Association between nasal shedding and fever that influenza A (H3N2) induces in dogs

<p>Abstract</p> <p>Background</p> <p>Avian origin canine influenza virus was reported in Korea. The dog to dog contact transmission of the avian origin canine influenza virus (CIV) H3N2 and CIV H3N8 was shown by experimental contact transmission. This study was focused on viral excretion and fever in order to elucidate the epidemiological associations which might be helpful to control the disease transmissions in CIV outbreak in dogs.</p> <p>Methods</p> <p>An influenza seronegative 10-week-old Beagle dog was experimentally inoculated with the canine influenza virus A/canine/01/2007, subtype H3N2. Eight hours after inoculation, the infected dog was cohoused with seven uninfected Beagle dogs. Clinical signs including fever were recorded for 14 days post inoculation.</p> <p>Results</p> <p>The infected dog and four of seven contact dogs in the study showed clinical signs (sneezing, nasal discharge and coughing) during the study. Viral shedding occurred in all of the animals tested and began on 1 to 6 DPI in dogs with clinical signs. Elevated body temperatures above 39.5°C (geometric mean temperature of 39.86°C±0.49) were observed in all symptomatic dogs. The mean viral titer during fever was 2.99 log EID₅₀/ml, which was significantly higher than the viral titer detected in the non fever.</p> <p>Conclusions</p> <p>The data show that contact dogs with a canine influenza infected dog shed different levels of virus in their nasal excretions and demonstrate that clinical signs, including fever, significantly correlate with the viral shedding.</p

Two Alternative Splicing Variants of AtERF73/HRE1, HRE1α and HRE1β, Have Differential Transactivation Activities in Arabidopsis

AtERF73/HRE1 is an AP2/ERF transcription factor in Arabidopsis and has two distinct alternative splicing variants, HRE1&alpha; and HRE1&beta;. In this study, we examined the differences between the molecular functions of HRE1&alpha; and HRE1&beta;. We found that HRE1&alpha; and HRE1&beta; are both involved in hypoxia response and root development and have transactivation activity. Two conserved motifs in the C-terminal region of HRE1&alpha; and HRE1&beta;, EELL and LWSY-like, contributed to their transactivation activity, specifically the four E residues in the EELL motif and the MGLWS amino acid sequence at the end of the LWSY-like motif. The N-terminal region of HRE1&beta; also showed transactivation activity, mediated by the VDDG motif, whereas that of HRE1&alpha; did not. The transactivation activity of HRE1&beta; was stronger than that of HRE1&alpha; in Arabidopsis protoplasts. Both transcription factors transactivated downstream genes via the GCC box. RNA-sequencing analysis further supported that both HRE1&alpha; and HRE1&beta; might regulate gene expression associated with the hypoxia stress response, although they may transactivate different subsets of genes in downstream pathways. Our results, together with previous studies, suggested that HRE1&alpha; and HRE1&beta; differentially transactivate downstream genes in hypoxia response and root development in Arabidopsis

Characteristics and Pathogenicity of the Cell-Adapted Attenuated Porcine Epidemic Diarrhea Virus of the Non-S INDEL Cluster

The high antigenic diversity of porcine epidemic diarrhea virus (PEDV) means that porcine epidemic diarrhea (PED) is a challenge for the global pig industry. Understanding the circulation of the virus to determine an optimal vaccine strategy is important in controlling the disease. In this study, we describe the genetic diversity of circulating PEDV based on the full sequences of spike genes of eight positive samples collected in Vietnam since 2018. Additionally, we developed a live attenuated vaccine candidate from the cell-adapted PEDV2 strain, which was continuously passaged until level 103 in VERO-CCL81 cells. PEDV2-p103, which belongs to the emerging non-S INDEL cluster, exhibited low virus shedding, did not induce lesions in the small intestine of challenged piglets, and had a high titer in the VERO-CCL81 cell at 48 h post-infection. These results suggest that the PEDV2-p103 strain could be a potential oral attenuated vaccine, and its immunogenicity and efficacy should be further assessed through in vivo tests

Comparison of the virulence of three H3N2 canine influenza virus isolates from Korea and China in mouse and Guinea pig models

Abstract Background Avian-origin H3N2 canine influenza virus (CIV) has been the most common subtype in Korea and China since 2007. Here, we compared the pathogenicity and transmissibility of three H3N2 CIV strains [Chinese CIV (JS/10), Korean CIV (KR/07), and Korean recombinant CIV between the classic H3N2 CIV and the pandemic H1N1 virus (MV/12)] in BALB/c mouse and guinea pig models. The pandemic H1N1 (CA/09) strain served as the control. Results BALB/c mice infected with H1N1 had high mortality and obvious body weight loss, whereas no overt disease symptoms were observed in mice inoculated with H3N2 CIV strains. The viral titers were higher in the group MV/12 than those in groups JS/10 and KR/07, while the mice infected with JS/10 showed higher viral titers in all tissues (except for the lung) than the mice infected with KR/07. The data obtained in guinea pigs also demonstrated that group MV/12 presented the highest loads in most of the tissues, followed by group JS/10 and KR/07. Also, direct contact transmissions of all the three CIV strains could be observed in guinea pigs, and for the inoculated and the contact groups, the viral titer of group MV/12 and KR/07 was higher than that of group JS/10 in nasal swabs. These findings indicated that the matrix (M) gene obtained from the pandemic H1N1 may enhance viral replication of classic H3N2 CIV; JS/10 has stronger viral replication ability in tissues as compared to KR/07, whereas KR/07 infected guinea pigs have more viral shedding than JS/10 infected guinea pigs. Conclusions There exists a discrepancy in pathobiology among CIV isolates. Reverse genetics regarding the genomes of CIV isolates will be helpful to further explain the virus characteristics