Coxsackievirus A21, Enterovirus 68, and Acute Respiratory Tract Infection, China - Vol. 18 No. 5 - May 2012 - Emerging Infectious Disease journal - CDC
Volume 18, Number 5—May 2012
Coxsackievirus A21, Enterovirus 68, and Acute Respiratory Tract Infection, China
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Human enteroviruses (HEVs) are small, nonenveloped RNA viruses belonging to the family Picornaviridae. HEVs are classified into 4 species (HEV-A to -D) according to their molecular and antigenic properties (1). HEVs are associated with diverse clinical syndromes, ranging from mild upper respiratory tract illnesses to severe and potentially fatal conditions, such as aseptic meningitis, encephalitis, myocarditis, acute flaccid paralysis, and hand-foot-and-mouth disease (1).
AbstractDuring August 2006–April 2010, in Beijing, China, 2 rare human enterovirus serotypes, coxsackievirus A21 and enterovirus 68, were detected most frequently in human enterovirus–positive adults with acute respiratory tract infections. Thus, during some years, these 2 viruses cause a substantial proportion of enterovirus-associated adult acute respiratory tract infections.
Although HEV serotypes can cocirculate, spatial and temporal factors determine the predominant serotype. For instance, in France and Spain, echovirus 11 and echovirus 6 are the predominant serotypes in patients with enterovirus respiratory infections (2,3). Clusters of the rare serotype enterovirus 68 (EV68), which causes severe respiratory infections in children, have been recently reported in the Philippines (4) and Japan (5). To help clinicians and public health officials better understand the epidemiologic and clinical profiles of HEV respiratory infections, temporal and geographic patterns of circulation, especially the dynamics of HEV serotype shift, need to be determined. We report that in some years in Beijing, People’s Republic of China, the rarely reported coxsackievirus A21 (CVA21) and EV68 are the predominant serotypes in adults with enterovirus-associated acute respiratory tract infection (ARTI).
From August 2006 through April 2010, throat and nasal swabs were collected from 6,942 (3,158 male and 3,784 female) adult patients (>15 years of age) at the time of admission to the Fever Clinic Department at the Peking Union Medical College Hospital for ARTI. The 6,942 participants were randomly selected by physicians, as described (6). To detect HEV, we amplified 350–400 bp of the viral protein 1 (VP1) gene by reverse transcription PCR (7) and verified the findings by sequence analysis (GenBank accession nos. JN168998–JN169120). According to results of BLAST analysis (www.ncbi.nlm.nih.gov), the HEV detected in a sample was assigned to the serotype with which the amplified sequence shared >75% nt or >88% aa sequence identity (8). All samples were simultaneously screened for influenza viruses (A, B, and C), human parainfluenza viruses (1–4), respiratory syncytial virus, human coronaviruses (229E, NL63, HKU1, and OC43), metapneumovirus, adenovirus, and rhinovirus (6).