Overweight and obese adult humans have a defective cellular immune response to pandemic H1N1 Influenza a virus

Paich, Heather A.; Sheridan, Patricia A.; Handy, Jean; Karlsson, Erik A.; Schultz‐Cherry, Stacey; Hudgens, Michael G.; Noah, Terry L.; Weir, Samuel S.; Beck, Melinda A.

doi:10.1002/oby.20383

Cited by 160 publications

(150 citation statements)

References 24 publications

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“…Recently, two human studies have supported this hypothesis and observed inhibited T cell activation and expression in IAV-vaccinated obese individuals [69, 74]. In one study [69], peripheral blood mononuclear cells (PBMCs) were obtained from obese subjects 12 months after immunization with the 2010–2011 seasonal IAV vaccine.…”

Section: Influenza a Virus (Iav)mentioning

confidence: 99%

The weight of obesity on the human immune response to vaccination

Painter

Ovsyannikova

Poland

2015

Vaccine

164

130

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Despite the high success of protection against several infectious diseases through effective vaccines, some sub-populations have been observed to respond poorly to vaccines, putting them at increased risk for vaccine-preventable diseases. In particular, the limited data concerning the effect of obesity on vaccine immunogenicity and efficacy suggests that obesity is a factor that increases the likelihood of a poor vaccine-induced immune response. Obesity occurs through the deposition of excess lipids into adipose tissue through the production of adipocytes, and is defined as a body-mass index (BMI) ≥ 30 kg/m2. The immune system is adversely affected by obesity, and these “immune consequences” raise concern for the lack of vaccine-induced immunity in the obese patient requiring discussion of how this sub-population might be better protected.

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Section: Influenza a Virus (Iav)mentioning

confidence: 99%

The weight of obesity on the human immune response to vaccination

Painter

Ovsyannikova

Poland

2015

Vaccine

164

130

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“…Furthermore, the evidence that macrophage phagocytic activity was impaired in obese mouse models indicated that innate immunity is defective in obesity (56,57). T cells (86). Thus, defects of CD4+ T cells impact on antibody production by B cells.…”

Section: Characterizations Of Related Immune Cells In Obesity Macrophagementioning

confidence: 99%

Is Obesity One of Physiological Factors which Exert Influenza Virus-induced Pathology and Vaccine Efficacy?

Cho

Nam

2014

J Bacteriol Virol

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Obesity has been considered a risk factor for infectious diseases including the influenza virus. Most epidemiological investigations indicated that obesity is connected to the severity of influenza, although there are some exceptions. Many studies using obese humans and animal models showed that immune response was impaired in the obese group, increasing susceptibility and severity of influenza virus. However, the exact mechanism by which obesity inhibits anti-viral immune response remains unknown. This review discusses current studies about the properties of immune cells in obesity. In obesity, the balance of adipokines is disrupted and the level of proinflammatory cytokine is increased compared with non-obese control. Moreover, macrophages induced systemic inflammation by secreting cytokines such as TNF-α and IL-6, antigen presenting capacity of dendritic cells was diminished which affect T cell responses, and influenza-specific antibody production seems reduced and decreased even faster after vaccination in obese mouse. The number of circulating T cells and proliferation of mitogen-stimulated T cells dropped and T cell memory was significantly low in influenza infected obese mouse. Therefore, obesity may be one of factors for disease progression in influenza virus infection and vaccine efficacy.

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“…Obesity: Obesity has commonly been reported in ICU submissions and patients dying from pdm(H1N1)09 [6,11,12,[15][16][17][18] and has been identified as a predictor of outcome in acute respiratory infection [19], possibly as a consequence of a defective cellular immune response to infection [20]. Of those admitted to an ICU in Australia and New Zealand in 2009, 28.6% (of which data was available) had a BMI of 35 kg/m 2 or greater [12].…”

Section: Factors Associated With Death or Hospitalisationmentioning

confidence: 99%

Risk Factors Associated with Severe Clinical Outcomes of Pandemic H1N1 Infection

Fullen¹

2014

JHVRV

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The clinical outcome of pandemic H1N1 influenza infection is dependent on the interplay of virus and host factors. Influenza virus infections can range from relatively mild infections of the upper respiratory tract to fatal disease of the lower respiratory tract. A range of host factors play a role in the severity of clinical disease in pdm(H1N1)09 infection. With the exception of neonates age was directly proportional to the severity of clinical outcome; obesity, COPD and pregnancy play a key role in clinical outcome of infection. An important determinant in the pathogenesis of influenza infection is the tissue tropism of the influenza virus. The D222G and D222N mutations of pdm(H1N1)09 influenza appear to have an increased tropism for the tissues of the lower respiratory tract and are disproportionally associated with severe clinical disease. These α2-3 salicylic acid tropic mutations, which have been associated with fatal cases of influenza infection, have also been preferentially selected for during sequential passage in embryonated eggs and viruses of avian origin. KeywordsInfluenza; Pandemic; H1N1; pdm(H1N1)09; Oseltamivir IntroductionThe current H1N1 influenza vaccine strain A/ California/7/2009 has a surprisingly high no detectable antibody (NDA) rate of approximately 52% in a population of 200 subjects screened (unpublished data). Studies have shown that the A/California/7/2009 strain of pandemic H1N1 influenza causes alveolar haemorrhage in the ferret model [1,2]; similar "swine flu" viruses A/Mexico/4482/2009 and A/ Netherlands/602/2009 also presented severe pathology in the ferret model [3,4]. As a consequence it is clear that infection with this group of viruses represents a significant risk of a severe clinical outcome. Furthermore, the severe symptoms that are associated with a subset of A/California/7/2009 infections are atypical for previous seasonal influenza infections. Co-morbidities and their impact on clinical outcome of infectionThe clinical outcomes of infection by pdm(H1N1)09 are considerably affected by one or more host factors and comorbidities. Here we discuss these co-morbidities and the impact that they have on clinical consequences to infection. Case fatality ratiosBy July 2009 63,479 cases of influenza like illness were reported in Mexico; of these cases 11% (6,945) were confirmed as H1N1 influenza; 92% of confirmed positive cases (6,407) were treated as outpatients, 7% (475) were admitted to hospital and survived and <1% died (63) [5]. During the early phase of the pandemic the case fatality ratio (CFR) was calculated to be approximately 0.4-0.6% [6]. In the UK an estimated 540,000 people had symptomatic H1N1 infection during a study period with a CFR of (0.026%) 26 deaths per 100,000 [7]. There is little published information for the CFRs of seasonal H1N1 or H3N2 influenza. However using data from the Health Protection Agency (HPA) we were able to determine the CFR for influenza infections admitted to intensive care units (ICU). 2/7 SymptomsA meta-analysis of H1N1...

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Overweight and obese adult humans have a defective cellular immune response to pandemic H1N1 Influenza a virus

Cited by 160 publications

References 24 publications

The weight of obesity on the human immune response to vaccination

The weight of obesity on the human immune response to vaccination

Is Obesity One of Physiological Factors which Exert Influenza Virus-induced Pathology and Vaccine Efficacy?

Risk Factors Associated with Severe Clinical Outcomes of Pandemic H1N1 Infection

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