Epstein-Barr virus reactivation and upper-respiratory illness in elite swimmers

Abstract

GLEESON, M., D. B. PYNE, J. P. AUSTIN, J. L. FRANCIS, R. L. CLANCY, W. A. MCDONALD, and P. A. FRICKER. Epstein-Barr virus reactivation and upper-respiratory illness in elite swimmers. Med. Sci. Sports Exerc., Vol. 34, No. 3, pp. 411–417, 2002. The aim of this study was to investigate the relationships between latent viral shedding of Epstein-Barr virus (EBV) in saliva, upper-respiratory illness, and mucosal immune suppression in a cohort of highly trained swimmers undertaking intensive training. Saliva was collected before selected training sessions from 14 elite male swimmers during a 30-d period of intensive training. Prior infection with EBV was determined by EBV antibody serology. Salivary IgA concentrations were measured by enzyme linked immunosorbent assay (ELISA), and EBV viral shedding (EBV-DNA) was detected by polymerase chain reaction (PCR). Symptoms of upper-respiratory illness were recorded daily. Eleven swimmers (79%) were seropositive for prior EBV infection. Seven EBV seropositive swimmers (64%) had EBV-DNA detected during the study period. Upper-respiratory symptoms (URS) were reported in six of seven swimmers in whom EBV-DNA was detected and in three of four swimmers with no EBV-DNA detection. No URS were reported in the EBV seronegative swimmers. There was a statistically significant relationship between EBV serology status and URS (P = 0.027). EBV-DNA was detected in saliva before the appearance of URS. Salivary IgA levels were significantly lower immediately before the URS (P = 0.01) compared with subsequent peak IgA levels and declined to pre-URS levels on average 11 d after the first appearance of URS. The time course of appearance of EBV-DNA in relation to URS suggests latent viral EBV shedding may be a contributing factor in the URS. The low levels of salivary IgA detected before the URS indicated transient mucosal immune suppression in the study cohort. The viral shedding may alternatively be a reflection of the altered immune control mechanisms that occur in response to intensive exercise and unrelated to the URS.