Pneumonia Caused by Rhinovirus

Imakita, Masami; Shiraki, Kimíyasu; Yutani, Chikao; Ishibashi‐Ueda, Hatsue

doi:10.1086/313723

Cited by 43 publications

(37 citation statements)

References 5 publications

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“…With the availability of recent molecular detection methods, the role of rhinoviruses in the pathogenesis of various clinical syndromes has been expanded. Once thought to be only associated with mild selflimiting upper respiratory tract infections, rhinoviruses have been recently linked with more serious lower airway illnesses, including bronchitis and pneumonia (10,14,21). These viral agents have also been associated with asthma and cystic fibrosis exacerbations in children (4,8,15,16).…”

Section: Discussionmentioning

confidence: 99%

“…Rhinoviruses are the leading cause of the common cold, a highly prevalent and benign infection of the upper respiratory tract usually devoid of significant systemic symptoms. However, it has been recently suggested that rhinoviruses may also replicate in the tracheobronchial tree and may cause viral pneumonitis in selected settings (10,14,23). The full scope of the disease burden associated with rhinovirus infections has not been completely elucidated since virus isolation is difficult and serology testing is limited by the large number (Ͼ100) of viral serotypes.…”

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Roleof Picornaviruses in Flu-Like Illnesses of Adults Enrolled in anOseltamivir Treatment Study Who Had No Evidence of Influenza VirusInfection

et al. 2002

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The primary objective of this study was to determine the role of picornavirus in flu-like episodes (temperature of >38.0°C plus one respiratory and one constitutional symptom) among otherwise healthy adults enrolled in a placebo-controlled, double-blind, randomized oseltamivir treatment study. Combined nasal and pharyngeal swabs were collected at baseline for influenza cultures and picornavirus reverse transcription (RT)-PCR. In addition, acute-and convalescent-serum samples were obtained for serological studies of common respiratory pathogens. From a total of 719 subjects enrolled in the clinical trial within 36 h of the onset of symptoms, 475 (66%) had evidence of recent influenza A or B virus infections by means of culture and/or serological testing. Of the 244 remaining patients, 36 (15%) presented a seroconversion for at least one of the common respiratory viruses or atypical pathogens. An RT-PCR assay for the picornavirus 5 noncoding region (NCR) was positive in a subset of 15 (19%) of 78 patients with flu-like illnesses of undetermined etiology. Sequence analysis of the picornavirus 5 NCR amplicons revealed that 14 (93%) of them had greater homology to rhinoviruses, whereas 1 (7%) was related to enteroviruses. Interestingly, median total symptom scores and oral temperatures of picornavirus-positive patients (n ‫؍‬ 15) and placebo-treated influenza virus-positive patients (n ‫؍‬ 161) were similar over a 3-week period. We conclude that, among the influenza virus-negative preselected cases of this study, rhinoviruses were relatively frequent pathogens associated with important respiratory and systemic symptoms.The Picornaviridae family, which contains single-stranded RNA viruses, is divided into various genera such as Rhinovirus, Enterovirus, and Hepatovirus. Rhinoviruses are the leading cause of the common cold, a highly prevalent and benign infection of the upper respiratory tract usually devoid of significant systemic symptoms. However, it has been recently suggested that rhinoviruses may also replicate in the tracheobronchial tree and may cause viral pneumonitis in selected settings (10,14,23). The full scope of the disease burden associated with rhinovirus infections has not been completely elucidated since virus isolation is difficult and serology testing is limited by the large number (Ͼ100) of viral serotypes. The recent development of reverse transcription (RT)-PCR assays based on amplification of the conserved 5Ј noncoding region (NCR) of picornaviruses has been shown to improve significantly the detection of rhinoviruses in clinical samples (1,12,13,25). In the present study, we used the latter approach to determine the role of picornaviruses in flu-like illnesses of adults enrolled in an influenza virus neuraminidase inhibitor trial based on a stringent clinical case definition.(This work was presented in part at the Third International Symposium on Respiratory Viral Infections, 1 December 2000, St. Lucia, West Indies [abstr. P4].) MATERIALS AND METHODS Study population.A placebo-controlled, doub...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Roleof Picornaviruses in Flu-Like Illnesses of Adults Enrolled in anOseltamivir Treatment Study Who Had No Evidence of Influenza VirusInfection

et al. 2002

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“…The lungs of infected mice were removed under anesthesia from at least 3 mice in each group on days 1 and 2 p.i. and fixed for hematoxylin and eosin staining or rapidly frozen in liquid nitrogen for immunohistochemical examination as described previously (Imakita et al, 2000;Kamiyama et al, 2001;Fukuda et al, 2003). Briefly, 6 µm thick serial sections of the frozen lungs were dried at room temperature, fixed with cold acetone, and then washed with TBS.…”

Section: Methodsmentioning

confidence: 99%

Interleukin 12 is a primary cytokine responding to influenza virus infection in the respiratory tract of mice

