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".

Ex Input:
Paragraph: Interferon-induced transmembrane proteins (IFITMs) have been recognized as important antiviral effectors of the innate immune system, both in cell culture and in infected humans. In particular, polymorphisms of the human IFITM3 gene have been shown to affect disease severity and progression in influenza A virus (FLUAV) and human immunodeficiency virus (HIV) infection, respectively. Rhesus macaques (Macaca mulatta) are commonly used to model human infections and the experimental inoculation of these animals with simian immunodeficiency virus (SIV) is one of the best models for HIV/AIDS in humans. However, information on the role of IFITM3 in SIV infection of rhesus macaques is currently lacking. We show that rhesus macaque (rh) IFITM3 inhibits SIV and FLUAV entry in cell culture, although with moderately reduced efficiency as compared to its human counterpart. We further report the identification of 16 polymorphisms in the rhIFITM3 gene, three of which were exonic and synonymous while the remainder was located in non-coding regions. Employing previously characterized samples from two cohorts of SIV-infected rhesus macaques, we investigated the relationship between these rhIFITM3 polymorphisms and both AIDS-free survival time and virus load. In cohort 1, several intronic polymorphisms were significantly associated with virus load or survival. However, an association with both parameters was not observed and significance was lost in most cases when animals were stratified for the presence of MHC allele Mamu-A1*001. Moreover, no significant genotype-phenotype associations were detected in cohort 2. These results suggest that, although IFITM3 can inhibit SIV infection in cell culture, genetic variation in rhIFITM3 might have only a minor impact on the course of SIV infection in experimentally infected animals.
Title: Rhesus macaque IFITM3 gene polymorphisms and SIV infection

Ex Output:
False

Ex Input:
Paragraph: Coronaviruses (CoVs) are positive-sense single-stranded RNA viruses and contain the largest known RNA genomes, ranging from 27 to 32 kilobases in length. CoVs are capable of transspecies movement as evidenced by the Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) epidemic in 2002-2003 [1,2]. Additionally, the emergence of Middle East Respiratory Syndrome coronavirus (MERS-CoV) in 2012 demonstrates that CoVs continue to cause severe and lethal human disease [3] . Exactly how CoVs maintain the integrity of their large genomes while generating the population diversity required for emergence and adaptation has been a major question in RNA virology. The discovery of 39-to-59 exoribonuclease (ExoN) activity within CoV nonstructural protein 14 (nsp14-ExoN), which is critical for CoV high-fidelity replication, has challenged the long-held paradigm that RNA viruses cannot proofread and raises the possibility of an entirely new model for how RNA viruses regulate replication fidelity. We will summarize: 1) the data supporting proofreading during CoV replication; 2) the possibility of a multi-protein fidelity complex, using E. coli DNA polymerase III as a conceptual framework; and 3) the promise of genetic and therapeutic interference with fidelity regulation as an approach for attenuation and treatment of CoVs.
Title: Coronaviruses as DNA Wannabes: A New Model for the Regulation of RNA Virus Replication Fidelity

Ex Output:
True

Ex Input:
Paragraph: Evolution of coronaviruses is facilitated by the strong selection, large population size, and great genetic diversity within the susceptible hosts. This predisposition is primarily due to high error rate, and limited proofreading capability of the viral polymerase and by recombination. These characteristics make coronaviruses an interesting model system to study the mechanisms involved in viral evolution and the ways viruses adapt to switch host or to gain novel functions. Here we describe the protocol to estimate selection pressures for the spike gene and evolutionary dynamics of bovine coronaviruses.
Title: Chapter 4 Estimation of Evolutionary Dynamics and Selection Pressure in Coronaviruses

Ex Output:
True