An outbreak of acute respiratory tract infection occurred in Shanxi Province, China, from March to April 2006. Of the 254 patients affected by this outbreak, 247 patients were students of a senior high school; 1 of these patients died during the outbreak. Serological tests and blood culture revealed no evidence of bacterial infection. The results of direct reverse transcription-PCR or PCR performed with clinical specimens collected from the patients, including the sole patient who died, were positive for human adenoviruses (HAdVs) but negative for influenza virus, measles virus, rubella virus, mumps virus, parainfluenza virus, respiratory syncytial virus, and human enteroviruses. These findings were confirmed by enzyme-linked immunosorbent assay for HAdV immunoglobulin A, the conventional neutralization test, and viral isolation and identification. Sequencing of the entire hexon gene revealed that HdAV type 11a (HAdV-11a) belonging to the B2 species of HAdV was the etiological agent responsible for the outbreak. However, both the analysis of the phylogenetic relationship and the similarity plot indicated that the sequence of the 3 end of the hexon gene outside the hypervariable regions the HAdV-11a strain isolated in this outbreak may be a recombinant with the sequence of the HAdV-14 strain of species B2. Although isolates of HAdV species B2 seldom cause respiratory infections, they may pose a new global challenge with regard to acute respiratory diseases; this possibility cannot be overlooked and should be carefully considered. Hence, the need to establish and improve both epidemiological and virological surveillance of HAdV infections in China should be emphasized.

Whole-genome sequencing of human adenovirus type 11 (HAdV-11) strain QS, isolated in China, was conducted, and its sequence was compared with the sequences of strains within the species of HAdVs. The HAdV-11 QS genome contains 34,755 nucleotides. Similar to the other HAdV subgenus B sequences, the HAdV-11 QS genome coded 37 functional proteins and could be divided into four early, two intermediate, and five late transcription regions. The amino acid sequences of the fiber and the hypervariable regions (HVRs) within the hexon gene of HAdV-11 QS were identical to the corresponding sequences of the HAdV-11a strain; further analyses that compared those amino acid sequences with the amino acid sequences of the HAdV species subgenus B:2 strains revealed that the highest degree of homology (>99.2%) existed between HAdV-11 QS and the prototypical HAdV-14 strain, except for a few coding sequences of HVRs within the hexon gene, DNA polymerase, pVI, and pre-terminal protein. This indicate that HAdV-11 strain QS, isolated in China, is a recombinant adenovirus of HAdV-14, and the recombination analyses also confirmed this finding. It is difficult to clarify the time and manner of the recombination, and further investigations are required to determine whether the emergence of recombination between HAdV-11a and HAdV-14 might increase virulence, thereby posing a new global challenge with regard to acute respiratory diseases in the near future.

The prevalence of T2DM is high among women, and postmenopause status might be a stable and significant risk factor for T2DM; especially, postmenopausal women with normal weight should not be ignored in addressing the risk.

Alzheimer’s disease (AD) is commonly an age-associated dementia with neurodegeneration. The pathogenesis of AD is complex and still remains unclear. The inflammation, amyloid β (Aβ), and neurofibrillary tangles as well misfolded tau protein in the brain may contribute to the occurrence and development of AD. Compared with tau protein, Aβ is less toxic. So far, all efforts made in the treatments of AD with targeting these pathogenic factors were unsuccessful over the past decades. Recently, many studies demonstrated that changes of the intestinal environment and gut microbiota via gut–brain axis pathway can cause neurological disorders, such as AD, which may be involved in the pathogenesis of AD. Thus, remodeling the gut microbiota by various ways to maintain their balance might be a novel therapeutic strategy for AD. In the review article, we analyzed the characteristics of gut microbiota and its dysbiosis in AD and its animal models and investigated the possibility of targeting the gut microbiota in the treatment of the patients with AD in the future.