhibitory effects were Herba agastaches, Flos chrysanthemi indici, Rhizoma anemarrhenae, Astragalus root and Baikal skullcap root and these were used in herbal formulations. Anti-NDV activities of 4 formulations were tested on the growth of NDV in the DF-1 fibroblast cell line.Formulation II, containing Baikal skullcap root, Astragalus root, Anemarrhena rhizome (1:1:2) and formulation IV containing Anemarrhena rhizome, Astragalus root and Flos chrysanthemi indici (1:1:1), which had strong anti-NDV activity in vitro, were used to determine the in vivo inhibitory effects of NDV-infection in chickens. After treatment with the two formulations serum IgY titres against NDV were improved, and morbidity was reduced in the NDV-infected chickens.The results suggest that the components in formulations II and IV acted synergistically to improve resistance to Newcastle disease and provide a basis for the developing an anti-NDV herbal medicine.

Development, characterization and optimization of a new suspension chicken-induced pluripotent cell line for the production of Newcastle disease vaccine

Traditionally, substrates for production of viral poultry vaccines have been embryonated eggs or adherent primary cell cultures. The difficulties and cost involved in scaling up these substrates in cases of increased demand have been a limitation for vaccine production. Here, we assess the ability of a newly developed chicken-induced pluripotent cell line, BA3, to support replication and growth of Newcastle disease virus (NDV) LaSota vaccine strain. The characteristics and growth profile of the cells were also investigated. BA3 cells could grow in suspension in different media to a high density of up to 7.0 × 106 cells/mL and showed rapid proliferation with doubling time of 21 h. Upon infection, a high virus titer of 1.02 × 108 EID50/mL was obtained at 24 h post infection using a multiplicity of infection (MOI) of 5. In addition, the cell line was shown to be free of endogenous and exogenous Avian Leukosis viruses, Reticuloendotheliosis virus, Fowl Adenovirus, Marek's disease virus, and several Mycoplasma species. In conclusion, BA3 cell line is potentially an excellent candidate for vaccine production due to its highly desirable industrially friendly characteristics of growing to high cell density and capability of growth in serum free medium.

Isolation and identification of Newcastle disease viruses from field outbreaks in chickens and pigeons

Eleven dead or sick birds submitted from farms in the year 2010 with a history of sudden death with respiratory and/or diarrhoeal signs were used for isolation and identification of Newcastle disease virus (NDV). All samples were subjected to routine necropsy. Pooled respiratory tissues were inoculated in embryonated chicken eggs and chicken embryo fibroblast (CEF) cell culture. The growth of NDV was confirmed by embryo mortality, cytopathic effects (CPE) in cell culture, haemagglutination (HA) and haemagglutination inhibition (HI) test. The presence of NDV was confirmed by reverse transcriptionpolymerase chain reaction (RT-PCR). At necropsy seven cases were tentatively diagnosed as Newcastle disease (ND). Out of seven ND-suspected samples, four yielded virus in both embryos and cell culture, while one was positive only in embryos, one only in cell culture and one sample was negative in both embryos and cell culture. RT-PCR successfully amplified a 766 bp fragment covering parts of Matrix and Fusion protein genes of NDV from the samples that were positive either in embryos or in cell culture. It is suggested that RT-PCR could be a rapid and sensitive tool for the detection of NDV. DOI: http://dx.doi.org/10.3329/bvet.v29i2.14341 Bangl. vet. 2012. Vol. 29, No. 2, 41-48

Engagement of new castle disease virus (NDV) matrix (M) protein with charged multivesicular body protein (CHMP) 4 facilitates viral replication

Newcastle disease virus (NDV) causes heavy economic losses to poultry industry across the globe every year. Although NDV matrix (M) protein is involved in virus budding and our previous data indicate that in ovo expression of M protein facilitates NDV replication, the underlying mechanism for the role of M protein in NDV replication is not clear. Using yeast two-hybrid system and immunoprecipitation approaches, we found that M protein interacted with host vacuolar sorting protein charged multivesicular body protein (CHMP) 4B and 4C. In addition, the colocalization of M protein and CHMP4B/C could be observed using a laser confocal scanning microscope. Knockdown of CHMP4B by siRNA or transient expression of CHMP4B/C dominant negative forms markedly inhibited NDV growth in DF-1 cells. Thus, cellular CHMP4s play a critical role in NDV replication.

