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As a unique mammalian host for influenza A viruses, dogs support the transmission of canine influenza viruses (CIVs) of H3N8 and H3N2 subtypes and are susceptible to infection by avian and human influenza viruses. A cross-sectional serological study was performed to assess the exposure history of dogs in Hong Kong to CIV and human influenza viruses. Among 555 companion dogs sampled in 2015–2017, 1.3 per cent and 9.5 per cent showed hemagglutination inhibition (HI) antibody titre to CIV of H3N8 or H3N2 subtypes and to A(H1N1)pdm09 human influenza viruses, respectively. Among 182 shelter dogs sampled in 2017–2018, none showed HI titre to CIV and 1.1 per cent reacted to H3N2 human influenza virus. There was a poor correlation between ELISA and HI test results. The higher seropositive rates to human influenza viruses suggests that the contact dynamics of dogs under urban settings may affect the exposure risk to human influenza viruses and CIVs.

Avian H7N9 influenza viruses may pose a further threat to humans by reassortment with human viruses, which could lead to generation of novel reassortants with enhanced polymerase activity. We previously established a novel statistical approach to study the polymerase activity of reassorted vRNPs (Influenza Other Respir Viruses. 2013;7:969-78). Here, we report the use of this method to study recombinant vRNPs with subunits derived from human H1N1, H3N2, and H7N9 viruses. Our results demonstrate that some reassortant vRNPs with subunits derived from the H7N9 and other human viruses can have much higher polymerase activities than the wild-type levels., published_or_final_version

Objectives Swine have been regarded as intermediate hosts in the spread of influenza from birds to humans but studies of the sialylated glycans that comprise their respiratory tract have not been extensively studied in the past. This study analyzed the sialylated N-glycan and O-glycan profile of swine trachea and lung and correlated this with ex-vivo infection of swine explants with avian influenza viruses. Sample Lungs and tracheal samples were obtained from normal farm and laboratory raised swine and used for ex vivo infection as well as mass spectrometric analysis. Infection of the ex vivo tissues used high pathogenic and low pathogenic avian viruses including the novel H7N9 virus that emerged in China in early 2013. Main outcome measures Assessment of successful replication was determined by TCID50 as well as virus immunohistochemistry. The N-glycan and O-glycan profiles were measured by MALDI-TOF and sialylated linkages were determined by sialidase treatment. Lectin binding histochemistry was also performed on formalin fixed tissue samples with positive binding detected by chromogen staining. Results The swine respiratory tract glycans differed from the human respiratory tact glycans in two main areas. There was a greater abundance of Gal-α-Gal linkages resulting in a relative decrease in sialylated glycans. The swine respiratory tract also had a greater proportion of glycans containing Neu5Gc and Siaα2-6 glycans than the human respiratory tract. Infection with avian viruses was confined primarily to lung bronchioles rather than trachea and parenchyma. Conclusions In contrast to previous studies we found that there was not as much expression of Siaα2-3 glycans on the surface of the trachea. Infection of Siaα2-3 binding avian viruses was restricted to the lower respiratory tract bronchioles. This finding may diminish the ability of the swine to act as an intermediary in the transmission of avian viruses to humans.

Please cite this paper as: Wong et al. (2012) Cigarette smoking as a risk factor for influenza-associated mortality: evidence from an elderly cohort. Influenza and Other Respiratory Viruses 7(4), 531–539. Background The effects of individual lifestyle factors on the mortality risk after influenza infection have not been explored. Objectives In this study, we assessed the modifying effects of cigarette smoking on mortality risks associated with influenza in a cohort of Hong Kong elders with a follow-up period of 1998–2009. Methods We used the Cox proportional hazards model with time-dependent covariates of weekly proportions of specimens positive for influenza (termed as influenza virus activity), to calculate the hazard ratio of mortality associated with a 10% increase in influenza virus activity for never, ex- and current smokers. Other individual lifestyle and socioeconomic factors as well as seasonal confounders were also added into the models. Results The overall hazard ratio associated with influenza was 1·028 (95% confidence interval, 1·006, 1·051) for all natural cause mortality and 1·035 (1·003, 1·068) for cardiovascular and respiratory mortality. We found that influenza-associated hazard ratio was greater in current and ex-smokers than in never smokers for mortality of all natural causes, cardiovascular and respiratory diseases. Conclusions The findings suggest that smoking might increase influenza-associated mortality risks among elders.

