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.

Ex Input:
The red-crowned crane is one of the rarest crane species, and its population is decreasing due to loss of habitat, poisoning, and infections. Using a viral metagenomics approach, we analyzed the virome of feces from wild and captive red-crowned cranes, which were pooled separately. Vertebrate viruses belonging to the families Picornaviridae, Parvoviridae, Circoviridae, and Caliciviridae were detected. Among the members of the family Picornaviridae, we found three that appear to represent new genera. Six nearly complete genomes from members of the family Parvoviridae were also obtained, including four new members of the proposed genus "Chapparvovirus", and two members of the genus Aveparvovirus. Six small circular DNA genomes were also characterized. One nearly complete genome showing a low level of sequence identity to caliciviruses was also characterized. Numerous viruses believed to infect insects, plants, and crustaceans were also identified, which were probably derived from the diet of red-crowned cranes. This study increases our understanding of the enteric virome of red-crowned cranes and provides a baseline for comparison to those of other birds or following disease outbreaks.

Ex Output:
The fecal virome of red-crowned cranes


Ex Input:
Background: In last three years, 96 suspected poultry farms from different provinces in China were diagnosed for avian infectious bronchitis (IB) survey. Finally, 221 IBV strains were confirmed by dwarf embryo test and RT-PCR assay. By virus recovery trials, 187 of the isolates caused the birds died or distressed from nephritis, which was accordant with the clinical record. Results: Based on epidemiology analysis of recent field isolates of nephropathogenic IB in vaccinated farms in China, YL6 strain were used for vaccination and evaluated by antibody titer and challenge tests. The immunoprotection test indicated that the practical application of vaccine based on the recent field strains could finely facilitate controlling the nephropathogenic IB. Conclusions: Our study was aim at setting a guide for safeguard against nephropathogenic IBV-caused disease in China.

Ex Output:
Epidemiology and immunoprotection of nephropathogenic avian infectious bronchitis virus in southern China


Ex Input:
Intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV) into susceptible mouse strains produces a chronic demyelinating disease in which mononuclear cell-rich infiltrates in the central nervous system (CNS) are prominent. Current evidence strongly supports an immune-mediated basis for myelin breakdown, with an effector role proposed for TMEV-specific, major histocompatibility complex (MHC) class II-restricted delayed-type hypersensitivity (DTH) responses in which lymphokine-activated macrophages mediate bystander demyelination. The present study examined the possibility that concomitant or later-appearing neuroantigen-specific autoimmune T cell responses, such as those demonstrated in chronic-relapsing experimental allergic encephalomyelitis (R-EAE), may contribute to the demyelinating process following TMEV infection. T cell responses against intact, purified major myelin proteins (myelin 10 basic protein (MBP) and proteohpid protein (PLP)), and against altered myelin constituents were readily demonstrable in SJL//J mice with R-EAE, but were not detectable in SJL//J mice with TMEV-induced demyehnating disease. TMEV-infected mice also did not display T cell responses against the peptide fragments of MBP(91-104) and PLP(139-151) recently shown to be encephalitogenic in SJL/J mice. In addition, induction of neuroantigen-specific tolerance to a heterogeneous mixture of CNS antigens, via the i.v. injection of syngeneic SJL//J splenocytes covalently coupled with mouse spinal cord homogenate, resulted in significant suppression of clinical and histologic signs of R-EAE and the accompanying MBPand PLP-specific DTH responses. In contrast, neuroantigen-specific tolerance failed to alter the development of clinical and histologic signs of TMEV-induced demyelinating disease or the accompanying virus-specific DTH and humoral immune responses. These findings demonstrate that TMEV-induced demyelinating disease can occur in the apparent absence of neuroantigen-specific autoimmune responses. The relationship of the present results to the immunopathology of multiple sclerosis is discussed.

Ex Output:

Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease III. Failure of neuroantigen-specific immune tolerance to affect the clinical course of demyelination