respiratory syncytial virus

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respiratory syncytial virus

April 22, 2012, 01:31 PM

strain A ,
nucleotide area of fusion protein and glycoprotein

more contagious than flu - almost all children
had it by age 3

lower mutation rate than flu, seasonal outbreaks
not segmented, 11 proteins,enveloped
~15000 nucleotides

strains A,B alternating
oversummers in USA,Europe ?

Infected dendritic cells act as a reservoir for RSV over summer

S24 Differentiated primary bronchial epithelial cell (pBECs), monocyte derived macrophages (MdMs) and monocyte derived dendritic cells (MODCs) transwell co-culture: Respiratory Syncytial Virus (RSV) infection of the apical and basolateral surfaces

http://thorax.bmj.com/content/65/Suppl_4/A14.1.abstract

Introduction and Objectives RSV causes winter epidemics of respiratory disease. Active infection is virtually absent in summer months. Infected ciliated airway epithelial cells, local macrophages and dendritic cells secrete cytokines including interleukins (IL) 6 and 8, promoting a strong neutrophilic response that is important in disease clearance and airway inflammation. In vitro , RSV is capable of infecting MoDCs. RSV inhibits their maturation and can remain dormant in these cells. Dormant RSV can be stimulated to replicate with exogenous nitric oxide. These MoDCs are then able to re-infect HeLa cells (a lab strain of immortalised cervical cells). The following hypothesis was explored: Infected dendritic cells act as a reservoir for RSV over summer months . Aim The aim of this study was to investigate the effect of RSV on pBEC and MoDc cell lines across a semi permeable membrane in the presence of MdMs. Methods Primary bronchial epithelial cells were seeded in the apical part of the transwell model at 1×106 cells per ml and differentiated over 21 days on an air liquid interface. MoDCs were seeded on the basolateral part of the transwells at 1×106 cells/ml. MdM were seeded on top of the epithelial layer in selected experiments (see [Abstract S24 Figure 1][1]). Red fluorescent RSV (rr-RSV) was added to the apical side at a concentration of 1×106 plaque forming units (pfu)/ml with un-infected MoDCs on the basolateral side, and uninfected pBECs in the apical side were co-cultured with MoDCs previously infected with rr-RSV at 5 × 105 pfu/ml. Controls were uninfected pBECs with uninfected MoDCs or with just media on basolateral side. Red fluorescence (marker for active infection) was measured at 24, 48 and 168 h by flow cytometry. ![Abstract S24 Figure 1][2]</img> Abstract S24 Figure 1 Results Directly exposed pBECs and MoDCs were infected at 24 h. Indirectly exposed pBECs were infected at 48 h. Indirectly exposed MoDCs were infected only when MdMs were present on the overlying epithelial cell layer. Conclusions RSV is able to infect MoDCs and pBEC across a semi-permeable membrane in our in vitro model of airway epithelium, supporting MoDCs as a potential summer reservoir of RSV. [1]: #F1 [2]: pending:yes

MoDCs as a potential summer reservoir of RSV.

mutation rate is ~1.0 e-3 /position/year in the whole genome
(flu:2.5e-3) , maybe more (~2.5e-3) in the usually sequenced glycoprotein area

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Genetic variability and molecular evolution of the human respiratory syncytial virus subgroup B attachment G protein - PubMed

http://www.ncbi.nlm.nih.gov/pubmed/15994810

Human respiratory syncytial virus (HRSV) is the most important cause of acute respiratory disease in infants. Two major subgroups (A and B) have been identified based on antigenic differences in the attachment G protein. Antigenic variation between and within the subgroups may contribute to reinfect …

a 45-year period, including 196 Belgian strains obtained over 22 epidemic seasons (1982 to 2004).

HRSV-B evolutionary rate (1.95 x 10(-3) nucleotide substitutions/site/year)
is similar to that previously estimated for HRSV-A (1.83 x 10(-3) nucleotide substitutions/site/year).
(G protein genetic variability )

The most recent common ancestor of the currently circulating subgroup B strains was
estimated to date back to around the year 1949.

The divergence between the two major subgroups was calculated to have occurred
approximately 350 years ago.

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USA 1994-2008
influenza hospitalizations : 635/M/year
RSV :553/M/year

Hospitalizations associated with influenza and respiratory syncytial virus in the United States, 1993-2008 - PubMed

http://www.ncbi.nlm.nih.gov/pubmed/22495079

Overall US hospitalization rates for influenza and RSV are similar; however, their age-specific burdens differ dramatically. Our estimates are consistent with those from previous studies focusing either on influenza or RSV. Our approach provides robust national comparisons of hospitalizations associ …

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I'm interested in expert panflu damage estimates
my current links: http://bit.ly/hFI7H ILI-charts: http://bit.ly/CcRgT
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respiratory syncytial virus