Primary chicken tracheal cell culture system for the study of infection with avian respiratory viruses

A major route of infection of avian influenza virus (AIV) and Newcastle disease virus (NDV) in chickens is through cells of the respiratory epithelium. Here we describe the development of a method for culture of tracheal epithelial cells from chicken embryos as well as their use in studies of infection with avian respiratory viruses such as low-pathogenicity AIV and lentogenic NDV. Positive immunostaining for cytokeratin, the presence of cilia and microvilli, and microarray analysis of transcribed RNA demonstrated that the isolated cells were epithelial in nature. Infection of the epithelial cell cultures with AIV and NDV was demonstrated using immunofluorescence or green fluorescence protein fluorescence microscopy, respectively. Growth curves of AIV and NDV in tracheal epithelial cells revealed that tracheal epithelial cells can fully support AIV and NDV growth and reinfection. This system, which mimics that of the natural infection, will be useful to study the mechanisms of early viral infection and cellular host transcriptional responses.

Interactions between escherichia coli and Newcastle disease virus in chickens.

We investigated the interaction between Newcastle disease virus (NDV) and Escherichia coli in cell cultures, embryonated eggs, and 8-wk-old chickens. We measured the interactions on the basis of bacterial adherence and NDV hemagglutination titer in chickens, chicken embryos, and chicken embryo cell culture. Depending on the inoculation order of E. coli, a significant alteration of the growth of NDV was observed in both chickens and chicken embryos. When certain strains of E. coli were given before NDV exposure, the virus titers were lowered. In chickens, the mean virus titer was significantly (P < 0.05) lowered in the crop, the proventriculus, the gizzard, and the jejunum. However, there were no significant differences (P < 0.05) between the two groups for NDV titers in the duodenum, ileum, and cecum. In chicken embryos, when E. coli serotypes O78 and O119:B14 were inoculated before NDV exposure, the mean NDV titers were significantly (P < 0.5) lowered. However, there were no significant differences (P < 0.05) in NDV titer between the two groups when E. coli serotypes O78:K80:NM and O1ab:K NM were inoculated 24 hr before NDV exposure. When NDV was given prior to E. coli exposure, NDV titer was higher in both chickens and chicken embryos. In chickens, when NDV was given 48 hr before E. coli inoculation, NDV was detected in the proventriculus, gizzard, jejunum, ileum, and cecum, whereas no virus was detected in the control groups (NDV only). In the crop, NDV was detected at a significantly (P < 0.05) higher titer in the E. coli-inoculated group when compared with the control group that received NDV alone. In chicken embryos, virus titer was significantly (P < 0.05) higher when NDV was given 24 hr before E. coli inoculation for all three NDV strains used (Ulster and V4 strains). Adherence of E. coli to chicken embryo kidney (CEK) cells was significantly higher (P < 0.05) when the CEK cells were infected first with NDV and then by E. coli. The mean bacterial count per microscopic field in NDV-uninfected monolayers was eight compared with 112 for the NDV-infected monolayers. In approximately 10% of the fields in NDV-infected monolayers, the bacteria were too numerous to count.

Studies on chicken peripheral blood monocytes

Freshly isolated chicken peripheral blood monocytes were used. They were found to be heterogeneous in morphology, but have chemotactic and phagocytic activities, and are capable of respiratory burst. These cells posses a genetic sequecee that can be amplified by a pair of MIP 1-beta primers, indicating that they contain MIP 1-beta chemokine. The RNA from monocytes infected with Newcastle disease virus (NDV) were reverse transcribed, and the transcribed cDNA contains a sequence which can be amplified by a pair of NDV primers, indicating that these cells can support the growth of NDV. NDV infection of monocytes does not alter the existence of MIP-1beta. This finding raises the possibility that monocytes can serve as reservoirs for NDV infection.

