Hand-foot-and-mouth disease (HFMD) and herpangina, which commonly affect young children, are enterovirus infections causing a variety of exanthems. HFMD is a self-limiting exanthematous eruption characterized by vesicles in the oral cavity, mainly in the buccal mucosa and tongue, and peripherally distributed cutaneous lesions on the hands and feet. Herpangina produces multiple oral ulcers affecting predominantly the posterior part of the oral cavity only [1–3]. These diseases are associated with different strains of enteroviruses, such as coxsackievirus A (CVA) 2, 5, 6, 10, 16; coxsackievirus B (CVB) 1, 2, 5; and enterovirus (EV) 71 [4–8].
Human enterovirus (HEV) genera containing the CVA, CVB, echovirus (ECV), and EV serotypes are transmitted mainly via the fecal-oral route and by contact with throat discharges or fluid from blisters . Generally, HEV outbreaks peak during the summer and early fall, and various serotypes are often associated with a single outbreak . Since 1993, when nationwide surveillance began in Korea, there have been reports of summer outbreaks of enteroviruses caused by ECV 5, 6, 7, 9, 13, 18, and 30; CVA 24; CVB 3 and 5; and EV 71 [11, 12]. Especially, outbreaks of HFMD and herpangina caused by HEV infection were reported in 2009 in Korea [13, 14].
Diagnosis of HEV infections is based on amplification of a highly conserved 5’ non-coding region (NCR) that is widely-targeted in diagnostic procedures [15, 16]. In addition to traditional virological methods to serotype HEV, reverse transcription-polymerase chain reaction (RT-PCR) based on amplification of the VP1 region have been recently developed [17–19]. Because the VP1 region is one of the main exposed regions of the viral capsid and has been suggested to include a serotype specific antigenic neutralization site, the BC loop in this region has been implicated with viral antigenicity, and substitutions resulting in conformational changes in this region are believed to play a role in host adaptation for HEVs [20, 21].
In this study, to compare epidemic patterns of HFMD and herpangina, specimens from patients with HFMD and herpangina disease were collected and analyzed along with demographic data. Molecular detection by 5’ NCR RT-PCR and sequencing of the VP1 region of HEVs were carried out.