OC43 strain‐related coronavirus antibodies in different age groups

Abstract

Serum antibodies against human coronavirus OC43 in different age groups were measured by complement fixation (CF), haemagglutination inhibition (HI), radial diffusion haemolysis-in-gel (HIG), and solid-phase radioimmunoassay (RIA) methods. Antigen grown in suckling mouse brain was used in all tests. Results obtained by the CF and HIG tests, and the RIA, were in good agreement with regard to the presence or absence of antibodies. Similar results were also obtained with the HI test if nonspecific haemagglutination inhibitors were first removed by treatment with phospholipase C and only titers of 1:20 or greater were considered positive. Children 6--23 months of age (n = 45) were without measurable coronavirus antibodies in all four assays. A rapid increase in the prevalence of antibodies then occurred in subsequent age groups, and practically all persons 6 years of age or older were found to have OC43 antibodies as measured by the HIG test or the RIA. The mean antibody levels determined by these two methods continued to increase, however, up to the age group of 10--14 years. This increase in antibody levels after the initial antibody incidence plateau may be due to boosting effects caused by related coronavirus strains, since OC43 antigens are known to cross-react with antibodies induced by other human coronaviruses. Taken together, these data suggest that OC43 virus, or an antigenically related coronavirus strain, is very common in Finland.

Prevalence of human coronavirus antibody in the population of southern iraq

“…Previous studies have analyzed the prevalence of HCV antibodies in the sera of various populations in North America [Cavallaro and Monto, 1970;Hamre and Beem, 1972;Hendley et al, 1972;Kaye et al, 1971;McIntosh et al, 19701, South America [Candeias et al, 19721, and Europe [Bradburne and Somerset, 1972;Hovi et al, 1979;Zakstelskaya et al, 19721 and shown that HCV antibodies are widespead in these populations. Several of these reports describe variations in the incidence of antibodies to HCVs depending on a number of factors including the population studied and the season the samples were taken.…”

“…Recent reports have suggested that these viruses may be associated with more severe diseases, and in particular gastroenteritis, but as yet there is no clear evidence to support this [Macnaughton and Davies, 19811. Several reports have analyzed the extent of infections in various populations in America and Europe by estimates of HCV antibodies in sera from patients and volunteers [Bradburne and Somerset, 1972;Candeias et al, 1970;Cavallaro and Monto, 1970;Hamre and Beem, 1972;Hendley et al, 1972;Hovi et al, 1979; Kaye et al, 1971;McIntosh et al, 1970;Zakstelskaya et al, 19721. A number of assays have been used, including neutralization, complement fixation, hemagglutination inhibition, and radioimmunoassay.…”

Viruses and Bacteria in the Etiology of the Common Cold

“…For measuring coronavirus antibodies, crude EIA antigens (microsomal fraction) were prepared from coronavirus OC43-and 229E-infected cells and uninfected control antigen RD cells (human embryonal rhabdomyosarcoma cells) as described for mouse brain homogenate (13). Seeds for virus and cells (originally from the American Type Culture Collection) were kindly provided by K. Holmes (University of Health Sciences, Bethesda, Md.).…”

Coronavirus infects and causes demyelination in primate central nervous system

“…Coronaviruses are ubiquitous animal pathogens that can produce neurologic or systemic illness in infected animals . In humans, coronaviruses are a leading upper respiratory tract pathogen (Hovi et al, 1979) and are associated with gastroenteritis (Resta et al, 1985) but have never been proven to cause serious human illness . However, two reports, one describing the isolation of coronavirus from the brains of two multiple sclerosis (MS) patients (Burks et al, 1980) and the other the electron microscopic observation of a coronavirus in an MS brain perivascular immunocyte (Tanaka et al, 1976), suggest that there may be an association between coronaviruses and human demyelinating disease .…”