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.
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Question: . Rapid detection of viral-specific antibodies by ELISA. Vet. I~unol. Immunopathol., 17: 453-464. The development of three separate rapid ELISAs for detecting antibodies in host serum to three different viruses is described. These include: 1. A direct antigen assay using enzyme labelled anti-canine Ig for detecting antibodies to canine parvovirus, 2. A competitive ELISA using a feline infectious peritonitis virus-specific monoclonal antibody labelled with enzyme, and 3. A competitive ELISA using an equine infectious anemia virus-specific monoclonal antibody and enzyme labelled antigen, p. 26. The utility and benefits of each of the three approaches is emphasized.

Answer: Rapid detection of viral-specific antibodies by ELISA


Question: Recent years have seen several advances in our understanding of immunity to virus infection of the lower respiratory tract, including to influenza virus infection. Here, we review the cellular targets of viruses and the features of the host immune response that are unique to the lungs. We describe the interplay between innate and adaptive immune cells in the induction, expression and control of antiviral immunity, and discuss the impact of the infected lung milieu on moulding the response of antiviral effector T cells. Recent findings on the mechanisms that underlie the increased frequency of severe pulmonary bacterial infections following respiratory virus infection are also discussed. Viruses are highly evolved and ubiquitous pathogens. Although infection with many viruses results in a mild, self-limited disease, other viruses can produce severe and frequently fatal infections. The respiratory tract is a major portal through which viruses enter to initiate infection. Whereas some viruses can initiate infection in the respiratory tract and then disseminate to other sites in the body, other viruses typically remain localized to the respiratory tract, where they replicate and induce tissue injury (see Supplementary information S1 (table)). Various defence mechanisms have evolved in the respiratory tract to prevent and control infection by viruses and other pathogens. The respiratory tract can be divided anatomically into the upper respiratory tract (including the nose, mouth and pharynx) and the lower respiratory tract (which consists of the trachea, bronchi and lungs), with the lymphoid tissue of Waldeyer's ring (including the pharyngeal and palatine tonsils) representing the line of demarcation. Because of the crucial role of the lower respiratory tract in respiration, we limit the focus of this Review to recent advances in our understanding of the host immune response to virus infection at this site.

Answer: Regulating the adaptive immune response to respiratory virus infection NIH Public Access


Question: The objective of the present study was to determine if chicken melanoma differentiation-associated gene 5 (MDA5) senses infectious bursal disease virus (IBDV) infection to initiate and amplify an innate immune response in the chicken MDA5 (chMDA5) signaling pathway. Chicken embryo fibroblast DF-1 cells were infected with IBDV LP1 at a multiplicity of infection (MOI) of 0.5 or 10. In addition, knockdown and overexpression of chMDA5 were performed by transfecting DF-1 cells with chMDA5targeting small interfering RNA (siRNA) or chMDA5expressing DNA. The transfected cells were infected with IBDV LP1 at an MOI of 10. Cell culture supernatants and lysates were collected at 2, 8, 16 and 24 hours postinfection (hpi) for IBDV titer determination and RNA extraction, respectively. IBDV RNA loads and mRNA expression levels of chicken MDA5, interferon-b (IFN-b) promoter stimulator 1 (IPS-1), interferon regulatory factor-3 (IRF-3), IFN-b, double-stranded RNA-dependent protein kinase (PKR), 2 0 ,5 0 -oligoadenylate synthetase (OAS), myxovirus resistance gene (Mx), and major histocompatibility complex class I (MHC class I) were determined by real-time RT-PCR. The IBDV titer increased up to 1.4 9 10 7 plaqueforming units (PFU)/mL at 24 hpi, and the IBDV RNA load reached 464 ng/lL at 24 hpi. The mRNA expression levels of chicken MDA5, IRF-3, IFN-b, PKR, OAS, Mx and MHC class I in IBDV-infected DF-1 cells exhibited significant (p \ 0.05) upregulation up to 906-, 199-, 26,310-, 12-, 66,144-, 64,039-and 33-fold, respectively. Expressed chMDA5 from transfection and double-stranded RNA from IBDV infection were localized or colocalized in the cytoplasm of DF-1 cells at 16 hpi. When chMDA5 was knocked down in DF-1 cells, IBDV titers and RNA loads were significantly higher (p \ 0.05) than those in DF-1 cells without chMDA5 knockdown at 24 hpi. The expression levels of chicken MDA5, IRF-3, IFN-b and MHC class I in chMDA5-knockdown DF-1 cells were significantly lower (p \ 0.05) at 16 and 24 hpi. DF-1 cells overexpressing chMDA5 by transfection with chMDA5 expressing DNA had significantly lower (p \ 0.05) IBDV titers and RNA loads at 16 and 24 hpi and showed significantly higher (p \ 0.05) expression of chicken MDA5, IRF-3, IFN-b, PKR, OAS, Mx and MHC class I at 2 hpi. The results indicated that chicken MDA5 recognized IBDV infection and that this interaction resulted in the activation of chMDA5-related innate immune genes and upregulation of chicken MHC class I.

Answer:
Chicken melanoma differentiation-associated gene 5 (MDA5) recognizes infectious bursal disease virus infection and triggers MDA5-related innate immunity