TASK DEFINITION: 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.
PROBLEM: Background: The HIV-1 RNA genome has a biased nucleotide composition with a surplus of As. Several hypotheses have been put forward to explain this striking phenomenon, but the A-count of the HIV-1 genome has thus far not been systematically manipulated. The reason for this reservation is the likelihood that known and unknown sequence motifs will be affected by such a massive mutational approach, thus resulting in replication-impaired virus mutants. We present the first attempt to increase and decrease the A-count in a relatively small polymerase (pol) gene segment of HIV-1 RNA. To minimize the mutational impact, a new mutational approach was developed that is inspired by natural sequence variation as present in HIV-1 isolates. This phylogeny-instructed mutagenesis allowed us to create replication-competent HIV-1 mutants with a significantly increased or decreased local A-count. The local A-count of the wild-type (wt) virus (40.2%) was further increased to 46.9% or reduced to 31.7 and 26.3%. These HIV-1 variants replicate efficiently in vitro, despite the fact that the pol changes cause a quite profound move in HIV-SIV sequence space. Extrapolating these results to the complete 9 kb RNA genome, we may cautiously suggest that the A-rich signature does not have to be maintained. This survey also provided clues that silent codon changes, in particular from G-to-A, determine the subtype-specific sequence signatures.

SOLUTION: HIV-1 tolerates changes in A-count in a small segment of the pol gene

PROBLEM: Please cite this article as: El-Shall N.A., Shewita R.S., Abd El-Hack M.E., AlKahtane A., Alarifi S., Alkahtani S., Abdel-Daim M.M. & Sedeik M.E., Effect of essential oils on the immune response to some viral vaccines in broiler chickens, with special reference to Newcastle disease virus, Poultry Science (2020), doi: https://doi.(Mohamed E. Abd El-Hack). 21 (1952±28.82) did not significantly (p>0.05) improve growth performance compared to 41 the non-treated birds (NC and VC) (1970±19.56 and 1904±38.66). Essential oils 42 showed an antiviral effect on vNDv in vivo (in chickens) as a preventive measure 43 (PRV) as well as some therapeutic effect (TTT) through decreasing the viral shedding 44 titres (loNC 0 ), mortality rate, and severity of clinical signs and post mortem lesions, in 45 addition to serum malondialdhyde (MDA) level. Regarding the other viruses, the EOs 46 mixture did not improve the immune response to the AI and IB vaccines but age (2108±341.05). The studied EOs mixture showed an immune stimulating response 49 to ND and IBD vaccines, antiviral effect against ND virus especially if administered 50 before the challenge, however it did not have a growth promoting effect. 51 52

SOLUTION: Journal Pre-proof Effect of essential oils on the immune response to some viral vaccines in broiler chickens, with special reference to Newcastle disease virus Effect of essential oils on the immune response to some viral vaccines in broiler 3 chickens, with special reference to Newcastle disease virus 4

PROBLEM: Porcine reproductive and respiratory syndrome virus (PRRSV) is not only a poor inducer of type I interferon but also inhibits the efficient induction of type I interferon by porcine transmissible gastroenteritis virus (TGEV) and synthetic dsRNA molecules, Poly I:C. However, the mechanistic basis by which PRRSV interferes with the induction of type I interferon in its natural host cells remains less well defined. The purposes of this review are to summarize the key findings in supporting the post-transcriptional control of type I interferon in its natural host cells and to propose the possible role of translational control in the regulation of type I interferon induction by PRRSV.

SOLUTION:
Post-Transcriptional Control of Type I Interferon Induction by Porcine Reproductive and Respiratory Syndrome Virus in Its Natural Host Cells