Sudden Infant Death Associated with Rhinovirus Infection.

A less than one-month-old infant with symptoms of rhinitis died unexpectedly in his sleep. He was not born prematurely and had no known underlying disease. Cerebrospinal fluid, nasopharyngeal and lung samples, and rectal swab were found to be positive for subgroup A rhinovirus, while the blood was negative. This case highlights the important finding that the rhinovirus, a common pathogen associated with upper respiratory tract infections, can sometimes, as the only pathogen, lead to complications such as a cerebrospinal infection and be involved in the sudden infant death syndrome (SIDS). Vigilance is necessary in case of viral infections in the infant's environment, and measures of hygiene and protection must be encouraged in order to reduce the risk of the SIDS.

Epidemiological characteristics and clinical outcomes of human rhinovirus infections in a hospitalized population. Severity is independently linked to RSV coinfection and comorbidities.

Human rhinovirus (hRV) is a predominant respiratory viral pathogen. The determinants that lead to adverse clinical outcomes in hospitalized patients are unclear. Our objective was to analyze the epidemiological and clinical characteristics of hRV infections in a hospitalized population and to compare non-severe and severe infections. The study was based on data from all patients with a respiratory episode admitted to Hospital from October 2015 to September 2016. During the study period, out of 2465 respiratory episodes, 434 were detected positive for hRV. Most of the coinfections involved the respiratory syncytial virus (RSV) and very few influenza viruses. A possible interference between rhinovirus and influenza virus is suggested. Airway involvement was present in a large part of hRV infections with 28.4 % (n = 48/169) of bronchiolitis and 3.6 % (n = 6/169) of bronchitis. One third of patients had at least one of the following severity criteria: need for oxygen therapy, hospitalization ≥ 5 days, and admission to the ICU. On multivariate analysis, a respiratory co-infection with RSV and the presence of a chronic respiratory disease (including a history of asthma) were shown to be independent risk factors for the onset of a severe infection in patients ≤ 2 years old. In a case control study based on 70 patients, hRV-A was the predominant lineage, followed closely by hRV-C. High viral load or viral genotypes were not associated with severe infection.

Different meteorological parameters influence metapneumovirus and respiratory syncytial virus activity.

BACKGROUND: Both human metapneumovirus (hMPV) and respiratory syncytial virus (RSV) cause epidemics during the cold season in temperate climates. OBJECTIVES: The purpose of this study was to find out whether climatic factors are associated with RSV and hMPV epidemics. STUDY DESIGN: Our study was based on data from 4300 patients admitted to the Dijon University Hospital for acute respiratory infection (ARI) over three winter seasons chosen for their dissimilar meteorological and virological patterns. Cases of hMPV and RSV were correlated with meteorological parameters recorded in the Dijon area. The relationship between virus data and local meteorological conditions was analyzed by univariate and multivariate negative binomial regression analysis. RESULTS: RSV detection was inversely associated with temperature and positively with relative humidity and air pressure, whereas hMPV was inversely associated with temperature and positively with wind speed. CONCLUSIONS: The association among meteorological variables and weekly ARIs cases due to RSV and hMPV demonstrated the relevance of climate factors as contributors to both hMPV and RSV activities. Meteorological drivers of RSV and hMPV epidemics are different. Low temperatures influence both hMPV and RSV activity. Relative humidity is an important predictor of RSV activity, but it does not influence hMPV activity.

RNA interference in vitro and in vivo using DsiRNA targeting the nucleocapsid N mRNA of human metapneumovirus.

Human metapneumovirus causes respiratory diseases with outcomes that can be severe in children, the immunocompromised, and the elderly. Synthetic small interfering RNAs (siRNAs) that silence targeted genes can be used as therapeutic agents. Currently, there is no specific therapy for hMPV. In this study, we designed Dicer-substrate siRNAs (DsiRNAs) that target metapneumovirus sequences on the mRNAs of the N, P, and L genes. In vitro, six DsiRNAs were shown to inhibit virus replication using cell proliferation tests. Of those, the DsiRNA that targets the most conserved mRNA sequence was then resynthesized in Evader™ format with heavy 2'-O-methyl modification of the guide strand. In a murine model, the prophylactic administration of this Evader™ DsiRNA was effective at partially inhibiting viral replication of hMPV (13×10(3) vs. 29×10(3)PFU/g of lung; p<0.01), which was not the case for the control, a mismatched DsiRNA. Inhibition was achieved without inducing cytokines or off-target effects. Moreover, the specificity of the siRNA mechanism of action was demonstrated in vitro and in vivo using 5'-RACE methodology. This in vivo approach of using a DsiRNA against hMPV is an important step in the development of synthetic siRNA as a therapeutic agent for this virus.

Human metapneumovirus genotypes and severity of disease in young children (n = 100) during a 7-year study in Dijon hospital, France.

Human metapneumovirus is a cause of respiratory tract infections at all ages. Our objectives were to analyze the distribution of the A and B genotypes over 7 years in Dijon and to investigate a possible association between hMPV genotypes and disease severity. During 2002-2009, we genotyped the 100 isolates from children <3 years old with hMPV. Phylogenetic analysis indicated a change in the distribution of hMPV genotype over the years. Severity was then measured by detailed clinical evaluation. The hospitalization rate was greater when genotype B was involved 72.5% versus 53.3% (P = 0.054). Those infected with genotype B tended to have a higher clinical score, as measured by Vicente et al. 2006 (P = 0.07). We showed that, although clinical severity is not clearly associated with hMPV genotype in this study, pathological signs on chest X-ray were observed more often in B subgroup (P < 0.01).