All IVIG preparations we examined contained high NATs to all HPeVs (Table 2).
Our findings indicate that using LLC-MK2 cells might be preferable in a neutralization assay for HPeVs because all 3 HPeVs replicate efficiently in LLC-MK2 cells and effects of using different cell lines can be excluded when interpreting results.
The remaining known HPeVs are clinically unexplored.
Centralized surveillance of this virus could provide deeper insight into the behavior of HPeV and might shed light on the clinical significance of the HPeVs other than type 3.
Although we used a new direct-sequence analysis method and a slightly older RT-PCR method to amplify the HPeV3 genome in this study, new laboratory diagnostic procedures for HPeVs have been developed during the past few years.
Phylogenetic analysis with the complete P1 amino acid sequences of fully sequenced HPeVs confirmed the existence of the 6 types defined by previous studies (Figure 1, panel A) (15).
Alignments showed that VP3/VP1, VP1/2A, and 2C/3A cleavage sites differed for PAK5045 relative to those of fully sequenced HPeVs strains, whereas the other 6 sites were conserved.
To identify possibly unrecognized HPeVs, we systematically searched for HPeVs in patients in Brazil with enteritis.
The primers used for RT-PCR were HPeV-head (forward primer; 5'-TTT GAA AGG GGT CTC CT-3') and HPeV-mid (reverse primer; 5'-CAT AAG TTC CAC AAG CGT GG-3') HPeV-head primer was designed as a conserved 5' end sequence of the HPeVs 5' UTR.
This association has increased the awareness of HPeVs as relevant pathogens in young children.
However, if the 3 patients with nosocomial HPeVs are excluded, the mean duration of hospitalization was 3.
Neonatal infections caused by other HPeVs and many enteroviruses have been reported, including outbreaks of respiratory diseases on neonatal wards (11).