The cause of this ARTI outbreak was HAdV-B55. This was another outbreak caused by this re-emerging virus. Continuous surveillance of respiratory adenovirus is necessary for disease control.

Objectives: No licensed vaccines or therapeutic agents for human metapneumovirus (hMPV) infection exist to date. We aimed to construct a multi-epitope peptide (MEP) of hMPV to show promising results for epitope-based vaccine development. Methods: Six independent algorithms were screened to predict B-cell epitopes of hMPV, and three algorithms were used to predict cytotoxic T lymphocyte and T helper (Th) lymphocyte epitopes. Predicted epitopes were assembled in series with the spacers GPGPG and KK introduced, termed MEP. Recombinant mep genes were inserted into pET32a(+) plasmid and expressed in Escherichia coli strain BL21 (DE3). BALB/c mice were immunized with MEP with different adjuvants. Antibody titer, lymphocyte proliferation, cytotoxic T lymphocyte (CTL) activity and splenocyte cytokines were detected 2 weeks later after the last immunization. Microneutralization assay was used to detect neutralizing antibodies. Results: Six B-cell epitopes, four CTL epitopes and two Th epitopes were screened to construct the mep gene. Expressed MEP induced >10⁴ antibodies in BALB/c mice, and produced anti-MEP antibody reacting with hMPV strains specifically as detected in indirect fluorescent assay (the titer was 160). The lymphocyte proliferation index, CTL activity and splenocyte cytokines of the MEP immunization groups were higher than in the control group (p < 0.05). Both IgG1 and IgG2a antibodies could be detected in the different groups, and balanced Th1/Th2 cytokines were secreted by splenocytes in these groups. The mean neutralizing titers of the MEP+CpG ODN, MEP+Alum and MEP+Alum+ CpG ODN groups were 87 (95% CI 50-126), 93 (95% CI 67-121) and 96 (95% CI 69-147), respectively. Conclusion: MEP of hMPV elicited both strong humoral immunity and cell-mediated immunity in mice. The anti-MEP serum could neutralize hMPV infection in vitro. Joint use of CpG ODN and aluminum hydroxide adjuvants obtained the best immune effects. This study may contribute to hMPV epitope-based vaccine development.

Influenza A virus infections occur in different species, causing mild to severe respiratory symptoms that lead to a heavy disease burden. Eurasian avian-like swine influenza A(H1N1) viruses (EAS-H1N1) are predominant in pigs and occasionally infect humans. An influenza A(H1N1) virus was isolated from a boy who was suffering from fever and headache and designated as A/Tianjin-baodi/1606/2018(H1N1). Full-genome sequencing and phylogenetic analysis revealed that A/Tianjin-baodi/1606/2018(H1N1) is a novel reassortant EAS-H1N1 containing gene segments from EAS-H1N1 (HA and NA), classical swine H1N1(NS) and A(H1N1)pdm09(PB2, PB2, PA, NP and M) viruses. The isolation and analysis of A/Tianjin-baodi/1606/2018(H1) provide further evidence that EAS-H1N1 poses a threat to human health and greater attention should be paid to surveillance of influenza virus infection in pigs and humans.

Active symptom surveillance was applied to three selected communities ( 160,147 persons) in Tianjin from 2010 to 2012. We examined 1089 individuals showing pertussis-like symptoms, of which 1022 nasopharyngeal specimens were tested for pertussis by polymerase chain reaction and 802 sera for anti-pertussis toxin antibodies. Of the total cases tested, 113 were confirmed, and their demographic, clinical, and vaccination-related data were collected. The annual incidence was 23.52 cases/100,000 persons among communities, which was 16.22 times that obtained via hospital reports for the same period (P < 0.001). The actual incidence in the 15-69 years age group was most significantly underestimated by hospitals, given that it was 43.08 times that of the reported hospital rate. Among the cases aged <15 years, 84.5% were individuals who had been fully vaccinated. The misdiagnosis rate was as high as 94.69%, and only 5.31% of the confirmed pertussis cases were properly diagnosed as pertussis at their first medical visit. Pertussis incidence in China has been severely underestimated and this was in part due to a high misdiagnosis rate. Adolescents and adults have become new high-risk populations. Future work should focus on reinforcing immunization programmes, especially among adolescents and adults.

No abstract

No abstract

No abstract

Pandemic influenza A (H1N1) 2009 virus (H1N1pdm09) was a novel tri-assortment virus that emerged in Mexico and North America in 2009 and caused the first influenza pandemic in the 21st century. This study investigated the prevalence pattern and molecular characteristics of H1N1pdm09 in three continuous years from April 2009 to March 2012 in populations of Tianjin, Northeast China. Totally, 3,068 influenza viruses (25.4 %) were detected from 12,089 respiratory specimens. Among them, 41.4 % (1,269/3,068) were H1N1pdm09 positive. 15.1 % (192/1,269) severe respiratory infection cases were H1N1pdm09 positive. H1N1pdm09 was the predominant prevalence subtype in October 2009-March 2010 (69.1 %, 930/1,346) and October 2010-March 2011 (42.1 %, 220/523). Eight isolated H1N1pdm09 viruses from severe infection/death cases in three different years were selected to sequence the whole genome through splicing the sequences following 46 PCRs. HA sequences of seven H1N1pdm09 isolates from mild infection cases were detected. Phylogenetic analysis showed that HA, NA, M, NP and NS genes of H1N1pdm09 viruses gathered together with swine influenza A (H1N1), whereas PB2 and PA genes originated from avian influenza virus, and PB1 gene originated from human seasonal influenza virus. Identity analysis indicated that all the genes were highly conserved. Compared with vaccine strain A/California/07/2009(H1N1), the maximal mutation gene was HA (0.7-2.6 %), then NA (0.6-1.7 %), last one was M (mutation rate 0-0.6 %). More site substitutions were observed in 2011 isolates than in 2009 and 2010 isolates of HA (p = 0.002), NA (p = 0.003) and PA (p = 0.001) proteins. The amino acid substitution rates were varied among eight gene segments, ranging from 7.39 × 10(-4) for PB2 to 7.40 × 10(-3) for NA. The higher d N / d S rates were observed in HA, PA and NS segments in H1N1pdm09 in Tianjin. Three HA amino acid site substitutions occurred at the HA receptor-binding sites and antigenic determinant, including S179N and K180T (located at antigenic site Sa) in A/Tianjinhedong/SWL44/2011(H1) and A/Tianjinjinnan/SWL41/2011(H1), and D239N (located at antigenic site Ca) in A/Tianjinninghe/SWL49/2009(H1). Antigenic drift may have occurred in H1N1pdm09 with time. No oseltamivir-resistance site substitution was observed at 275 and 295 sites. Amino acid residue site at 31 in M2 protein was N in all 8 isolates, which suggested that H1N1pdm09 was resistant to amantadine.