Growth of newcastle disease virus in chicken macrophages

Chicken macrophages were isolated from chicken peripheral blood, cultured in vitro, and infected with Newcastle disease virus (NDV) after reaching semiconfluence. Infected macrophages supported the growth and replication of NDV. Virus-infected macrophages exhibited features of apoptosis as determined by agarose gel electrophoresis, thymidine release assays and flow cytometry. Electron microscopical examination also showed the appearance of intact virus particles, fragmented chromatin and apoptotic bodies. This evidence demonstrates that NDV infection of chicken macrophages causes chicken macrophages to undergo apoptosis.

Identification of Field Isolates of Infectious Bronchitis Virus by Interference with the La Sota Strain of Newcastle Disease Virus

The interference phenomenon of infectious bronchitis virus (IBV) with growth of Newcastle disease virus (NDV) in embryonating chicken eggs (ECE) was used as a diagnostic method. Fifteen field isolates obtained from presumptively infectious-bronchitis-affected chickens were analyzed by the IBV-NDV interference test. Eight isolates were capable of interfering with the growth of the La Sota strain of NDV, as measured by hemagglutination (HA) activity when IBV was inoculated 10 hr before NDV into ECE. The interference was considered specific for IBV, because it could be eliminated by adding homologous anti-IBV serum. The sensibility of this method could be demonstrated, because in some cases low-passage levels of IBV isolates showing HA interference ability were not capable of producing lesions in ECE. Furthermore, serologically negative IBV samples did not interfere with NDV growth. From these results, the IBV-NDV interference test appears to be a potential diagnostic alternative for identifying IBV field isolates.

Characterization of the virus isolated from HeLa cells persistently infected with Sendai virus (HVJ).

