Rhinovirus Infections in an Industrial Population. Iv. Infections Within Families of Employees During Two Fall Peaks of Respiratory Illness1

Jo, Hendley; Jm, Gwaltney; Ws, Jordan

doi:10.1093/oxfordjournals.aje.a120928

Cited by 80 publications

(40 citation statements)

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“…Since neutralizing antibody is not detected until 14 days after infection (4), recovery from illness, which occurs within 7-10 days of infection, is probably mediated by other agents. On the other hand, resistance to illness and infection has been associated with high pre-existing neutralizing antibody titres (4)(5)(6)(7), a finding which we have recently confirmed (8).…”

Section: Introductionsupporting

confidence: 77%

The time course of the humoral immune response to rhinovirus infection

et al. 1989

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SUMMARYThe specific humoral immune response of 17 volunteers to infection with human rhinovirus type 2 (HRV-2) has been measured both by neutralization and by ELISA. Six volunteers who had HRV-2-specific antibodies in either serum or nasal secretions before HRV-2 inoculation were resistant to infection and illness. Of the remaining 11 volunteers who had little pre-existing HRV-2-specific antibody, one was immune but 10 became infected and displayed increases in HRV-2-specific antibodies. These antibodies first increased 1-2 weeks after infection and reached a maximum at 5 weeks. All six resistant volunteers who had high pre-existing antibody and eight of the volunteers who became infected maintained their HRV-2-specific antibody for at least 1 year. At this time they were protected against reinfection. Two volunteers showed decreases in HRV-2-specific antibodies from either serum or nasal secretions. They became infected but not ill after HRV-2 inoculation 1 year later.

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Section: Introductionsupporting

confidence: 77%

The time course of the humoral immune response to rhinovirus infection

et al. 1989

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“…Furthermore, if volunteers became infected, these antibodies were clearly associated with reduction of symptoms, including the amount of nasal secretion. Other studies have demonstrated that resistance to disease and infection from respiratory viruses is mediated by circulating antibodies (Edmondson et al 1966;Hendley, Gwaltney & Jordan, 1969;Couch et al 1984) and similar results were obtained by Hamre & Beem (1972) and Reed (1984) with coronavirus. In contrast, other workers have noted the protective effect of secretory antibodies (Smith et al 1966;Mills et al 1971;Perkins et al 1969;Clements et al 1983).…”

supporting

confidence: 58%

Effect of specific humoral immunity and some non-specific factors on resistance of volunteers to respiratory coronavirus infection

Callow

1985

J. Hyg.

118

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SUMMARYThirty-three volunteers were inoculated intranasally with coronavirus 229E, and their responses monitored by antibody rises, symptomatology and virus excretion. These were related to their pre-trial immune status as indicated by concentrations of specific antibodies and non-specific proteins in serum and nasal washings. Both circulating and local specific antibodies were associated with protection from infection and disease, but only specific IgA antibodies of either type appeared to shorten the period of virus shedding. Although total secretory IgA was significantly associated only with reduction of symptoms, total protein in nasal washings appeared to protect against infection also, indicating that other locally produced proteins, not identified, may be associated with resistance.Two of the many factors which may affect the concentration of circulating and local protective proteins and thus influence the outcome of virus inoculation, namely, sex of the volunteer and the interval since the previous cold, were examined. Male volunteers or volunteers who had had evidence of a recent respiratory infection were less likely to be infected, but if they were infected, they had lower clinical scores and stopped shedding virus earlier than the rest. These groups possessed higher concentrations of specific antibodies and non-specific proteins in their pre-challenge sera and/or nasal washings. The significance of these findings is discussed.

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“…In children, this pattern strongly reflects the school calendar (15)(16)(17). A wave of asthma exacerbations in children ensues shortly after the return to school after summer break (shown in Fig.…”

mentioning

confidence: 91%

Respiratory virus transmission dynamics determine timing of asthma exacerbation peaks: Evidence from a population-level model

Eggo

Scott

Galvani

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Asthma exacerbations exhibit a consistent annual pattern, closely mirroring the school calendar. Although respiratory viruses-the "common cold" viruses-are implicated as a principal cause, there is little evidence to link viral prevalence to seasonal differences in risk. We jointly fit a common cold transmission model and a model of biological and environmental exacerbation triggers to estimate effects on hospitalization risk. Asthma hospitalization rate, influenza prevalence, and air quality measures are available, but common cold circulation is not; therefore, we generate estimates of viral prevalence using a transmission model. Our deterministic multivirus transmission model includes transmission rates that vary when school is closed. We jointly fit the two models to 7 y of daily asthma hospitalizations in adults and children (66,000 events) in eight metropolitan areas. For children, we find that daily viral prevalence is the strongest predictor of asthma hospitalizations, with transmission reduced by 45% (95% credible interval =41-49%) during school closures. We detect a transient period of nonspecific immunity between infections lasting 19 (17-21) d. For adults, hospitalizations are more variable, with influenza driving wintertime peaks. Neither particulate matter nor ozone was an important predictor, perhaps because of the large geographic area of the populations. The school calendar clearly and predictably drives seasonal variation in common cold prevalence, which results in the "back-to-school" asthma exacerbation pattern seen in children and indirectly contributes to exacerbation risk in adults. This study provides a framework for anticipating the seasonal dynamics of common colds and the associated risks for asthmatics.

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Rhinovirus Infections in an Industrial Population. Iv. Infections Within Families of Employees During Two Fall Peaks of Respiratory Illness1

Cited by 80 publications

References 0 publications

The time course of the humoral immune response to rhinovirus infection

The time course of the humoral immune response to rhinovirus infection

Effect of specific humoral immunity and some non-specific factors on resistance of volunteers to respiratory coronavirus infection

Respiratory virus transmission dynamics determine timing of asthma exacerbation peaks: Evidence from a population-level model

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