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.

Q: Recently, AdvanSure™️ kit based on multiplex real-time PCR was developed for simultaneous detection of 14 respiratory viruses (RVs). We compared the performance of AdvanSure with those of Seeplex®️ RV 15 ACE and culture by determining their sensitivities and specificities against a composite reference standard. Four hundred thirty-seven respiratory samples were tested by modified shell vial culture method, RV 15 ACE, and AdvanSure. One hundred fourteen samples (26.2%) out of 437 samples were positive by culture, while additional 91 (20.8%) were positive by AdvanSure or RV15. One hundred twelve of 114 culture-positive samples were positive by AdvanSure except 2 samples (1 adenovirus, 1 respiratory syncytial virus [RSV]). Overall, the sensitivities of culture, RV15, and AdvanSure were 74.5%, 89.8%, and 95.1%, respectively. Sensitivities of culture, RV15, and AdvanSure for each virus tested were as follows: 91/100/96% for influenza A, 60/0/100% for influenza B, 63/95/97% for RSV, 69/81/89% for adenovirus, and 87/93/93% for parainfluenza virus. For viruses not covered by culture, sensitivities of RV15 and AdvanSure were as follows: 77/88% for rhinovirus, 100/100% for coronavirus OC43, 40/100% for coronavirus 229E/NL63, 13/100% for metapneumovirus, and 44/100% for bocavirus. The overall specificities of culture, RV15, and AdvanSure were 100/98.9/ 99.5%, respectively. Of 45 coinfected specimens, AdvanSure detected 41 specimens (91.1%) as coinfected, while RV15 detected 27 specimens (60.0%) as coinfected. AdvanSure assay demonstrated exquisite performance for the detection of RVs and will be a valuable tool for the management of RV infection.

A: Evaluation of the AdvanSure™️ real-time RT-PCR compared with culture and Seeplex RV15 for simultaneous detection of respiratory viruses
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Q: 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.

A: HIV-1 tolerates changes in A-count in a small segment of the pol gene
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Q: Enterovirus (EV) 71 infection is known to cause hand-foot-and-mouth disease (HFMD) and in severe cases, induces neurological disorders culminating in fatality. An outbreak of EV71 in South East Asia in 1997 affected over 120,000 people and caused neurological disorders in a few individuals. The control of EV71 infection through public health interventions remains minimal and treatments are only symptomatic. Recently, human scavenger receptor class B, member 2 (SCARB2) has been reported to be a cellular receptor of EV71. We expressed human SCARB2 gene in NIH3T3 cells (3T3-SCARB2) to study the mechanisms of EV71 entry and infection. We demonstrated that human SCARB2 serves as a cellular receptor for EV71 entry. Disruption of expression of SCARB2 using siRNAs can interfere EV71 infection and subsequent inhibit the expression of viral capsid proteins in RD and 3T3-SCARB2 but not Vero cells. SiRNAs specific to clathrin or dynamin or chemical inhibitor of clathrin-mediated endocytosis were all capable of interfering with the entry of EV71 into 3T3-SCARB2 cells. On the other hand, caveolin specific siRNA or inhibitors of caveolae-mediated endocytosis had no effect, confirming that only clathrin-mediated pathway was involved in EV71 infection. Endocytosis of EV71 was also found to be pHdependent requiring endosomal acidification and also required intact membrane cholesterol. In summary, the mechanism of EV71 entry through SCARB2 as the receptor for attachment, and its cellular entry is through a clathrin-mediated and pHdependent endocytic pathway. This study on the receptor and endocytic mechanisms of EV71 infection is useful for the development of effective medications and prophylactic treatment against the enterovirus.

A:
Human SCARB2-Mediated Entry and Endocytosis of EV71
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