In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

Input: Consider Input: Paragraph: Introduction-HIV-1 uses a programmed -1 ribosomal frameshift to generate Gag-Pol, the precursor of its enzymes, when its full-length mRNA is translated by the ribosomes of the infected cells. This change in the reading frame occurs at a so-called slippery sequence that is followed by a specific secondary structure, the frameshift stimulatory signal. This signal controls the frameshift efficiency. The synthesis of HIV-1 enzymes is critical for the virus replication and therefore, the -1 ribosomal frameshift could be the target of novel antiviral drugs. Areas covered-This review examines various approaches used to select drugs interfering with the -1 frameshift of HIV-1. These include the selection and modification of chemical compounds that specifically bind to the frameshift stimulatory signal, the use of antisense oligonucleotides targeting this signal and the selection of compounds that modulate HIV-1 frameshift, by using bicistronic reporters where the expression of the second cistron depends upon HIV-1 frameshift. Expert opinion-The most promising approach is the selection and modification of compounds specifically targeting HIV-1 frameshift stimulatory signal. The use of antisense oligonucleotides binding to the frameshift stimulatory signal is still questionable. The use of bicistronic reporters preferentially selects compounds that modulate the frameshift by targeting the ribosomes, which is less promising. 
 Title: Targeting frameshifting in the human immunodeficiency virus

Output: True


Input: Consider Input: Paragraph: Data are limited regarding 2 new human polyomaviruses, KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV), in immunocompromised patients. We used realtime PCR to test for these and 12 respiratory viruses in 2,732 nasal wash samples collected during the fi rst year after allogeneic hematopoietic cell transplantation from 222 patients. Specimens were collected weekly until day 100; then at least every 3 months. One year after hematopoietic cell transplantation, the cumulative incidence estimate was 26% for KIPyV and 8% for WUPyV. Age <20 years predicted detection of KIPyV (hazard ratio [HR] 4.6) and WUPyV (HR 4.4), and detection of a respiratory virus in the previous 2 weeks predicted KIPyV detection (HR 3.4). Sputum production and wheezing were associated with detection of KIPyV in the past week and WUPyV in the past month. There were no associations with polyomavirus detection and acute graft versus host disease, cytomegalovirus reactivation, neutropenia, lymphopenia, hospitalization, or death. 
 Title: WU and KI Polyomaviruses in Respiratory Samples from Allogeneic Hematopoietic Cell Transplant Recipients

Output: False


Input: Consider Input: Paragraph: Restriction factors are antiviral components of intrinsic immunity which constitute a first line of defense by blocking different steps of the human immunodeficiency virus (HIV) replication cycle. In immune cells, HIV infection is also sensed by several pattern recognition receptors (PRRs), leading to type I interferon (IFN-I) and inflammatory cytokines production that upregulate antiviral interferon-stimulated genes (ISGs). Several studies suggest a link between these two types of immunity. Indeed, restriction factors, that are generally interferon-inducible, are able to modulate immune responses. This review highlights recent knowledge of the interplay between restriction factors and immunity inducing antiviral defenses. Counteraction of this intrinsic and innate immunity by HIV viral proteins will also be discussed. of PAMPs by PRRs induces signaling cascades and leads to the transcription of pro-inflammatory cytokines and type I interferons (IFN-I), the most powerful antiviral effectors. Once produced by cells in which PRRs have been activated, IFN-I are secreted and bind, in an autocrine or paracrine manner, to the membrane receptor IFNAR (IFN-α/β receptor chain) to induce signal transduction driving the transcription of interferon-stimulated genes (ISGs). There are hundreds of ISGs encoding antiviral proteins such as the protein kinase R (PKR) or the 2 -5 -oligoadenylate synthetase 1 (OAS1) [13, 14] . Thus, ISGs are crucial to switch cells into an antiviral state. Interestingly, even if HIV restriction factors have been described as intrinsic immune effectors, most of them are IFN-inducible and can be defined as ISGs linking intrinsic and innate immunity. Moreover, by exerting their antiviral functions or by additional pathways, some restriction factors have been described to shape innate and adaptive immune responses highlighting an intimate relationship between restriction factors and immunity [15, 16] . In this review, we summarize the recent knowledge of the interplay between restriction factors and immunity focusing only on restriction factors that belong to the ISG family. After a description of restriction factors antiviral mechanisms and their induction by IFN, we will discuss how they can modulate immunity, in particular, innate immune responses. Moreover, since HIV-1 proteins are able to counteract many restriction factors, we will also mention viral mechanisms used to escape from intrinsic and innate immunity. Taken together, this review will allow a better understanding of the intricate interplay between restriction factors-mediated intrinsic immunity and innate immunity. 
 Title: cells Interplay between Intrinsic and Innate Immunity during HIV Infection


Output: False