Downloaded from www.microbiologyresearch.org by IP: 54.70.40.11 On: Fri, 07 Dec 2018 07:56:14 Comparative genomic analysis of two strains of human adenovirus type 3 isolated from children with acute respiratory infection in southern China Qiwei Zhang, 1,2 Xiaobo Su, 3 Sitang Gong, 2 Qiyi Zeng, 2 Bing Zhu, 2 Zaohe Wu, 3 Tao Peng, 4 Chuyu Zhang 1 and Rong Zhou 2,3 Correspondence Chuyu Zhang Zhang_whu@yahoo.com.cn Rong Zhou zhou3218@yahoo.com 1 State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China 2 Central Laboratory, Guangzhou Children’s Hospital, Guangzhou 510120, China 3 South China Sea Institute of Oceanology, LED, Chinese Academy of Sciences, Guangzhou 510301, China 4 Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou 510663, China Received 9 September 2005 Accepted 8 February 2006 Human adenovirus type 3 (HAdV-3) is a causative agent of acute respiratory disease, which is prevalent throughout the world, especially in Asia. Here, the complete genome sequences of two field strains of HAdV-3 (strains GZ1 and GZ2) isolated from children with acute respiratory infection in southern China are reported (GenBank accession nos DQ099432 and DQ105654, respectively). The genomes were 35 273 bp (GZ1) and 35 269 bp (GZ2) and both had a G+C content of 51 mol%. They shared 99 % nucleotide identity and the four early and five late regions that are characteristic of human adenoviruses. Thirty-nine protein- and two RNA-coding sequences were identified in the genome sequences of both strains. Protein pX had a predicted molecular mass of 8?3 kDa in strain GZ1; this was lower (7?6 kDa) in strain GZ2. Both strains contained 10 short inverted repeats, in addition to their inverted terminal repeats (111 bp). Comparative whole-genome analysis revealed 93 mismatches and four insertions/deletions between the two strains. Strain GZ1 infection produced a typical cytopathic effect, whereas strain GZ2 did not; non-synonymous substitutions in proteins of GZ2 may be responsible for this difference. INTRODUCTION Adenoviruses (AdVs) are responsible for 5–10 % of lower respiratory tract infections in infants and children and infect a very broad spectrum of hosts, including cattle, duck, possum, dog, tree shrew, fish, frog, corn snake, and equine, ovine, porcine and simian animals (Davison et al., 2000; Farkas et al., 2002; Kova ´cs et al., 2003). They can be divided into four genera, Atadenovirus, Aviadenovirus, Mastadeno- virus, Siadenovirus, and unassigned species (Benko ˝ et al., 2000, 2002; Shenk, 2001; Davison et al., 2003; Kova ´cs et al., 2003). Since the first human adenovirus (HAdV) was isolated (Rowe et al., 1953), 51 different HAdV serotypes have been identified within the genus Mastadenovirus and they can be classified into six species (HAdV-A to -F) based on a variety of parameters, including oncogenicity in rodents, electrophoretic mobility (Wadell, 1979) and DNA or genome identity (Garon et al., 1973; Green et al., 1979; Wadell et al., 1980; Wadell, 1984; De Jong et al., 1999), as well as the classical gold standards of serum neutralization and haemagglutination-inhibition tests (Davison et al., 2003). HAdV-B species have been divided further into two groups: B1, including HAdV-3, -7, -16, -21 and -50, and SAdV-21; and B2, including HAdV-11, -14, -34 and -35 (Wold et al., 1979; Stone et al., 2003). HAdV-B group B1 viruses have been isolated from patients with febrile respiratory disease, especially fatal acute respiratory disease (ARD) (Hierholzer, 1995; Erdman et al., 2002). Members of group B2, with the exception of HAdV-11a and -14 (Van der Veen, 1963; Mei et al., 1998), are associated with persistent infections of kidney and urinary tract (Myerowitz et al., 1975; Shields et al., 1985). Of the 51 HAdV serotypes, about one-third are associated with human diseases. Adenovirus infections can occur endemically or as outbreaks. HAdV-B group B1 (HAdV-3, The GenBank/EMBL/DDBJ accession numbers for the human adenovirus type 3 strain GZ1 and GZ2 sequences reported in this paper are DQ099432 and DQ105654, respectively. 0008-1515 G 2006 SGM Printed in Great Britain 1531 Journal of General Virology (2006), 87, 1531–1541 DOI 10.1099/vir.0.81515-0