Deaths associated with human adenovirus-14p1 infections, Europe, 2009-2010

Abstract

Human adenovirus (HAdV) serotype 14 is rarely identified. However, an emerging variant, termed HAdV-14p1, recently has been described in the United States in association with outbreaks of acute respiratory disease with high rates of illness and death. We retrospectively analyzed specimens confirmed positive for HAdV by immunofluorescence, virus culture, or real-time PCR during July 1, 2009-July 31, 2010, and describe 9 cases of HAdV-14p1 infection with characteristic mutations in the fiber and E1A genes that are phylogenetically indistinguishable from the viruses previously detected in the United States. Three patients died; 2 were immunocompromised, and 1 was an immunocompetent adult. We propose that surveillance should be increased for HAdV-14p1 and recommend that this virus be considered in the differential diagnosis of sudden-onset acute respiratory disease, particularly fatal infections, for which an etiology is not clear.

Figure 1

Maximum-likelihood trees of the full-length fiber (A), E1A (B), and hexon (C) open reading frames of adenovirus B2 subgenera. Phylogenetic analysis was performed by using reference sequences from GenBank for the adenovirus B2 subgenera, including prototype reference strains. The query sequences from this study are identical and are represented in boldface. The tree was built in PAUP* (23) on the basis of the HKY85 model of evolution and for the fiber tree also with a β distribution and used midpoint rooting. Bootstrap resampling (n = 1,000) was performed by using the neighbor-joining algorithm. Scale bars indicate nucleotide substitutions per site.

Figure 2

Comparative restriction enzyme analysis of viral DNA extracted from the prototype human adenovirus (HAdV) 14 de Wit strain and the first detected HAdV-14 case isolated in Dublin, Ireland, November 2009. All odd-numbered lanes (e.g., 1, 3) contain the de Wit strain and all even-numbered lanes (e.g., 2, 4) contain the Dublin 2009 strain, with restriction enzyme digests as follows: lanes 1 and 2 with BamHI; lanes 3 and 4 with BclI; lanes 5 and 6 with BglII; lanes 7 and 8 with BstEII; lanes 9 and 10 with DraI; lanes 11 and 12 with HindIII; lanes 13 and 14 with PstI; lanes 15 and 16 with SmaI; lanes 17 and 18 with XbaI. Outer lanes are molecular markers (1 Kb +100 bp; BioRad, Hercules, CA, USA).