<i>Streptococcus pneumoniae</i> and <i>Haemophilus influenzae</i> at the initial stage of influenza

Takano, Misao; Ozaki, Kyoko; Nitahara, Yoshiyuki; Higuchi, Wataru; Takano, Tomomi; Nishiyama, Akihito; Yamamoto, Tatsuo

doi:10.1111/j.1442-200x.2009.02861.x

Cited by 11 publications

(7 citation statements)

References 26 publications

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“…Since Streptococcus pneumoniae carriage is highest in children (36, 37), S. pneumoniae colonization often precedes IAV infection in childhood (38, 39). Given that infant mice support efficient S. pneumoniae colonization in the URT (25, 40), we investigated the impact of S. pneumoniae colonization on IAV transmission.…”

Section: Resultsmentioning

confidence: 99%

An Infant Mouse Model of Influenza Virus Transmission Demonstrates the Role of Virus-Specific Shedding, Humoral Immunity, and Sialidase Expression by Colonizing Streptococcus pneumoniae

Ortigoza

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Zafar

et al. 2018

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This study provides insight into the role of the virus strain, age, immunity, and URT flora on IAV shedding and transmission efficiency. Using the infant mouse model, we found that (i) differences in viral shedding of various IAV strains are dependent on specific hemagglutinin (HA) and/or neuraminidase (NA) proteins, (ii) host age plays a key role in the efficiency of IAV transmission, (iii) levels of IAV-specific immunoglobulins are necessary to limit infectiousness, transmission, and susceptibility to IAV, and (iv) expression of sialidases by colonizing S. pneumoniae antagonizes transmission by limiting the acquisition of IAV in recipient hosts. Our findings highlight the need for strategies that limit IAV shedding and the importance of understanding the function of the URT bacterial composition in IAV transmission. This work reinforces the significance of a tractable animal model to study both viral and host traits affecting IAV contagion and its potential for optimizing vaccines and therapeutics that target disease spread.

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Section: Resultsmentioning

confidence: 99%

An Infant Mouse Model of Influenza Virus Transmission Demonstrates the Role of Virus-Specific Shedding, Humoral Immunity, and Sialidase Expression by Colonizing Streptococcus pneumoniae

Ortigoza

Blaser

Zafar

et al. 2018

mBio

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“…This is surprising given that the nasopharynx, a non-sterile environment extensively colonized by a diverse bacterial flora, is the first location encountered by IAV. Since Spn carriage is highest in children (36, 37), Spn colonization often precedes IAV infection in childhood (38, 39). Given that infant mice support efficient Spn colonization in the URT (25, 40), we investigated the impact of Spn colonization on IAV transmission.…”

Section: Resultsmentioning

confidence: 99%

An infant mouse model of influenza virus transmission demonstrates the role of virus-specific shedding, humoral immunity, and sialidase expression by colonizingStreptococcus pneumoniae