Microbiology and ImmunologyVolume 27, Issue 2 p. 207-211 NoteFree Access Characterization of the Virus Isolated from HeLa Cells Persistently Infected with Sendai Virus (HVJ) Tetsuya Yoshida, Tetsuya Yoshida Department of Bacteriology, Nagoya, Cancer Research Institute, Aichi, 466Search for more papers by this authorMichinari Hamaguchi, Michinari Hamaguchi Department of Virology and Cell Biology, Cancer Research Institute, Aichi, Nagoya, 466Search for more papers by this authorHiroshi Naruse, Hiroshi Naruse Department of Pediatrics, Nagoya University School of Medicine, Aichi, Nagoya, 466Search for more papers by this authorKazuo Nishikawa, Kazuo Nishikawa Department of Pediatrics, Nagoya University School of Medicine, Aichi, Nagoya, 466Search for more papers by this authorYoshiyuki Nagai, Yoshiyuki Nagai Department of Virology and Cell Biology, Cancer Research Institute, Aichi, Nagoya, 466Search for more papers by this author Tetsuya Yoshida, Tetsuya Yoshida Department of Bacteriology, Nagoya, Cancer Research Institute, Aichi, 466Search for more papers by this authorMichinari Hamaguchi, Michinari Hamaguchi Department of Virology and Cell Biology, Cancer Research Institute, Aichi, Nagoya, 466Search for more papers by this authorHiroshi Naruse, Hiroshi Naruse Department of Pediatrics, Nagoya University School of Medicine, Aichi, Nagoya, 466Search for more papers by this authorKazuo Nishikawa, Kazuo Nishikawa Department of Pediatrics, Nagoya University School of Medicine, Aichi, Nagoya, 466Search for more papers by this authorYoshiyuki Nagai, Yoshiyuki Nagai Department of Virology and Cell Biology, Cancer Research Institute, Aichi, Nagoya, 466Search for more papers by this author First published: February 1983 https://doi.org/10.1111/j.1348-0421.1983.tb03575.xCitations: 3AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL REFERENCES 1Kimura, Y., Ito, Y., Shimokata, K., Nishiyama, Y., Nagata, I., and Kitoh, J. 1975. Temperature-sensitive virus derived from BHK cells persistently infected with HVJ (Sendai virus). J. Virol. 15: 55– 63. 2Maeno, K., Yoshii, S., Nagata, I., and Matsumoto, T. 1966. Growth of Newcastle disease virus in a HVJ carrier culture of HeLa cells. Virology 29: 255– 263. 3Naruse, H., Nagai, Y., Yoshida, T., Hamaguchi, M., Matsumoto, T., Isomura, S., and Suzuki, S. 1981. The polypeptides of munps virus and their synthesis in infected chick embryo cells. Virology 112: 119– 130. 4Ogura, H., Sato, H., and Hatano, M. 1981. Temperature-sensitive HVJ (Sendai virus) with altered P polypeptide derived from persistently infected cell lines. J. Gen. Virol. 55: 469– 473. 5Roux, L., and Holland, J.J. 1979. Role of defective interfering particles of Sendai virus in persistent infections. Virology 93: 91– 103. 6Sato, H., Ogura, H., and Hatano, M. 1981. An intracellular interaction between a temperature- sensitive mutant and the original wild-type HVJ (Sendai virus) is responsible for the establishment and maintenance of HVJ persistent infection. J. Gen. Virol. 55: 459– 468. 7Yoshida, T., Hamaguchi, M., Naruse, H., and Nagai, Y. 1982. Persistent infection by a temperature-sensitive mutant isolated from a Sendai virus (HVJ) carrier culture: Its initiation and maintenance without aid of defective interfering particles. Virology 120: 329– 339. 8Yoshida, T., Nagai, Y., Maeno, K., Iinuma, M., Hamaguchi, M., Matsumoto, T., Nagayoshi, S., and Hoshino, M. 1979. Studies on the role of M protein in virus assembly using a ts mutant of HVJ (Sendai virus). Virology 92: 139– 154. Citing Literature Volume27, Issue2February 1983Pages 207-211 ReferencesRelatedInformation

Relation of interferon production to the limited replication of Newcastle disease virus in L cells.

Growth of Newcastle disease virus (NDV) in L cells, where the virus undergoes limited replication, has been compared to that in fully permissive BHK-21 host cells. The synthesis of viral proteins and the production of infectious progeny were found to occur normally at early times of infection in L cells. However, the subsequent amplification of viral protein synthesis did not take place and instead of infectious virions, non-infectious haemagglutinin was the predominant product. This shift of replication pattern from complete to incomplete virus production seemed to be temporally related to the appearance and accumulation of interferon (IFN) in the system. The addition of specific antiserum against mouse IFN to the infected L cell cultures was able to circumvent such restriction of virus growth. In the presence of the antiserum, synthesis of viral proteins was found to progress normally, with the production of a high amount of infectious progeny comparable to that of the permissive system. These results suggest that the limited replication of NDV in L cells may be due to interference by the endogenously produced IFN during the course of infection.

Enhancement of fusion from within by antiviral antibody in cells infected with Newcastle disease virus.