Hama

Kurokawa²,

Imakita³

et al. 2009

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. Abbreviations: BALF = bronchoalveolar lavage fluid; IFN = interferon; IL = interleukin; i.n. = intranasal; MAb(s) = monoclonal antibody(ies); p.i. = post infection; TNF = tumor necrosis factor Interleukin 12 is a primary cytokine responding to influenza virus infection in the respiratory tract of mice Summary. -We have reported previously that an increase in interleukin 12 (IL-12) production in the lungs of mice infected with Influenza A virus or an intranasal (i.n.) administration of IL-12 to the infected mice alleviated pneumonia (Tsurita et al., J. Pharmacol. Exp. Therapeut. 298, 362-368, 2001). In this study, we found that in the bronchoalveolar lavage fluids (BALF) obtained from mice infected i.n. with Influenza A virus IL-12 was elevated on day 1 post infection (p.i.) and was followed by tumor necrosis factor α (TNF-α), IL-18, and interferons α, β, and γ (IFN-α, -β, and -γ) on day 2 p.i. Histochemical analyses of the infected lungs on day 1 p.i. showed the presence of IL-12 and IL-12 mRNA in mononuclear and macrophage-like cells and colocalization of macrophages with viral antigen, while other cytokines were absent. Thus, IL-12 was produced by macrophages infiltrating the infected epithelium as the first response cytokine and its production at the site of infection may direct an early immune defense to alleviate the severity of infection.

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“…The resultant supernatants were used as the cell-free virus stocks, and their virus titers ranged from 3.3 ϫ 10 3 to 2.3 ϫ 10 5 PFU/ml in this study. The Towne strain of cytomegalovirus (CMV) (18,28) and rhinovirus 13 (13) were propagated in HEL cells, and adenovirus 5 (19) was propagated in Hep2 cells. CMV, rhinovirus 13, and adenovirus 5 were prepared from the infected cells by three cycles of freezing and thawing.…”

Section: Cells and Virusesmentioning

confidence: 99%

Neutralizing Anti-gH Antibody of Varicella-Zoster Virus Modulates Distribution of gH and Induces Gene Regulation, Mimicking Latency

Shiraki

Daikoku

Takemoto

et al. 2011

J Virol

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The anti-glycoprotein H (gH) monoclonal antibody (anti-gH-MAb) that neutralizes varicella-zoster virus (VZV) inhibited cell-to-cell infection, resulting in a single infected cell without apoptosis or necrosis, and the number of infectious cells in cultures treated with anti-gH-MAb declined to undetectable levels in 7 to 10 days. Anti-gH-MAb modulated the wide cytoplasmic distribution of gH colocalized with glycoprotein E (gE) to the cytoplasmic compartment with endoplasmic reticulum (ER) and Golgi markers near the nucleus, while gE retained its cytoplasmic distribution. Thus, the disintegrated distribution of gH and gE caused the loss of cellular infectivity. Varicella-zoster virus (VZV) infection causes varicella, and then VZV becomes latent in the sensory ganglia. The reactivation of VZV caused zoster in every age group, especially in the elderly, at rates of 3 to 8 per 1,000 person-years in a study of 48,388 zoster patients (46). The major complication of zoster is chronic pain (postherpetic neuralgia); the pain is related to peripheral nerve injury and the activation of brain-derived neurotrophic factor by anti-immediate early (IE) 62 antibody (12). However, the mechanism of VZV latency is not clear. Studies of the latent human ganglia revealed the difference between gene regulation in VZV and herpes simplex virus (HSV). Transcripts from genes 21, 29, 62, 63, and 66 of VZV and the product from gene 63 have been identified in latently infected human ganglia (4-7, 16, 17, 20, 22, 51), in contrast to the presence of noncoding latency-associated transcripts of HSV (29, 40).The thymus leukemia antigen on the cell surface is lost due to anti-thymus leukemia antibody treatment, and this phenomenon is defined as the antigenic modulation of eukaryotic cells (25). Antigenic modulation also is observed in measles virusinfected cells. Antibodies to viral surface antigens modulate measles virus expression in the infected cells, and anti-hemagglutinin antibody reduces the expression of viral fusion protein, matrix protein, and phosphoprotein in measles virus-infected cells (9-11, 14, 26). The biological importance of antigenic modulation has been recognized in various cells by clearing the cell surface expression of the respective antigen with the relevant monoclonal antibody, including monoclonal antibody treatment for immunotherapy in B cells (30,31), red blood cells (52), a human thymic myoid cell line (48), B cells (2,3,45), and differentiating murine embryonic stem cells and embryo fibroblasts (39).VZV expresses the viral glycoproteins glycoprotein E (gE), glycoprotein B (gB), and glycoprotein H (gH) on the surface of infected cells. Anti-gH monoclonal antibody (anti-gH-MAb) neutralizes viral infectivity and inhibits cell-to-cell infection and plaque formation in vitro, while monoclonal antibodies to gE and gB and zoster convalescent-phase sera do not inhibit cell-to-cell infection. When infected cells were treated with anti-gH-MAb after cell-free virus infection, single-cell infection was observed without morphologi...

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Pneumonia Caused by Rhinovirus

Cited by 43 publications

References 5 publications

Roleof Picornaviruses in Flu-Like Illnesses of Adults Enrolled in anOseltamivir Treatment Study Who Had No Evidence of Influenza VirusInfection

Roleof Picornaviruses in Flu-Like Illnesses of Adults Enrolled in anOseltamivir Treatment Study Who Had No Evidence of Influenza VirusInfection

Interleukin 12 is a primary cytokine responding to influenza virus infection in the respiratory tract of mice

Neutralizing Anti-gH Antibody of Varicella-Zoster Virus Modulates Distribution of gH and Induces Gene Regulation, Mimicking Latency

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