Influenza Influenza viruses are classified as genera A, B, and C, in accordance with the antigenic differences in their nucleoproteins (NP) and matrix 1 (M1) proteins (28). Influenza A (IAV) and B (IBV) viruses can result in severe upper respiratory disease in humans, while influenza C viruses (ICV) cause relatively mild disease (9, 23). Among influenza viruses, IAV and IBV are very similar in terms of genome structure and organization. IBV, along with influenza A(H3N2) and A(H1N1) viruses [including A(H1N1)pdm09 virus], cause seasonal influenza epidemics annually (9, 23). In the United States alone during 1976 to 2007, approximately 3,000 to 49,000 deaths each year have been attributed to these epidemics (42). Some reports indicate that in older children and healthy adults, influenza A(H3N2) virus is responsible for the most severe cases, followed by IBV, while influenza A(H1N1) virus infections tend to manifest as the mildest cases of illness (1,5,23,25). In some seasons, however, IBV may be the predominate strain responsible for influenza activities. This was best exemplified by the 1979-1980 season, in which IBV was the predominant strain circulating in the United States; therefore, it was responsible for influenza outbreaks and excess pneumonia and influenza deaths nationwide (39). Furthermore, IBV has been reported to be associated with central nervous system complications, such as Reye's syndrome and encephalitis in children (1).IBVs continue to circulate worldwide alongside IAVs. Actively circulating IBVs are divided into two genetically and antigenically

Influenza A viruses are usually non-pathogenic in wild aquatic birds, their natural reservoir. However, from May to July 2005, at Qinghai Lake in China, an unprecedented outbreak of highly pathogenic H5N1 avian influenza virus caused the death of thousands of wild migratory waterbirds. Herein, H5N1 influenza virus from bar-headed geese collected during the outbreak was characterized. Genomic analysis showed that A/Bar-headed Goose/Qinghai/0510/05 (Bh H5N1 virus) is a reassortant virus. Amino acid residue (lysine) at position 627 in the PB2 gene of the Bh H5N1 virus was the same as that of the human H5N1 virus (A/HK/483/97) and different from that of H5N1 avian influenza viruses deposited in GenBank. Antigenic analysis showed that significant antigenic variation has occurred in the Bh H5N1 virus. The Bh H5N1 virus induced systemic infections and caused 100 % mortality in chickens and mice, and 80 % mortality in ducks and geese. Bh H5N1 virus titres were higher in multiple organs of chickens, ducks and geese than in mice, and caused more severe histological lesions in chickens, ducks and mice than in geese. These results support the need to pay close attention and create control programmes to prevent the transmission of highly pathogenic avian influenza virus from wild migratory waterbirds into domestic chickens, ducks, geese and mammalian hosts.

Porcine circovirus 3 (PCV3) has been identified as a putative swine pathogen with a subset of infections resulting in stillborn and mummified fetuses, encephalitis and myocarditis in perinatal, and periarteritis in growing pigs. Three PCV3 isolates were isolated from weak-born piglets or elevated stillborn and mummified fetuses. Full-length genome sequences from different passages and isolates (PCV3a1 ISU27734, PCV3a2 ISU58312, PCV3c ISU44806) were determined using metagenomics sequencing. Virus production in cell culture was confirmed by qPCR, IFA, and in situ hybridization. In vivo replication of PCV3 was also demonstrated in CD/CD pigs (n = 8) under experimental conditions. Viremia, first detected at 7 dpi, was detected in all pigs by 28 dpi. IgM antibody response was detected between 7–14 dpi in 5/8 PCV3-inoculated pigs but no IgG seroconversion was detected throughout the study. Pigs presented histological lesion consistent with multi systemic inflammation characterized by myocarditis and systemic perivasculitis. Viral replication was confirmed in all tissues by in situ hybridization. Clinically, all animals were unremarkable throughout the study. Although the clinical relevance of PCV3 remains under debate, this is the first isolation of PCV3 from perinatal and reproductive cases of PCV3-associated disease and in vivo characterization of PCV3 infection in a CD/CD pig model.

No abstract

We retrospectively analysed the epidemiological data of all hand, foot, and mouth disease (HFMD) cases from the largest paediatric infectious diseases centre in Shanghai between 2007 and 2010. A total of 28 058 outpatients were diagnosed with HFMD, of which 3948 (14.07%) were hospitalized, 730 (2.60%) had complications with neurological disorders and pulmonary oedema/haemorrhage, and 11 (0.04%) died. The peak season was the summer months. Boys were more affected than girls. Since 2008, the major population group affected has shifted from native Shanghainese children attending preschool to migrant children and younger children cared for at home. Children aged 1-4 years constituted 82.27% of cases. EV-A71 was tested in clinical samples taken from severe cases in 2009 and 2010, and from most inpatients in 2010. EV-A71 was positive in 99.17% and 86.31% of severe cases, respectively in 2009 and 2010. All 12 cases with pulmonary oedema or haemorrhage were infected with EV-A71. Ten (90.90%) of 11 fatal cases were attributable to EV-A71 infection. In 2010, EV-A71-positive cases accounted for 54.12% of inpatients. The dominant circulation of EV-A71 led to the outbreak of HFMD and occurrence of severe and fatal cases.

No abstract

To determine the prevalence of porcine circovirus 2 (PCV2) genotypes in the USA during 2010-2011, 5 years after widespread PCV2 vaccination, serum samples from clinically normal pigs that were PCV2 vaccinated (n51177), non-vaccinated (n5378) or of unknown vaccination status (n5120), and 100 lung samples from pigs diagnosed with PCV-associated disease (PCVAD) were tested. The presence of PCV2, PCV1, PCV1-2a and porcine parvovirus (PPV) DNA was determined by PCR. Determination of the PCV2 genotype was done by differential PCR and sequencing. The prevalence of PCV2a and PCV2b in serum samples was 7.7 % (129/1675) and 8.4 % (141/1675), respectively. PCV2a DNA was only detected in non-vaccinated pigs. For the 100 PCVAD pigs, the prevalence of PCV2a and PCV2b in lung tissues was 13.0 and 65.0 %, respectively. Partial PCV2 ORF2 sequences (9-563 nt) were obtained from 85 PCV2 DNA-positive samples (24 normal pigs and 61 PCVAD cases). Phylogenetic analysis revealed that 12.9 % (11/85) of the sequences belonged to the 2E clade and the PCV2a genotype and 87.1 % (74/85) belonged to the 1B clade and the PCV2b genotype. The alignment of putative PCV2 capsid amino acid sequences revealed possible recombination or mutation between PCV2a and PCV2b genotypes. Chimeric PCV1-2a was not detected in any of the samples and the prevalence rates of PCV1 and PPV were low. Our results suggest PCV2b is more prevalent than PCV2a in PCVAD cases and in vaccinated herds PCV2b circulation is common. The data generated in this study provide novel information on the distribution of PCV2 genotypes in vaccinated pig populations.

No abstract