Microbiology and ImmunologyVolume 23, Issue 10 p. 1037-1041 Original ArticleFree Access Enhancement of fusion from within by Antiviral Antibody in Cells Infected with Newcastle Disease Virus Masao Iinuma, Masao Iinuma Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this authorKoichiro Maeno, Koichiro Maeno Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this authorHiroshi Nagura, Hiroshi Nagura Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this authorToshisada Matsumoto, Toshisada Matsumoto Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this author Masao Iinuma, Masao Iinuma Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this authorKoichiro Maeno, Koichiro Maeno Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this authorHiroshi Nagura, Hiroshi Nagura Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this authorToshisada Matsumoto, Toshisada Matsumoto Department of Virology, Cancer Research Institute, and First Department of Pathology, Nagoya University School of Medicine, NagoyaSearch for more papers by this author First published: October 1979 https://doi.org/10.1111/j.1348-0421.1979.tb00534.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL REFERENCES 1Harter, D.H., and Choppin, P.W. 1967. Cell-fusing activity of Visna virus particles. Virology 31: 279– 288. 2Iinuma, M., Maeno, K., and Matsumoto, T. 1973. Studies on the assembly of Newcastle disease virus: An arginine-dependent step in virus replication. Virology 51: 205– 215. 3Iinuma, M., Nagai, Y., Maeno, K., Yoshida, T., and Matsumoto, T. 1971. Studies on the assembly of Newcastle disease virus: Incorporation of structural proteins into virus particles. J. Gen. Virol. 12: 239– 247. 4Iinuma, M., Yoshida, T., Nagai, Y., Maeno, K., Matsumoto, T., and Hoshino, M. 1971. Sub-units of NDV: Hemagglutinin and neuraminidase subunits of Newcastle disease virus. Virology 46: 663– 677. 5Kohn, A. 1965. Polykaryocytosis induced by Newcastle disease virus in monolayers of animal cells. Virology 26: 228– 245. 6Ludwing, H., Becht, H., and Rott, R. 1974. Inhibition of herpesvirus induced cell fusion by concanavalin A, antisera, and 2-deoxy-D-glucose. J. Virol. 14: 307– 314. 7Maeno, K., and Kilbourne, E.D. 1970. Developmental sequence and intracellular sites of synthesis of three structural protein antigens of influenza A2 virus. J. Virol. 5: 153– 164. 8Maeno, K., Yoshida, T., Iinuma, M., Nagai, Y., Matsumoto, T., and Asai, J. 1970. Isolation of hemagglutinin and neuraminidase subunits of hemagglutinating virus of Japan. J. Virol. 6: 492– 499. 9Maeno, K., Yoshii, S., Nagata, I., and Matsumoto, T. 1966. Growth of Newcastle disease virus in a HVJ carrier culture of HeLa cells. Virology 29: 255– 263. 10Nishiyama, Y., Ito, Y., Shimokata, K., Kimura, Y., and Nagata, I. 1976. Polykaryocyte formation induced by VSV in mouse L cells. J. Gen. Virol. 32: 85– 96. 11Okada, Y. 1969. Factors in fusion of cells by HVJ. Current Topics in Microbiol, and Immunol. 48: 102– 128. 12Okada, Y., and Tadokoro, J. 1962. Analysis of giant polynuclear cell formation caused by HVJ virus from Ehrlich's ascites tumor cells. II. Quantitative analysis of giant polynuclear formation. Expt. Cell. Res. 26: 108– 118. 13Okada, Y., Yamada, K., and Tadokoro, J. 1964. Effect of antiserum on the cell fusion reaction caused by HVJ. Virology 22: 397– 409. 14Poste, G. 1970. Virus-induced polykaryocytosis and the mechanism of cell fusion. Advances in Virus Research 16: 303– 356. 15Rankin, A.M., Fisher, L.E., and Bussell, R.H. 1972. Cell fusion by canine distemper virus-infected cells. J. Virol. 10: 1179– 1183. 16Seto, J.T., Becht, H., and Rott, R. 1974. Effect of specific antibodies on biological functions of the envelope components of Newcastle disease virus. Virology 61: 354– 360. 17Wainberg, M.A., and Howe, C. 1972. Antibody-mediated fusion of FL amnion cells infected with parainfluenza virus type 2. Immunol. Commun. 1: 481– 489. Citing Literature Volume23, Issue10October 1979Pages 1037-1041 ReferencesRelatedInformation

Studies on the assembly of Newcastle disease virus: An arginine-dependent step in virus replication

