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.

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.
Hopf bifurcation analysis of a delayed SEIR epidemic model with infectious force in latent and infected period

In trial 1, phase 1, 48 male Holstein calves initially 2 to 4 d of age were transported 3.5 h to the research facility. Calves were randomly selected to either receive a s.c. injection of Zuprevo (Merck Animal Health, Summit, NJ; 4 mg of tildipirosin/kg of BW; TIL) the day after arrival (d 0) and again at weaning (d 42) or receive no injections (CON). Calves were fed 0.66 kg of milk replacer DM daily for 39 d and then 0.33 kg daily for 3 d. A starter was fed free choice for the 56 d of phase 1. In trial 1, phase 2, the same calves from phase 1 grouped by CON and TIL were moved to group pens (4 pens per treatment, 4 calves per pen) for the next 56 d. The starter was blended with 5% chopped grass hay and fed free choice. Trial 2 was similar to trial 1, phase 2 and used 48 two-month-old male Holstein calves. Calves were randomly selected to receive either a s.c. injection of Zuprevo (4 mg of tildipirosin/kg of BW; TIL) on d 0 or no injections (CON). In trial 1, phase 1, preweaning ADG and BCS change; postweaning starter intake and hip width change; overall starter intake, ADG, and hip width change; final hip width; and final BCS were greater for TIL than CON. During phase 2 of trial 1 and trial 2, calf ADG and hip width change were greater for TIL than CON. Overall, in transported Holstein calves, TIL improved ADG and structural growth by approximately 13%.
Case Study: Control of respiratory disease in male Holstein calves with tildipirosin and effect on health and growth from 0 to 4 months of age

Background: Interaction between immune system and Chandipura virus (CHPV) during different stages of its life cycle remain poorly understood. The exact route of virus entry into the blood and CNS invasion has not been clearly defined. The present study was undertaken to assess the population in PBMC that supports the growth of virus and to detect active virus replication in PBMC as well as its subsets. Methods: PBMC subsets viz.: CD3 + , CD14 + , CD19 + , CD56 + cells were separated and infected with CHPV. The infected cells were then assessed for transcription (N gene primer) and replication (NP gene primer) of CHPV by PCR. The supernatant collected from infected cells were titrated in Baby Hamster Kidney (BHK) cells to assess virus release. The cytokine and chemokine expression was quantified by flow cytometry. Results: Amplification of N and NP gene was detected in CD14 + (monocyte) and CD19 + (B cell), significant increase in virus titre was also observed in these subsets. It was observed that, although the levels of IL-6 and IL-10 were elevated in CD14 + cells as compared to CD19 + cells, the differences were not significant. However the levels of TNF and IL-8 were significantly elevated in CD14 + cells than in CD19 + cells. The levels of chemokine (CXCL9, CCL5, CCL2, CXCL10) were significantly elevated in CHPV infected PBMC as compared to uninfected cells. CCL2 and CXCL9 were significantly increased in CHPV infected CD14 + cells as compared to CD19 + cells. Conclusion: CD14 + and CD19 + cells support active replication of CHPV. High viral load was detected in CD14 + cells infected with CHPV hence it might be the primary target cells for active replication of CHPV. An elevated levels of cytokines and chemokines observed in CD14 + cells may help in predicting the pathogenecity of CHPV and possible entry into the central nervous system.
Monocytes and B cells support active replication of Chandipura virus