Mucosal IgG Levels Correlate Better with Respiratory Syncytial Virus Load and Inflammation than Plasma IgG Levels

Vissers, Marloes; Ahout, Inge M. L.; Jonge, Marien I. de; Ferwerda, Gerben

doi:10.1128/cvi.00590-15

Cited by 33 publications

(31 citation statements)

References 14 publications

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“…[43][44][45] Indeed, high titers of pre-existent mucosal IgG are correlated with reduced viral loads in hRSV-infected infants. 46 Similar correlation have been obtained for nasal IgA levels in naturally infection and in experimental challenges in healthy adults. 47,48 On the other hand, it has been described in mice that antibodies play a major role during reinfection, even more than in the first infection, giving a principal role to T cells in the clearance of the virus during the first hRSV challenge.…”

Section: The Humoral Response Against Hrsv Infectionsupporting

confidence: 65%

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

et al. 2016

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Human Respiratory syncytial virus (hRSV) and human metapneumovirus (hMPV) are the two major etiological viral agents of lower respiratory tract diseases, affecting mainly infants, young children and the elderly. Although the infection of both viruses trigger an antiviral immune response that mediate viral clearance and disease resolution in immunocompetent individuals, the promotion of long-term immunity appears to be deficient and reinfection are common throughout life. A possible explanation for this phenomenon is that hRSV and hMPV, can induce aberrant T cell responses, which leads to exacerbated lung inflammation and poor T and B cell memory immunity. The modulation of immune response exerted by both viruses include different strategies such as, impairment of immunological synapse mediated by viral proteins or soluble factors, and the induction of pro-inflammatory cytokines by epithelial cells, among others. All these viral strategies contribute to the alteration of the adaptive immunity in order to increase the susceptibility to reinfections.In this review, we discuss current research related to the mechanisms underlying the impairment of T and B cell immune responses induced by hRSV and hMPV infection. In addition, we described the role each virulence factor involved in immune modulation caused by these viruses.

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Section: The Humoral Response Against Hrsv Infectionsupporting

confidence: 65%

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

et al. 2016

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“…Vissers et al studied a cohort of infants hospitalized with RSV infection in the Netherlands to determine the importance of serum versus mucosal antibody, presumed to be maternally derived given the young age of the infants (mean, 53 days). The authors found that RSV-specific mucosal IgG concentrations, but not plasma IgG concentrations, inversely correlated with viral load (4). While the results are provocative, the study was limited by its small sample size and cross-sectional design.…”

mentioning

confidence: 78%

“…In this issue of Clinical and Vaccine Immunology, two articles address important obstacles in the path to a successful RSV vaccine (3,4). Acosta and colleagues provide a history and perspective on the vaccine-enhanced RSV illness that occurred in the 1960s.…”

mentioning

confidence: 99%

Progress toward a Respiratory Syncytial Virus Vaccine

Neuzil

2016

Clin Vaccine Immunol

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Respiratory syncytial virus is the leading cause of serious lower respiratory disease in young children throughout the world. An estimated 3.4 million children younger than 5 years of age are hospitalized each year with severe respiratory syncytial virus (RSV) lower respiratory tract infection, with the highest incidence in children younger than 6 months of age. Up to 200,000 deaths occur annually, with most deaths occurring in children younger than 1 year of age and in developing-country settings (1). Unfortunately, options for prevention and control are limited. No RSV vaccine is licensed anywhere in the world. While prophylactic treatment with RSV-specific neutralizing antibody is effective in reducing RSV morbidity in infants, its use is currently limited to select populations in high-resource settings because of its expense and because of challenges with its delivery (2). Prevention of severe RSV disease through active immunization of infants would be optimal but has been extremely challenging to implement, given the young age by which immunity is necessary and the legacy of vaccine-enhanced illness leading to deaths in a number of young children after receipt of a formalin-inactivated RSV vaccine in the 1960s.In this issue of Clinical and Vaccine Immunology, two articles address important obstacles in the path to a successful RSV vaccine (3, 4). Acosta and colleagues provide a history and perspective on the vaccine-enhanced RSV illness that occurred in the 1960s. The devastating results from those trials have thwarted vaccine efforts for the past 5 decades. The authors summarize the large and important body of work that has informed our understanding of immune responses in seronegative infants. The authors caution that RSV vaccines triggering high levels of interleukin-4 (IL-4) and/or IL-13 are associated with enhanced disease in animal models and should be excluded as potential candidates for infant immunization. Likewise, vaccines eliciting nonneutralizing antibody may also be quite risky in seronegative individuals (3).The second article addresses the important issue of identifying a correlate of protection, which if established could make vaccine licensure easier to achieve. Vissers et al. studied a cohort of infants hospitalized with RSV infection in the Netherlands to determine the importance of serum versus mucosal antibody, presumed to be maternally derived given the young age of the infants (mean, 53 days). The authors found that RSV-specific mucosal IgG concentrations, but not plasma IgG concentrations, inversely correlated with viral load (4). While the results are provocative, the study was limited by its small sample size and cross-sectional design. It will be important to replicate these results in larger populations in other locales. Nonetheless, such innovative work is needed to inform measures of vaccine-induced immunity and accelerate RSV vaccine development.The RSV experience reminds us that vaccine development is by nature a prolonged, risky, and increasingly expensive process. Laborato...

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“…This is unlike other respiratory infections, such as with influenza virus, in which antibodies persist and confer lifelong protection against the original infecting strain. However, nasal anti-RSV IgA levels correlate with protection from experimental infection in adults 89 , while levels of nasal (maternally derived) anti-RSV IgG correlate with lower viral load in infants 90 . Furthermore, anti-RSV antibodies have been found in amniotic fluid 91 and could potentially be protective to the lungs of newborns.…”

Section: Adaptive Immune Responses To Rsvmentioning

confidence: 98%

Respiratory syncytial virus infection: an innate perspective

Johansson

2016

F1000Res

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Respiratory syncytial virus (RSV) is a common cause of upper respiratory tract infection in children and adults. However, infection with this virus sometimes leads to severe lower respiratory disease and is the major cause of infant hospitalisations in the developed world. Several risk factors such as baby prematurity and congenital heart disease are known to predispose towards severe disease but previously healthy, full-term infants can also develop bronchiolitis and viral pneumonia during RSV infection. The causes of severe disease are not fully understood but may include dysregulation of the immune response to the virus, resulting in excessive recruitment and activation of innate and adaptive immune cells that can cause damage. This review highlights recent discoveries on the balancing act of immune-mediated virus clearance versus immunopathology during RSV infection.

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Mucosal IgG Levels Correlate Better with Respiratory Syncytial Virus Load and Inflammation than Plasma IgG Levels

Cited by 33 publications

References 14 publications

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

Progress toward a Respiratory Syncytial Virus Vaccine

Respiratory syncytial virus infection: an innate perspective

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