Palivizumab epitope–displaying virus-like particles protect rodents from RSV challenge

Schickli, Jeanne H.; Whitacre, David C.; Tang, Roderick S.; Kaur, Jasmine; Lawlor, Heather; Peters, C; Jones, Joyce; Peterson, Darrell L.; McCarthy, Michael; Nest, Gary Van; Milich, David R.

doi:10.1172/jci78450

Cited by 43 publications

(35 citation statements)

References 39 publications

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“…[26][27][28][29] The ineffectiveness of the natural infection to induce long-term immunity has hampered vaccine generation and currently there is no licensed vaccine available to prevent the bronchiolitis and pneumonia caused either by hRSV or hMPV. [30][31][32][33][34] However, several candidate vaccines are in different stages of development for preventing the diseases caused by these viral agents. Candidate vaccines for hRSV and hMPV employ different approaches, including a chimeric virus (hMPV), 35 live attenuated virus (hRSV), 36 and purified proteins (hRSV), 37 among others.…”

Section: Introductionmentioning

confidence: 99%

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: Introductionmentioning

confidence: 99%

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

et al. 2016

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“…Replication-defective gene-based single-cycle vectors (15,16), subunit vaccines adjuvanted with various Toll-like receptor (TLR) agonists (17), viruslike particles (VLPs) with protective antigens (18)(19)(20), and new formulations with the prefusion conformation of RSV F (21-25) defy our traditional understanding of replicating and nonreplicating vaccines, posing new questions for the field and for human studies. This challenge is particularly significant for RSV because a vaccine designed to protect infants and toddlers against RSV in the 1960s primed for a severe form of respiratory illness upon RSV infection, known as enhanced RSV disease (ERD).…”

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confidence: 99%

Brief History and Characterization of Enhanced Respiratory Syncytial Virus Disease

Acosta

Caballero

Polack

2016

Clin Vaccine Immunol

199

173

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In 1967, infants and toddlers immunized with a formalin-inactivated vaccine against respiratory syncytial virus (RSV) experienced an enhanced form of RSV disease characterized by high fever, bronchopneumonia, and wheezing when they became infected with wild-type virus in the community. Hospitalizations were frequent, and two immunized toddlers died upon infection with wild-type RSV. The enhanced disease was initially characterized as a "peribronchiolar monocytic infiltration with some excess in eosinophils." Decades of research defined enhanced RSV disease (ERD) as the result of immunization with antigens not processed in the cytoplasm, resulting in a nonprotective antibody response and CD4؉ T helper priming in the absence of cytotoxic T lymphocytes. This response to vaccination led to a pathogenic Th2 memory response with eosinophil and immune complex deposition in the lungs after RSV infection. In recent years, the field of RSV experienced significant changes. Numerous vaccine candidates with novel designs and formulations are approaching clinical trials, defying our previous understanding of favorable parameters for ERD. This review provides a succinct analysis of these parameters and explores criteria for assessing the risk of ERD in new vaccine candidates. R espiratory syncytial virus (RSV) is the leading respiratory cause of hospitalization in infants and young children in the United States and in the world (1, 2). Most severe infections occur in young infants, with the peak incidence of lower respiratory tract illness (LRTI) occurring between 2 and 4 months of age (3-5). In the United States, hospitalization rates have risen during the last decades (6), and while premature babies and infants with chronic lung disease and/or congenital heart disease are at increased risk for severe presentations, the majority of hospitalizations occur in previously healthy infants. Recent estimates of global mortality suggest that between 66,000 and 234,000 infants and young children die every year due to RSV (1, 2). Ninety-nine percent of deaths occur in the developing world (2). A significant proportion of these fatalities are thought to occur in the community. The need for preventive interventions against the virus is indisputable.The virus. RSV is a member of the pneumovirus genus of the family Paramyxoviridae. The virus is a negative-sense RNA virus with a nonsegmented encapsidated genome and a lipid envelope (7). The envelope is a host plasma membrane-derived lipid bilayer containing three virally encoded transmembrane glycoproteins: the fusion (F) protein, the attachment (G) protein, and the small hydrophobic (SH) protein. RSV F is the main neutralizing antigen, highly conserved and essential for virus viability (7). The secondary protective antigen eliciting neutralizing antibodies is the RSV G protein. Both neutralizing antigens are the main candidates for novel vaccines and targets for monoclonal antibodies.A new scenario. The world of RSV vaccines is experiencing important changes. In recent years, epidemiologic...

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“…One of these substitutions, Asn268Ile, may affect the neutralization of HRSV (Bates et al, 2014), whereas other substitutions may not have such an effect (Bates et al, 2014;Schickli et al, 2015).…”

mentioning

confidence: 99%

Molecular evolution of the fusion protein gene in human respiratory syncytial virus subgroup A

Kimura

Nagasawa

Tsukagoshi

et al. 2016

Infection, Genetics and Evolution

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Palivizumab epitope–displaying virus-like particles protect rodents from RSV challenge

Cited by 43 publications

References 39 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

Brief History and Characterization of Enhanced Respiratory Syncytial Virus Disease

Molecular evolution of the fusion protein gene in human respiratory syncytial virus subgroup A

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