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]: Background: While it is known that acute respiratory illness (ARI) is caused by an array of viruses, less is known about co-detections and the resultant comparative symptoms and illness burden. This study examined the co-detections, the distribution of viruses, symptoms, and illness burden associated with ARI between December 2012 and March 2013. Methods: Outpatients with ARI were assayed for presence of 18 viruses using multiplex reverse transcriptase polymerase chain reaction (MRT-PCR) to simultaneously detect multiple viruses. Results: Among 935 patients, 60% tested positive for a single virus, 9% tested positive for ≥1 virus and 287 (31%) tested negative. Among children (<18 years), the respective distributions were 63%, 14%, and 23%; whereas for younger adults (18-49 years), the distributions were 58%, 8%, and 34% and for older adults (≥50 years) the distributions were 61%, 5%, and 32% (P < 0.001). Co-detections were more common in children than older adults (P = 0.01), and less frequent in households without children (P = 0.003). Most frequently co-detected viruses were coronavirus, respiratory syncytial virus, and influenza A virus. Compared with single viral infections, those with co-detections less frequently reported sore throat (P = 0.01), missed fewer days of school (1.1 vs. 2 days; P = 0.04), or work (2 vs. 3 days; P = 0.03); other measures of illness severity did not vary. Conclusions: Among outpatients with ARI, 69% of visits were associated with a viral etiology. Co-detections of specific clusters of viruses were observed in 9% of ARI cases particularly in children, were less frequent in households without children, and were less symptomatic (e.g., lower fever) than single infections.
[A]: influenza season


[Q]: In this paper, we analyze a delayed SEIR epidemic model in which the latent and infected states are infective. The model has a globally asymptotically stable disease-free equilibrium whenever a certain epidemiological threshold, known as the basic reproduction number R 0 , is less than or equal to unity. We investigate the effect of the time delay on the stability of endemic equilibrium when R 0 > 1. We give criteria that ensure that endemic equilibrium is asymptotically stable for all time delays and a Hopf bifurcation occurs as time delay exceeds the critical value. We give formulae for the direction of Hopf bifurcations and the stability of bifurcated periodic solutions by applying the normal form theory and the center manifold reduction for functional differential equations. Numerical simulations are presented to illustrate the analytical results.
[A]: Hopf bifurcation analysis of a delayed SEIR epidemic model with infectious force in latent and infected period


[Q]: Background H3N2 influenza viruses circulating in humans and European pigs originate from the pandemic A/Hong Kong/68 virus. Because of slower antigenic drift in swine, the antigenic divergence between swine and human viruses has been increasing. It remains unknown to what extent this results in a reduced cross-protection between recent human and swine H3N2 influenza viruses. Objectives We examined whether prior infection of pigs with an old [A/Victoria/3/75 (A/Vic/75)] or a more recent [A/Wisconsin/67/ 05 (A/Wis/05)] human H3N2 virus protected against a European swine H3N2 virus [sw/Gent/172/08 (sw/Gent/08)]. Genetic and antigenic relationships between sw/Gent/08 and a selection of human H3N2 viruses were also assessed. Results After challenge with sw/Gent/08, all challenge controls had high virus titers in the entire respiratory tract at 3 days postchallenge and nasal virus excretion for 5-6 days. Prior infection with sw/Gent/08 or A/Vic/75 offered complete virological protection against challenge. Pigs previously inoculated with A/Wis/05 showed similar virus titers in the respiratory tract as challenge controls, but the mean duration of nasal shedding was 1Á3 days shorter. Unlike sw/Gent/08-and A/Vic/75-inoculated pigs, A/Wis/05-inoculated pigs lacked cross-reactive neutralizing antibodies against sw/Gent/08 before challenge, but they showed a more rapid antibody response to sw/Gent/08 than challenge controls after challenge. Cross-protection and serological responses correlated with genetic and antigenic differences. Conclusions Infection immunity to a recent human H3N2 virus confers minimal cross-protection against a European swine H3N2 virus. We discuss our findings with regard to the recent zoonotic infections of humans in the United States with a swine-origin H3N2 variant virus. Please cite this paper as: Qiu et al. (2013) Prior infection of pigs with a recent human H3N2 influenza virus confers minimal cross-protection against a European swine H3N2 virus.
[A]:
Prior infection of pigs with a recent human H3N2 influenza virus confers minimal cross-protection against a European swine H3N2 virus