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Showing papers by "D. James Nokes published in 2009"


Journal ArticleDOI
02 Dec 2009-PLOS ONE
TL;DR: Maternal-specific RSV Ab decline rapidly following birth, however, evidence of protection against severe disease by RSV-matAb during the first 6–7 months is provided, suggesting that boosting maternal-specific Ab byRSV vaccination may be a useful strategy to consider.
Abstract: Background Respiratory syncytial virus (RSV) is the major cause of lower respiratory tract infection in infants. The rate of decay of RSV-specific maternal antibodies (RSV-matAb), the factors affecting cord blood levels, and the relationship between these levels and protection from infection are poorly defined. Methods A birth cohort (n = 635) in rural Kenya, was studied intensively to monitor infections and describe age-related serological characteristics. RSV specific IgG antibody (Ab) in serum was measured by the enzyme linked immunosorbent assay (ELISA) in cord blood, consecutive samples taken 3 monthly, and in paired acute and convalescent samples. A linear regression model was used to calculate the rate of RSV-matAb decline. The effect of risk factors on cord blood titres was investigated. Results The half-life of matAb in the Kenyan cohort was calculated to be 79 days (95% confidence limits (CL): 76–81 days). Ninety seven percent of infants were born with RSV-matAb. Infants who subsequently experienced an infection in early life had significantly lower cord titres of anti-RSV Ab in comparison to infants who did not have any incident infection in the first 6 months (P = 0.011). RSV infections were shown to have no effect on the rate of decay of RSV-matAb. Conclusion Maternal-specific RSV Ab decline rapidly following birth. However, we provide evidence of protection against severe disease by RSV-matAb during the first 6–7 months. This suggests that boosting maternal-specific Ab by RSV vaccination may be a useful strategy to consider.

140 citations


Journal ArticleDOI
TL;DR: S Severity data suggest that the justification for RSV vaccination will be based on the prevention of morbidity, not mortality, and an effective vaccine for children aged >2 months (outside the age group of poor responders) could prevent a large portion of RSV disease.
Abstract: Background.Although necessary for developing a rationale for vaccination, the burden of severe respiratory syncytial virus (RSV) disease in children in resource‐poor settings remains poorly defined. Methods.We conducted prospective surveillance of severe and very severe pneumonia in children aged <5 years admitted from 2002 through 2007 to Kilifi district hospital in coastal Kenya. Nasal specimens were screened for RSV antigen by immunofluorescence. Incidence rates were estimated for the well‐defined population. Results.Of 25,149 hospital admissions, 7359 patients (29%) had severe or very severe pneumonia, of whom 6026 (82%) were enrolled. RSV prevalence was 15% (20% among infants) and 27% during epidemics (32% among infants). The proportion of case patients aged 3 months was 65%, and the proportion aged 6 months was 43%. Average annual hospitalization rates were 293 hospitalizations per 100,000 children aged <5 years (95% confidence interval, 271–371 hospitalizations per 100,000 children aged <5 years) and 1107 hospitalizations per 100,000 infants (95% confidence interval, 1012–1211 hospitalizations per 100,000 infants). Hospital admission rates were double in the region close to the hospital. Few patients with RSV infection had life‐threatening clinical features or concurrent serious illnesses, and the associated mortality was 2.2%. Conclusions.In this low‐income setting, rates of hospital admission with RSV‐associated pneumonia are substantial; they are comparable to estimates from the United States but considerably underestimate the burden in the full community. An effective vaccine for children aged >2 months (outside the age group of poor responders) could prevent a large portion of RSV disease. Severity data suggest that the justification for RSV vaccination will be based on the prevention of morbidity, not mortality.

138 citations



Journal ArticleDOI
17 Jul 2009-Science
TL;DR: The causes of epidemics of rotavirus, a major, global endemic virus, are investigated, with implications for childhood vaccination and the risk of future, widespread pandemics.
Abstract: Epidemic viruses, such as severe acute respiratory syndrome (SARS) and influenza A, cause diseases that rapidly spread to many people, and seem to attract more scientific and public attention than do endemic viruses, which are continually present in populations. Yet endemic viruses cause far greater disability and death. But epidemic viruses are endemic somewhere, or will become so, and endemic viruses are often recurrently epidemic. So developing a full understanding of the mechanisms that promote and drive endemicity is key to reducing the overall burden of viral disease and reducing the risk of future, widespread pandemics. On page 290 of this issue, Pitzer et al. ( 1 ) investigate the causes of epidemics of rotavirus, a major, global endemic virus.

4 citations