Growth of Newcastle disease virus in HeLa cells deprived of various amino acids was investigated. Of all amino acids in Eagle's MEM, only arginine was found to be essential for the synthesis of infectious progeny virus. Omission of any one or all of the other amino acids from the culture medium permitted limited virus production, but none whatever could be detected in the absence of medium-arginine. Although the arginine-deprived cells had synthesized a large quantity of nucleocapsid antigen, hemagglutinin and neuraminidase at the later stage of infection, neither hemadsorption on the cell surface nor release of infectious virus could be detected. When arginine was restored to the culture, hemadsorption reaction and release of virus became soon detectable and the virus titer increased rapidly. Simultaneous addition of cycloheximide with arginine did not result in such a recovery of virus production. Immunofluorescent staining of NDV-infected cells with antiviral antibody showed that the cells incubated in normal medium exhibited clear fluorescence at the cell surface, but the surface of arginine-deprived cells did not show any detectable fluorescence, whereas either cells showed distinct cytoplasmic fluorescence when stained after fixation. These results suggest that arginine plays a specific role in the synthesis of a protein which might be an essential for virus maturation.

Growth of Newcastle disease virus in fertile eggs of the Japanese quail ( Coturnix coturnix japonica)

Five strains of Newcastle disease virus (NDV) were inoculated into the allantoic cavities of six-day fertile quail eggs and nine-day fertile hen eggs. The mean embryo infective dose (EID 50) was higher and the mean embryo death time (EDT 50) was shorter in quail eggs than in hen eggs. The F strain killed all the quail embryos, but hardly any chick embryos. The HA and EID 50 titres of allantoic fluids were higher from hen eggs than from quail eggs. It is considered that fertile quail eggs have some advantages over hen eggs for use in the virological laboratory.

Mechanism of enhancement of Newcastle disease virus growth in cultured cells by co-infecting hog cholera virus.

The mechanism of the enhanced replication of Newcastle disease (ND) virus in swine testicle (ST) cells infected with hog cholera (HC) virus (END phenomenon) was studied. Two mechanisms appeared to operate, one being the suppression of interferon production by the coinfecting HC virus and the other a still undefined mechanism not related to interferon. The first mechanism was suggested by the facts that interferon production by ND virus was inhibited by prior infection with HC virus, and that ND virus growth was suppressed by exogenous interferon in both HC infected and uninfected ST cell cultures. The reason for the inhibition of interferon production is unknown; it is neither due to a decreased ND virus adsorption to ST cells nor due to the production of some factor blocking the interferon production. The possibility of an additional mechanism emerged when the effects of 20-methylcholanthrene and actinomycin D were examined. These substances suppressed the interferon induction by ND virus but increased the viral growth only slightly, while in HC infected cells actinomycin D reduced ND virus replication to a marked extent. It thus seems that the second mechanism, which is not related to interferon and which is sensitive to actinomycin D, may be more important than the suppression of interferon production in END phenomenon. Poly I∶C treatment, which could confer on uninfected cells resistance to ND and WEE viruses without inducing detectable amounts of interferon, did not affect the growth of these viruses in HC infected cells. This phenomenon presumably shares a common mechanism with the END phenomenon.

Specific requirement of serine for the growth of Newcastle disease virus

Eagle's MEM, which is free of serine, was unable to support the growth of Newcastle disease virus (NDV) in a clonal subline (S3T) of HeLa S3 cells which requires serine for optimum growth. Full growth of poliovirus was, however, achieved in the same condition. Eagle's MEM supplemented with l-serine at an optimum concentration of 1 m M supported the full growth of NDV. Kinetic experiments revealed that except in the first 2 hours after infection continued presence of exogenous serine was essential for the multiplication of NDV. At any time after 2 hours, upon the addition of serine and after certain periods of time lag (which could be overcome by 8 hours after infection), the logarithmic increase of the NDV progeny occurred at the same rate. In the serine-free medium, the synthesis of viral RNA or some virus-specific antigen(s) was found to proceed in the NDV-infected cells, while neither hemagglutinin production nor hemadsorption was observed. The possible role of serine for the growth of NDV was discussed.