Ortigoza

Blaser

Zafar

et al. 2018

Preprint

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1 9 2 0 2 1 2 2 Word count: Abstract (368), Text (4692) 2 3 2 ABSTRACT 2 4 2 5The pandemic potential of influenza A viruses (IAV) depends on the infectivity of 2 6 the host, transmissibility of the virus, and susceptibility of the recipient. While virus traits 2 7 supporting IAV transmission have been studied in detail using ferret and guinea pig 2 8 models, there is limited understanding of host traits determining transmissibility and 2 9 susceptibility because current animal models of transmission are not sufficiently 3 0 tractable. Although mice remain the primary model to study IAV immunity and 3 1 pathogenesis, the efficiency of IAV transmission in adult mice has been inconsistent. 2Here we describe an infant mouse model which support efficient transmission of IAV. 3We demonstrate that transmission in this model requires young age, close contact, 3 4 shedding of virus particles from the upper respiratory tract (URT) of infected pups, the 3 5 use of a transmissible virus strain, and a susceptible recipient. We characterize 3 6shedding as a marker of infectiousness that predicts the efficiency of transmission 3 7 among different influenza virus strains. We also demonstrate that transmissibility and 3 8 susceptibility to IAV can be inhibited by humoral immunity via maternal-infant transfer of 3 9 IAV-specific immunoglobulins, and modifications to the URT milieu, via sialidase activity 4 0 of colonizing Streptococcus pneumoniae (Spn). Due to its simplicity and efficiency, this 4 1 model can be used to dissect the host's contribution to IAV transmission and explore 4 2 new methods to limit contagion.4 3 3 IMPORTANCE 4 4 4 5This study provides insight into the role of the virus strain, age, immunity, and 4 6 URT flora on IAV shedding and transmission efficiency. Using the infant mouse model, 4 7 we found that: (a) differences in viral shedding of various IAV strains is dependent on 4 8 specific hemagglutinin (HA) and/or neuraminidase (NA) proteins; (b) host age plays a 4 9 key role in the efficiency of IAV transmission; (c) levels of IAV-specific immunoglobulins 5 0 are necessary to limit infectiousness, transmission, and susceptibility to IAV; and (d) 5 1 expression of sialidases by colonizing Spn antagonize transmission by limiting the 5 2 acquisition of IAV in recipient hosts. Our findings highlight the need for strategies that 5 3 limit IAV shedding, and the importance of understanding the function of the URT 5 4 bacterial composition in IAV transmission. This work reinforces the significance of a 5 5tractable animal model to study both viral and host traits affecting IAV contagion, and its 5 6 potential for optimizing vaccines and therapeutics that target disease spread. 5 7 5 8 5 9

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“…Individuals colonized with S. pneumoniae who subsequently encounter an influenza virus infection may therefore have sufficient levels of IFN-a and IFN-b in the respiratory tract to mitigate IAV infection. Such a scenario may be most relevant to children, who, due to their high rate of pneumococcal carriage [9], are likely to be colonized with S. pneumoniae prior to contracting IAV [104]. Indeed, mice colonized first with the pneumococcus and then infected with influenza virus have significantly lower viral titers in the nasopharynx compared with mice infected with influenza virus alone [81].…”

Section: Inhibitory Effects Of S Pneumoniae On Viral Replicationmentioning

confidence: 97%

Interactions Between Streptococcus Pneumoniae and Influenza Virus: A Mutually Beneficial Relationship?

et al. 2012

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Historically, most research on infectious diseases has focused on infections with single pathogens. However, infections with pathogens often occur in the context of pre-existing viral and bacterial infections. Clinically, this is of particular relevance for coinfections with Streptococcus pneumoniae and influenza virus, which together are an important cause of global morbidity and mortality. In recent years new evidence has emerged regarding the underlying mechanisms of influenza virus-induced susceptibility to secondary pneumococcal infections, in particular regarding the sustained suppression of innate recognition of S. pneumoniae. Conversely, it is also increasingly being recognized that there is not a unidirectional effect of the virus on S. pneumoniae, but that asymptomatic pneumococcal carriage may also affect subsequent influenza virus infection and the clinical outcome. Here, we will review both aspects of pneumococcal influenza virus infection, with a particular focus on the age-related differences in pneumococcal colonization rates and invasive pneumococcal disease.

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Streptococcus pneumoniae and Haemophilus influenzae at the initial stage of influenza

Cited by 11 publications

References 26 publications

An Infant Mouse Model of Influenza Virus Transmission Demonstrates the Role of Virus-Specific Shedding, Humoral Immunity, and Sialidase Expression by Colonizing Streptococcus pneumoniae

An Infant Mouse Model of Influenza Virus Transmission Demonstrates the Role of Virus-Specific Shedding, Humoral Immunity, and Sialidase Expression by Colonizing Streptococcus pneumoniae

An infant mouse model of influenza virus transmission demonstrates the role of virus-specific shedding, humoral immunity, and sialidase expression by colonizingStreptococcus pneumoniae

Interactions Between Streptococcus Pneumoniae and Influenza Virus: A Mutually Beneficial Relationship?

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