Four clinical isolates of SARS coronavirus were serially passaged in two primate cell lines (FRhK4 and Vero E6). Viral genetic sequences encoding for structural proteins and open reading frames 6–8 were determined in the original clinical specimen, the initial virus isolate (passage 0) and at passages 5, 10, and 15. After 15 passages, a total of 15 different mutations were identified and 12 of them were non‐synonymous mutations. Seven of these mutations were recurrent mutation and all located at the spike, membrane, and Orf 8a protein encoding sequences. Mutations in the membrane protein and a deletion in ORF 6–8 were already observed in passage 0, suggesting these amino acid substitutions are important in the adaptation of the virus isolate in primate cell culture. A mutation in the spike gene (residue 24079) appeared to be unique to adaptation in FRhK4 cells. It is important to be aware of cell culture associated mutations when interpreting data on molecular evolution of SARS coronavirus. J. Med. Virol. 76:435–440, 2005. © 2005 Wiley‐Liss, Inc.

Human cytomegalovirus (HCMV), human herpesvirus-6 (HHV-6), and human herpesvirus-7 (HHV-7) DNA in peripheral blood leukocytes (PBL) of 61 bone marrow transplant recipients was monitored weekly during the first 12 weeks post-transplantation by a nested polymerase chain reaction (PCR). Thirty-seven (61%), 17 (28%), and 32 (53%) of patients had one or more PBL specimens positive for HCMV, HHV-6 or HHV-7 DNA, respectively. HHV-7 DNA in PBL during the early post-transplant period was associated with a longer time to neutrophil engraftment (mean 28.8 days vs 19.8 days; P = 0.01). In two patients who failed to engraft, HHV-6 DNA and HHV-7 DNA was detected in plasma and PBL, respectively, early in their post-transplant period. Patients with HCMV disease were more likely to have concurrent HHV-7 DNA in PBL prior to onset of disease than were patients with asymptomatic HCMV infection, suggesting that HHV-7 may be a cofactor in the progression from HCMV infection to HCMV disease. In the 17 patients (179 specimens) in whom viral DNA in plasma was studied (in addition to PBL), a positive result was found only in 3. In each, viral DNA in plasma appeared to correlate with clinically significant disease. HHV-7 DNA in plasma was associated with encephalitis in an allograft recipient.

Diagnosis of significant infections by human herpesvirus 6 (HHV6) and 7 (HHV7) in transplant patients has proved difficult because both viruses are ubiquitous and can cause persistent infections in their hosts. The significance of viral DNA detected in peripheral blood leukocytes (PBLs; DNAemia) by PCR is therefore unclear. The interpretation of serological results is complicated by the fact that both primary and secondary infections with other herpesviruses may be associated with a concurrent antibody response to HHV6. Fifty-four renal allograft recipients were studied prospectively and their serological response to HHV6, HHV7 and CMV were compared with the detection of viral DNAemia from the homologous and heterologous viruses. Serum and heparinished blood samples were collected prospectively from 54 renal allograft recipients. DNA was extracted from PBLs and tested for the presence of HHV6, HHV7 and CMV DNA by PCR. Antibodies to HHV6 and HHV7 were measured by an indirect immunofluorescence test and to CMV by an anticomplement immunofluorescence (ACIF) test. CMV IgM antibodies were detected by a commercial enzyme immunoassay. CMV and HHV7 DNAemia were each significantly associated with serological responses to the homologous virus but no such association was found for HHV6 DNAemia. However, patients with consecutively positive DNAemia to any of the viruses (including HHV6) were more likely to have a homologous serological response. Patients who had detectable CMV IgM without a concurrent rise in CMV antibodies were significantly less likely to have CMV DNAemia (odds ratio = 0.16; 95% CI 0.02-0.9). CMV IgM antibodies may be associated with HHV6 or HHV7 DNAemia (odds ratio 2.3; 95% CI 0.5-15). This serological profile may reflect a crossreactive response to HHV6, HHV7 or other herpesviruses. CMV IgM should not be used in isolation for the diagnosis of CMV infection or disease in this group of patients.