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.

Example Input: Over the past several decades, significant advances have been made in identifying factors that contribute to the pathogenesis of multiple sclerosis (MS) and have culminated in the approval of some effective therapeutic strategies for disease intervention. However, the mechanisms by which environmental factors, such as infection, contribute to the pathogenesis and/or symptom exacerbation remain to be fully elucidated. Relapse frequency in MS patients contributes to neurological impairment and, in the initial phases of disease, serves as a predictor of poor disease prognosis. The purpose of this review is to examine the evidence that supports a role for peripheral infection in modulating the natural history of this disease. Evidence supporting a role for infection in promoting exacerbation in animal models of MS is also reviewed. Finally, a few mechanisms by which infection may exacerbate symptoms of MS and other neurological diseases are discussed. Those who comprise the majority of MS patients acquire approximately two upper-respiratory infections per year; furthermore, this type of infection doubles the risk for MS relapse, underscoring the contribution of this relationship as being potentially important and particularly detrimental.
Example Output: infection as an environmental trigger of multiple sclerosis disease exacerbation

Example Input: Recent years have seen several advances in our understanding of immunity to virus infection of the lower respiratory tract, including to influenza virus infection. Here, we review the cellular targets of viruses and the features of the host immune response that are unique to the lungs. We describe the interplay between innate and adaptive immune cells in the induction, expression and control of antiviral immunity, and discuss the impact of the infected lung milieu on moulding the response of antiviral effector T cells. Recent findings on the mechanisms that underlie the increased frequency of severe pulmonary bacterial infections following respiratory virus infection are also discussed. Viruses are highly evolved and ubiquitous pathogens. Although infection with many viruses results in a mild, self-limited disease, other viruses can produce severe and frequently fatal infections. The respiratory tract is a major portal through which viruses enter to initiate infection. Whereas some viruses can initiate infection in the respiratory tract and then disseminate to other sites in the body, other viruses typically remain localized to the respiratory tract, where they replicate and induce tissue injury (see Supplementary information S1 (table)). Various defence mechanisms have evolved in the respiratory tract to prevent and control infection by viruses and other pathogens. The respiratory tract can be divided anatomically into the upper respiratory tract (including the nose, mouth and pharynx) and the lower respiratory tract (which consists of the trachea, bronchi and lungs), with the lymphoid tissue of Waldeyer's ring (including the pharyngeal and palatine tonsils) representing the line of demarcation. Because of the crucial role of the lower respiratory tract in respiration, we limit the focus of this Review to recent advances in our understanding of the host immune response to virus infection at this site.
Example Output: Regulating the adaptive immune response to respiratory virus infection NIH Public Access

Example Input: Facing the threats of infectious diseases, we take various actions to protect ourselves, but few studies considered an evolving system with competing strategies. In view of that, we propose an evolutionary epidemic model coupled with human behaviors, where individuals have three strategies: vaccination, self-protection and laissez faire, and could adjust their strategies according to their neighbors' strategies and payoffs at the beginning of each new season of epidemic spreading. We found a counter-intuitive phenomenon analogous to the well-known Braess's Paradox, namely a better condition may lead to worse performance. Specifically speaking, increasing the successful rate of self-protection does not necessarily reduce the epidemic size or improve the system payoff. The range and degree of the Braess's Paradox are sensitive to both the parameters characterizing the epidemic spreading and the strategy payoff, while the existence of the Braess's Paradox is insensitive to the network topologies. This phenomenon can be well explained by a mean-field approximation. Our study demonstrates an important fact that a better condition for individuals may yield a worse outcome for the society.
Example Output:
Braess's Paradox in Epidemic Game: Better Condition Results in Less Payoff