Answer questions 1-5 using the following information. Jesse was infected with in
ID: 167889 • Letter: A
Question
Answer questions 1-5 using the following information.
Jesse was infected with influenza A for the first time while at school. She fully recovered. One year later she once again got infected with the same strain of influenza. How many days after the primary influenza infection began would you expect the influenza virus titer to start declining? Would you expect the influenza virus levels to exhibit different kinetics during the second infection? Explain why or why not. How many days after the primary influenza infection began would you expect lymphocytes to hit their maximal number? Explain How many days after the primary influenza infection began would you expert antibody class switching to occur? How would this be different during the secondary influenza infection? Explain. How many days after the primary infection would maximal I F N - alpha and beta produced? Explain How many days after the primary infection would neutrophils home to the site of infection? ExplainExplanation / Answer
1.In otherwise healthy adults, influenza virus shedding (the time during which a person might be infectious to another person) increases sharply one-half to one day after infection, peaks on day 2 and persists for an average total duration of 5 days—but can persist as long as 9 days. In those who develop symptoms from experimental infection (only 67% of healthy experimentally infected individuals), symptoms and viral shedding show a similar pattern, but with viral shedding preceding illness by one day. Children are much more infectious than adults and shed virus from just before they develop symptoms until two weeks after infection. In immunocompromised people, viral shedding can continue for longer than two weeks.Mutations leading to resistant virus typically have an associated fitness cost such that either virus production (p) is lowered or the infection rate () is lowered.To reduce the effects that drug-resistant mutations have on viral dynamics during treatment, combination therapy can be used.
2.Cytotoxic T lymphocytes were not detected until 6 to 14 DPI and disappeared by day 21.Both the cytotoxic T-lymphocyte-mediated and the antibody-mediated immune responses tend to be detected after peak viral replication.
4. Interferons (IFNs), particularly of type I (IFN-/), tumor necrosis factor alpha, and other cytokines, such as interleukin-6, become elevated early after infection. Type I IFNs are produced by infected epithelial cells and other host cells, such as macrophages, monocytes, and dendritic cells, in response to the presence of viral double-stranded RNA . High IFN titers are detected 1 day after virus shedding begins and generally peak simultaneously with, or up to 1 day after, virus titer peak.
5.Increased viral replication, increased numbers of alveolar macrophages (AMs) and neutrophils, and elevated cytokines and chemokines have all been associated with influenza lethality. Macrophages and neutrophils are recruited to the airways by cytokines and chemokines in order to ingest and kill bacteria.At days 3 – 7 days post-influenza infection, enhanced neutrophil recruitment was seen with secondary bacterial challenge. At weeks 2 – 6 post-influenza infection, bacterial super-infection resulted in lower numbers of neutrophils recruited to the co-infected airways, which was associated with sustained desensitization of alveolar macrophages to bacterial toll-like receptor ligands.