Echovirus type 30 (E30) (genus, Enterovirus; family,Picornaviridae) has caused large outbreaks of aseptic meningitis in many regions of the world in the last 40 years. U.S. enterovirus surveillance data for the period 1961 to 1998 indicated that the annual proportion of E30 isolations relative to total enterovirus isolations has fluctuated widely, from a low of 0% in 1966 to a high of 42% in 1998. Peaks of E30 isolations occurred in the years 1968 to 1969, 1981 to 1984, 1990 to 1993, and 1997 to 1998, coincident with large nationwide outbreaks of E30-associated aseptic meningitis. Analysis of the complete VP1 sequence (876 nucleotides) of 136 E30 strains isolated in geographically dispersed regions of the United States and nine other countries between 1956 and 1998 indicated that the currently circulating E30 strains are genetically distinct from those isolated 30 to 40 years ago. Phylogenetic reconstruction demonstrated the existence of at least four distinct genetic groups, three of which have not been isolated in North America since 1981. Two of the three groups disappeared during periods when E30 was isolated infrequently. All North American E30 strains isolated after 1988 were closely related to one another, and all post-1993 isolates were of the same lineage within this group. Surveillance data indicate that E30 causes large national outbreaks of 2- to 4-year durations, separated by periods of relative quiescence. Our results show that shifts in the overall genetic diversity of E30 and the predominant genetic type correlate temporally with the dynamics of E30 isolation. The sequence data also provide a basis for the application of molecular techniques for future epidemiologic investigations of E30 disease.
SUMMARYThe polypeptides induced by canine distemper virus (CDV) strains have been characterized by polyacrylamide slab gel electrophoresis of infected cell lysates labelled with 35S-methionine, 14C-amino acids, ZH-glucosamine and 3H-mannose, or 32P-orthophosphate. Seven virus-induced polypeptides have been assigned the following nomenclature and mol. wt.: a large polypeptide L (I8OOOO); a large glycoprotein H (77 ooo); a nucleocapsid-associated protein P (73 ooo); the nucleocapsid protein N (60oo0); the smaller glycoprotein Fo (590oo); a membrane protein M (35oo0) and a small polypeptide S (I5OOO). During pulse-chase experiments with 3H-glucosamine and l~C-amino acids the intensity of the Fo band decreases and that of the F1 and F2 bands increases; the H polypeptide band becomes more diffuse and the S-protein disappears. The N-and P-but not the M-proteins have been found to be phosphorylated. The polypeptide pattern of the Onderstepoort strain of CDV has been compared with that of two other CDV and with I7 measles and subacute sclerosing panencephalitis (SSPE) strains. Differences in the mobilities of various polypeptides have been observed between CDV and measles and SSPE strains; however, the only consistent difference is the mol. wt. of the M-protein of CDV strains which is smaller by 2ooo than that of MV and this may be a biochemical marker to distinguish CDV from measles and SSPE virus strains.
The relatedness of enteroviral isolates associated with two recent outbreaks in Canada was assessed using direct sequencing of amplicons derived from a large portion of the 5' nontranslated region (NTR) of the viral genome. The amplicons of 60 echovirus 30 isolates originating from seven different provinces in 1991 were found to share 99% or greater sequence identity. Recent coxsackievirus B1 isolates characterised in the same manner were identical to each other. When the 5' NTR sequence of these isolates was compared to prototype strains a difference of 11-15% in nucleotide composition was observed. These results indicate that the variability of nucleotide sequence found in 5' NTRs can be utilized to identify rapidly enteroviral strains associated with particular outbreaks and distinguish them from other strains and serotypes.
IMPORTANCEIn the United States, Black and Hispanic children have higher rates of asthma and asthma-related morbidity compared with White children and disproportionately reside in communities with economic deprivation.OBJECTIVE To determine the extent to which neighborhood-level socioeconomic indicators explain racial and ethnic disparities in childhood wheezing and asthma. DESIGN, SETTING, AND PARTICIPANTSThe study population comprised children in birth cohorts located throughout the United States that are part of the Children's Respiratory and Environmental Workgroup consortium. Cox proportional hazard models were used to estimate hazard ratios (HRs) of asthma incidence, and logistic regression was used to estimate odds ratios of early and persistent wheeze prevalence accounting for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, and region and decade of birth.EXPOSURES Neighborhood-level socioeconomic indicators defined by US census tracts calculated as z scores for multiple tract-level variables relative to the US average linked to participants' birth record address and decade of birth. The parent or caregiver reported the child's race and ethnicity.MAIN OUTCOMES AND MEASURES Prevalence of early and persistent childhood wheeze and asthma incidence. RESULTSOf 5809 children, 46% reported wheezing before age 2 years, and 26% reported persistent wheeze through age 11 years. Asthma prevalence by age 11 years varied by cohort, with an overall median prevalence of 25%. Black children (HR, 1.47; 95% CI, and Hispanic children (HR, 1.29; 95% CI, 1.09-1.53) were at significantly increased risk for asthma incidence compared with White children, with onset occurring earlier in childhood. Children born in tracts with a greater proportion of low-income households, population density, and poverty had increased asthma incidence. Results for early and persistent wheeze were similar. In effect modification analysis, census variables did not significantly modify the association between race and ethnicity and risk for asthma incidence; Black and Hispanic children remained at higher risk for asthma compared with White children across census tracts socioeconomic levels. CONCLUSIONS AND RELEVANCEAdjusting for individual-level characteristics, we observed neighborhood socioeconomic disparities in childhood wheeze and asthma. Black and Hispanic children had more asthma in neighborhoods of all income levels. Neighborhood-and individual-level characteristics and their root causes should be considered as sources of respiratory health inequities.
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