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:
This is a study on the Avian coronavirus IBV and chicken host-relationship from the codon usage point of view based on fifty-nine non-redundant IBV S1 sequences (nt 1-507) from strains detected worldwide and chicken tissuespecific protein genes sequences from IBV-replicating sites. The effective number of codons (ENC) values ranged from 36 to 47.8, indicating a high-to-moderate codon usage bias. The highest IBV codon adaptation index (CAI) value was 0.7, indicating a distant virus versus host synonymous codons usage. The ENC 9 GC3 % curve indicates that both mutational pressure and natural selection are the driving forces on codon usage pattern in S1. The low CAI values agree with a low S protein expression and considering that S protein is a determinant for attachment and neutralization, this could be a further mechanism besides mRNA transcription attenuation for a low expression of this protein leading to an immune camouflage.

Ex Output:
Avian coronavirus Spike Glycoprotein Ectodomain Shows a Low Codon Adaptation to Gallus gallus with Virus-Exclusive Codons in Strategic Amino Acids Positions


Ex Input:
SARS-CoV-2, a member of the coronavirus family, is responsible for the current COVID-19 pandemic. Based on our analysis of hepatitis C virus and coronavirus replication, and the molecular structures and activities of viral inhibitors, we previously demonstrated that three nucleotide analogues inhibit the SARS-CoV RNA-dependent RNA polymerase (RdRp). Here, using polymerase extension experiments, we have demonstrated that the active triphosphate form of Sofosbuvir (a key component of the FDA approved hepatitis C drug EPCLUSA), is incorporated by SARS-CoV-2 RdRp, and blocks further incorporation. Using the same molecular insight, we selected the active triphosphate forms of three other anti-viral agents, Alovudine, AZT (an FDA approved HIV/AIDS drug) and Tenofovir alafenamide (TAF, an FDA approved drug for HIV and hepatitis B) for evaluation as inhibitors of SARS-CoV-2 RdRp. We demonstrated the ability of these three viral polymerase inhibitors, 3'-fluoro-3'-deoxythymidine triphosphate, 3'-azido-3'deoxythymidine triphosphate and Tenofovir diphosphate (the active triphosphate forms of Alovudine, AZT and TAF, respectively) to be incorporated by SARS-CoV-2 RdRp, where they also terminate further polymerase extension. These results offer a strong molecular basis for these nucleotide analogues to be evaluated as potential therapeutics for COVID-19.

Ex Output:
Nucleotide Analogues as Inhibitors of SARS-CoV-2 Polymerase


Ex Input:
Detailed information on the source, spread and evolution of respiratory syncytial virus (RSV) during seasonal community outbreaks remains sparse. Molecular analyses of attachment (G) gene sequences from hospitalized cases suggest that multiple genotypes and variants co-circulate during epidemics and that RSV persistence over successive seasons is characterized by replacement and multiple new introductions of variants. No studies have defined the patterns of introduction, spread and evolution of RSV at the local community and household level. We present a whole genome sequence analysis of 131 RSV group A viruses collected during 6-month household-based RSV infection surveillance in Coastal Kenya, 2010 within an area of 12 km 2 . RSV infections were identified by regular symptom-independent screening of all household members twice weekly. Phylogenetic analysis revealed that the RSV A viruses in nine households were closely related to genotype GA2 and fell within a single branch of the global phylogeny. Genomic analysis allowed the detection of householdspecific variation in seven households. For comparison, using only G gene analysis, household-specific variation was found only in one of the nine households. Nucleotide changes were observed both intra-host (viruses identified from same individual in follow-up sampling) and inter-host (viruses identified from different household members) and these coupled with sampling dates enabled a partial reconstruction of the within household transmission chains. The genomic evolutionary rate for the household dataset was estimated as 2.307 Â 10 À 3 (95% highest posterior density: 0.935-4.165Â 10 À 3 ) substitutions/site/year. We conclude that (i) at the household level, most RSV infections arise from the introduction of a single virus variant followed by accumulation of household specific variation and (ii) analysis of complete virus genomes is crucial to better understand viral transmission in the community. A key question arising is whether prevention of RSV introduction or spread within the household by vaccinating key transmitting household members would lead to a reduced onward community-wide transmission.

Ex Output:

Transmission patterns and evolution of respiratory syncytial virus in a community outbreak identified by genomic analysis