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: Coronaviridae and causes highly contagious respiratory disease in chickens. Innate immunity plays significant roles in host defense against IBV. Here, we explored the interaction between IBV and the host innate immune system. Severe histopathological lesions were observed in the tracheal mucosa at 3-5 days post inoculation (dpi) and in the kidney at 8 dpi, with heavy viral loads at 1-11 and 1-28 dpi, respectively. The expression of mRNAs encoding Toll-like receptor (TLR) 3 and TLR7 were upregulated at 3-8 dpi, and that of TIR-domain-containing adapter-inducing interferon (IFN) (TRIF) was upregulated at 21 dpi in the trachea and kidney. Myeloid differentiation primary response protein 88 (MyD88) was upregulated in the trachea during early infection. Tumor necrosis factor receptor-associated factor (TRAF) 3 and TRAF6 were upregulated expression in both tissues. Moreover, melanoma differentiation-associated protein 5 (MDA5), laboratory of genetics and physiology 2 (LGP2), stimulator of IFN genes (STING), and mitochondrial antiviral signaling protein (MAVS), as well as TANK binding kinase 1 (TBK1), inhibitor of kappaB kinase (IKK) , IKK, IKK, IFN regulatory factor (IRF) 7, nuclear factor of kappaB (NF-B), IFN-, IFN-, various interleukins(ILs), and macrophage inflammatory protein-1 (MIP-1) were significantly upregulated in the trachea and downregulated in the kidney. These results suggested that the TLR and MDA5 signaling pathways and innate immune cytokine were induced after IBV infection. Additionally, consistent responses to IBV infection were observed during early infection, with differential and complicated responses in the kidney.

Output: Responses of the Toll-like receptor and melanoma differentiation- associated protein 5 signaling pathways to avian infectious bronchitis virus infection in chicks

Input: Consider Input: Coronaviruses most often infect the respiratory or intestinal tract. Transmissible gastroenteritis virus (TGEV), a group 1 coronavirus, infects the porcine small intestine. Piglets up to the age of 3 weeks die from diarrhea caused by the viral gastroenteritis unless they are protected by antibodies. In addition to the cellular receptor, porcine aminopeptidase N, the TGEV spike protein binds to sialic acid residues. We have shown that the sialic acid binding activity mediates the binding of TGEV to a mucin-like glycoprotein present in porcine brush border membranes. This was shown by performing a virus overlay binding assay with proteins obtained from brush border membranes by lectin precipitation. Because of the reactivity with specific lectins we assume that the recognized glycoprotein has the characteristics of a mucin.

Output: Identification of Sugar Residues Involved in the Binding of TGEV to Porcine Brush Border Membranes

Input: Consider Input: In many systems transfer between the endoplasmic reticulum and the Golgi apparatus is blocked at temperatures below 16C. In virus-infected cells in culture, a special membrane compartment is seen to accumulate. Our studies with rat liver show a similar response to temperature both in situ with slices and in vitro with isolated transitional endoplasmie reticulum fractions. With isolated transitional endoplasmic reticulum fractions, when incubated in the presence of nucleoside tripbosphate and a cytosol fraction, temperature dependent formation of vesicles occurred with a Ql0 of "2 but was apparent only at temperatures greater than 12C. A similar response was seen in situ at 12C and 16C where fusion of transition vesicles with cis Golgi apparatus, but not their formation, was blocked and transition vesicles accumulated in large numbers. At 18C and below and especially at 8C and 12C, the cells responded by accumulating smooth tubular transitional membranes near the cis Golgi apparatus face. With cells and tissue slices at 20C neither transition vesicles nor the smooth tubular elements accumulated. Those transition vesicles which formed at 3"/C were of a greater diameter than those formed at 4C both in situ and in vitro. The findings show parallel responses between the temperature dependency of transition vesicle formation in vitro and in situ and suggest that a subP0Pulation of the transitional endoplasmic reticulum may be morphologically and functionally homologous to the 16C compartment observed in vitally-infected cell lines grown at low temperatures. transition vesicle --endoplasmie reticulum --temperature --rat liver
Output: Identification of the 16C compartment of the endoplasmic reticulum in rat liver and cultured hamster kidney cells