The Unexpected Impact of Vaccines on Secondary Bacterial Infections Following Influenza

Smith, Amber M.; Huber, Victor C.

doi:10.1089/vim.2017.0138

Cited by 29 publications

(26 citation statements)

References 263 publications

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“…The models assume all individuals in the population have identical immunity generated by exposure to influenza in the past. They will also need to taking into account the prior immune history to influenza infection that may lead to mild and/or asymptomatic infections, mild infection as a result of the vaccination and effect of influenza vaccine on secondary bacterial infections [ 58 – 61 ]. Finally, we have assumed that there is no inherent fitness difference in the two strains (in the absence of immunity) and need to consider the process of generation of variation and how vaccination can change the tempo of antigenic evolution which has been considered in a recent paper [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

Intermediate levels of vaccination coverage may minimize seasonal influenza outbreaks

et al. 2018

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For most pathogens, vaccination reduces the spread of the infection and total number of cases; thus, public policy usually advocates maximizing vaccination coverage. We use simple mathematical models to explore how this may be different for pathogens, such as influenza, which exhibit strain variation. Our models predict that the total number of seasonal influenza infections is minimized at an intermediate (rather than maximal) level of vaccination, and, somewhat counter-intuitively, further increasing the level of the vaccination coverage may lead to higher number of influenza infections and be detrimental to the public interest. This arises due to the combined effects of: competition between multiple co-circulating strains; limited breadth of protection afforded by the vaccine; and short-term strain-transcending immunity following natural infection. The study highlights the need for better quantification of the components of vaccine efficacy and longevity of strain-transcending cross-immunity in order to generate nuanced recommendations for influenza vaccine coverage levels.

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Section: Discussionmentioning

confidence: 99%

Intermediate levels of vaccination coverage may minimize seasonal influenza outbreaks

et al. 2018

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“…Throughout influenza virus infection, epithelial cells are infected and die, and inflammation accumulates as host immune responses work to halt virus spread. As lung tissue becomes injured and the host immune response weakens, bacterial pathogens readily invade and cause pneumonia . Heightened lethality occurs when bacteria invade during the virus resolution phase with the maximum synergistic effect at 7 days post‐influenza …”

Section: Influenza‐bacteria Coinfection Kineticsmentioning

confidence: 99%

“…As lung tissue becomes injured and the host immune response weakens, bacterial pathogens readily invade and cause pneumonia. 3,4,[6][7][8][9][10]124 Heightened lethality occurs when bacteria invade during the virus resolution phase with the maximum synergistic effect at 7 days post-influenza. 112 Following bacterial infection, viral loads rebound and bacterial titers increase to high levels within ~24 hours (Figure 4).…”

Section: Host-pathogen Regulation During Influenzapneumococcal Coinmentioning

confidence: 99%

Host‐pathogen kinetics during influenza infection and coinfection: insights from predictive modeling

Smith

2018

Immunological Reviews

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SummaryInfluenza virus infections are a leading cause of morbidity and mortality worldwide. This is due in part to the continual emergence of new viral variants and to synergistic interactions with other viruses and bacteria. There is a lack of understanding about how host responses work to control the infection and how other pathogens capitalize on the altered immune state. The complexity of multi‐pathogen infections makes dissecting contributing mechanisms, which may be non‐linear and occur on different time scales, challenging. Fortunately, mathematical models have been able to uncover infection control mechanisms, establish regulatory feedbacks, connect mechanisms across time scales, and determine the processes that dictate different disease outcomes. These models have tested existing hypotheses and generated new hypotheses, some of which have been subsequently tested and validated in the laboratory. They have been particularly a key in studying influenza‐bacteria coinfections and will be undoubtedly be useful in examining the interplay between influenza virus and other viruses. Here, I review recent advances in modeling influenza‐related infections, the novel biological insight that has been gained through modeling, the importance of model‐driven experimental design, and future directions of the field.

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“…The discovery of antibiotics and the development of influenza and bacterial vaccines have significantly reduced the chances of recurrence of catastrophic pandemics like the Spanish influenza of 1918 [102]. However, influenza and other respiratory viruses remain among the main causes of bacterial complications and of CAP.…”

Section: Resultsmentioning

confidence: 99%

The problem of bacterial complications post respiratory viral infections

Egorov

2018

Microbiology Independent Research Journal (MIR Journal)

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Every person over the course of their lifetime is repeatedly infected by a variety of respiratory viruses that represent risk factors for the development of bacterial complications. The most dangerous among the etiological factors of acute respiratory viral diseases is the influenza A virus. This virus is capable of causing catastrophic pandemics with high mortality mainly due to secondary bacterial pneumonia. As has been shown in numerous recent studies, the main mechanism of provoking bacterial infections irrespective of the type of respiratory virus is the imbalanced response of the antiviral innate immunity -excessive interferon response and uncontrolled inflammation. The probability of severe bacterial complications in the course of acute respiratory viral infections is determined by both the virulence of the virus itself and by the composition of the respiratory microbiota at the time of the viral infection as well as by the genetic characteristics of the organism. The occurrence of severe bacterial complications is also affected by the chronic diseases that have an impact on the regulation of the innate immune response. This review summarizes the current concept of the mechanisms of the development of post viral bacterial complications as well as the potential prevention strategies for these complications.

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The Unexpected Impact of Vaccines on Secondary Bacterial Infections Following Influenza

Cited by 29 publications

References 263 publications

Intermediate levels of vaccination coverage may minimize seasonal influenza outbreaks

Intermediate levels of vaccination coverage may minimize seasonal influenza outbreaks

Host‐pathogen kinetics during influenza infection and coinfection: insights from predictive modeling

The problem of bacterial complications post respiratory viral infections

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