In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Input: Consider Input: Infectious bronchitis (IB) and Newcastle disease (ND) are common viral diseases of chickens, which are caused by infectious bronchitis virus (IBV) and Newcastle disease virus (NDV), respectively. Vaccination with live attenuated strains of IBV-H120 and NDV-LaSota are important for the control of IB and ND. However, conventional live attenuated vaccines are expensive and result in the inability to differentiate between infected and vaccinated chickens. Therefore, there is an urgent need to develop new efficacious vaccines. In this study, using a previously established reverse genetics system, we generated a recombinant IBV virus based on the IBV H120 vaccine strain expressing the haemagglutinin-neuraminidase (HN) protein of NDV. The recombinant virus, R-H120-HN/5a, exhibited growth dynamics, pathogenicity and viral titers that were similar to those of the parental IBV H120, but it had acquired hemagglutination activity from NDV. Vaccination of SPF chickens with the R-H120-HN/5a virus induced a humoral response at a level comparable to that of the LaSota/H120 commercial bivalent vaccine and provided significant protection against challenge with virulent IBV and NDV. In summary, the results of this study indicate that the IBV H120 strain could serve as an effective tool for designing vaccines against IB and other infectious diseases, and the generation of IBV R-H120-HN/5a provides a solid foundation for the development of an effective bivalent vaccine against IBV and NDV.

Output: Recombinant infectious bronchitis virus (IBV) H120 vaccine strain expressing the hemagglutinin-neuraminidase (HN) protein of Newcastle disease virus (NDV) protects chickens against IBV and NDV challenge


Input: Consider Input: Ca 2+ is one of the most universal and versatile signaling molecules and is involved in almost every aspect of cellular processes. Viruses are adept at utilizing the universal Ca 2+ signal to create a tailored cellular environment that meets their own demands. This review summarizes most of the known mechanisms by which viruses perturb Ca 2+ homeostasis and utilize Ca 2+ and cellular Ca 2+ -binding proteins to their benefit in their replication cycles. Ca 2+ plays important roles in virion structure formation, virus entry, viral gene expression, posttranslational processing of viral proteins and virion maturation and release. As part of the review, we introduce an algorithm to identify linear "EF-hand" Ca 2+ -binding motifs which resulted in the prediction of a total of 93 previously unrecognized Ca 2+ -binding motifs in virus proteins. Many of these proteins are nonstructural proteins, a class of proteins among which Ca 2+ interactions had not been formerly appreciated. The presence of linear Ca 2+ -binding motifs in viral proteins enlarges the spectrum of Ca 2+ -virus interplay and expands the total scenario of viral calciomics. (J.J. Yang). for structural integrity or functionality; and (3) critical virus-host interactions depend on cellular Ca 2+ -regulated proteins or pathways. This review, which aims to stimulate future studies on the roles of Ca 2+ in virus infection, is focused on such interplay by highlighting recent discoveries in the biological roles of Ca 2+ in virus infection. 0143-4160/$ -see front matter

Output: Viral calciomics: Interplays between Ca 2+ and virus


Input: Consider Input: An assay for the microsomal hydroxylation of lauric acid (LA), based on HPLC with flowthrough radiochemical detection, has been developed. Conditions were optimized for resolution and quantitation of three microsomal metabolites of LA, one of which has not been reported previously as a metabolite of LA in mammalian microsomal incubations. These products, 12-(w)-hydroxy-LA, 1 1-(w-1)-hydroxy-LA, and a novel metabolite, IO-(o-2)-hydroxy-LA, were isolated by HPLC and identified by gas chromatography/mass spectrometry. In the presence of NADPH, the formation of all three metabolites was linear with time and microsomal protein concentration. Hydrogen peroxide also supported the microsomal metabolism of LA, although the ratio of metabolites was substantially different than that produced by NADPH-supported microsomes. Several biochemical probes (metyrapone, a-naphthoflavone, 2diethylaminoethyl-2,2diphenylvalerate hydrochloride, and lo-undecynoic acid) were used to dissociate the three LA hydroxylase activities. These experiments suggest that the site-specific hydroxylation [w-, (w-l)-, (w-2)-] of LA may be catalyzed by different isozymes of cytochrome P-450.


Output: Determination of Microsomal Laurie Acid Hydroxylase Activity by HPLC with Flow-Through Radiochemical Quantitation