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]: Viruses use a limited set of host pathways for infection. These pathways represent bona fide antiviral targets with low likelihood of viral resistance. We identified the salicylanilide niclosamide as a broad range antiviral agent targeting acidified endosomes. Niclosamide is approved for human use against helminthic infections, and has anti-neoplastic and antiviral effects. Its mode of action is unknown. Here, we show that niclosamide, which is a weak lipophilic acid inhibited infection with pH-dependent human rhinoviruses (HRV) and influenza virus. Structure-activity studies showed that antiviral efficacy and endolysosomal pH neutralization co-tracked, and acidification of the extracellular medium bypassed the virus entry block. Niclosamide did not affect the vacuolar H + -ATPase, but neutralized coated vesicles or synthetic liposomes, indicating a proton carrier mode-of-action independent of any protein target. This report demonstrates that physico-chemical interference with host pathways has broad range antiviral effects, and provides a proof of concept for the development of host-directed antivirals.
[A]: Niclosamide Is a Proton Carrier and Targets Acidic Endosomes with Broad Antiviral Effects


[Q]: Human parainfluenza viruses (HPIVs) are common causes of severe pediatric respiratory viral disease. We characterized wild-type HPIV2 infection in an in vitro model of human airway epithelium (HAE) and found that the virus replicates to high titer, sheds apically, targets ciliated cells, and induces minimal cytopathology. Replication of an experimental, live attenuated HPIV2 vaccine strain, containing both temperature sensitive (ts) and non-ts attenuating mutations, was restricted >30-fold compared to rHPIV2-WT in HAE at 32°C and exhibited little productive replication at 37°C. This restriction paralleled attenuation in the upper and lower respiratory tract of African green monkeys, supporting the HAE model as an appropriate and convenient system for characterizing HPIV2 vaccine candidates.
[A]: Growth restriction of an experimental live attenuated human parainfluenza virus type 2 vaccine in human ciliated airway epithelium in vitro parallels attenuation in African green monkeys


[Q]: The present study was undertaken to evaluate chikungunya virus (CHIKV) proteins for RNAi suppressor activity. We systematically analyzed all nine CHIKV proteins for RNAi suppressor activity using Sf21 RNAi sensor cell line based assay. Two non-structural proteins, namely, nsP2 and nsP3 were found to exhibit RNAi suppressor activity. We further validated the findings in natural hosts, namely in Aedes and in mammalian cell lines and further through EMSA and Agrobacterium infiltration in GFP silenced transgenic tobacco plants. Domains responsible for maximum RNAi suppressor activity were also identified within these proteins. RNA binding motifs in these domains were identified and their participation in RNAi suppression evaluated using site directed mutagenesis. Sequence alignment of these motifs across all species of known alphaviruses revealed conservation of these motifs emphasizing on a similar role of action in other species of alphaviruses as well. Further validation of RNAi suppressor activity of these proteins awaits establishment of specific virus infection models. RNA interference (RNAi) is a conserved evolutionary mechanism designed to impart an antiviral defence system across organisms ranging from plants, fungi, arthropods and nematodes 1-4 . The phenomenon, triggered by the production of double stranded RNA (dsRNA) by the pathogen upon infection, leads to the activation of the RNA interference silencing complex (RISC) by loading of dsRNA/siRNA into the complex ultimately leading to cleavage of the viral RNA 5,6,7 . Several components of RISC participate in the cleavage, most important being ribonuclease III Dicer (DCR) and Argonaute protein (AGO). Dicer acts on dsRNA to generate small RNA (sRNA) that are loaded into the AGO, resulting in cleavage 8,9 ; however, some RNAi pathways are independent of Dicer and other components like RNA-dependent RNA polymerase (RdRP) produce short RNA transcripts that directly bind to AGO 10 . Similarly, much is now known about the Piwi pathway that is specifically active in the germline 11 . In response to RNAi in plants and insects, viruses infecting these systems utilise some of their own proteins/sequence elements that counteract the antiviral RNAi pathway 12 . These viral suppressors of RNAi (VSRs) act through different mechanisms, either by binding to long dsRNA and protecting them from Dicer 7,13 or short RNAs 14 or through multi-mode mechanisms 15,16 . Recently it has been shown that some viruses encode host-specific VSRs due to co-evolution of the virus and the host, emphasising on the importance of analysing suppressor activity in relevant host 17 . Amongst medically important pathogenic viruses, arboviruses form an important subset of viruses due to the complexity of their host preferences 18 . These viruses, mainly constituted by genera flavivirus and alphavirus,
[A]:
Analysis of chikungunya virus proteins reveals that non-structural proteins nsP2 and nsP3 exhibit RNA interference (RNAi) suppressor activity OPEN