Evidence of H10N8 influenza virus infection among swine in southern China and its infectivity and transmissibility in swine.

Infection with a novel H10N8 influenza virus in humans was first described in China in December 2013, which raised concerns related to public health. This novel virus was subsequently confirmed to have originated from a live poultry market. However, whether this virus can infect other mammals remains unclear. In the present study, antibody specific for H10N8 influenza virus was detected in swine herds in southern China during serological monitoring for swine influenza virus. The pathogenicity and transmissibility of this H10N8 influenza virus to swine was examined. The results showed that swine are susceptible to infection with human-origin H10N8 influenza virus, which causes viral shedding, severe tissue lesions, and seroconversion, while infection with avian-origin H10N8 influenza virus causes only seroconversion and no viral shedding. Importantly, human-origin H10N8 influenza virus can inefficiently be transmitted between swine and cause seroconversion through direct contact. This study provides a new perspective regarding the ecology of H10N8 influenza virus and highlights the importance of epidemiological monitoring of the H10N8 influenza virus in different animal species, which will be helpful for preventing and controlling future infections by this virus.

The 150-Loop Restricts the Host Specificity of Human H10N8 Influenza Virus.

Adaptation of influenza A viruses to new hosts are rare events but are the basis for emergence of new influenza pandemics in the human population. Thus, understanding the processes involved in such events is critical for anticipating potential pandemic threats. In 2013, the first case of human infection by an avian H10N8 virus was reported, yet the H10 hemagglutinin (HA) maintains avian receptor specificity. However, the 150-loop of H10 HA, as well as related H7 and H15 subtypes, contains a two-residue insert that can potentially block human receptor binding. Mutation of the 150-loop on the background of Q226L and G228S mutations, which arose in the receptor-binding site of human pandemic H2 and H3 viruses, resulted in acquisition of human-type receptor specificity. Crystal structures of H10 HA mutants with human and avian receptor analogs, receptor-binding studies, and tissue staining experiments illustrate the important role of the 150-loop in H10 receptor specificity.

PB2-588 V promotes the mammalian adaptation of H10N8, H7N9 and H9N2 avian influenza viruses.

Human infections with avian influenza H7N9 or H10N8 viruses have been reported in China, raising concerns that they might cause human epidemics and pandemics. However, how these viruses adapt to mammalian hosts is unclear. Here we show that besides the commonly recognized viral polymerase subunit PB2 residue 627 K, other residues including 87E, 292 V, 340 K, 588 V, 648 V, and 676 M in PB2 also play critical roles in mammalian adaptation of the H10N8 virus. The avian-origin H10N8, H7N9, and H9N2 viruses harboring PB2-588 V exhibited higher polymerase activity, more efficient replication in mammalian and avian cells, and higher virulence in mice when compared to viruses with PB2-588 A. Analyses of available PB2 sequences showed that the proportion of avian H9N2 or human H7N9 influenza isolates bearing PB2-588 V has increased significantly since 2013. Taken together, our results suggest that the substitution PB2-A588V may be a new strategy for an avian influenza virus to adapt mammalian hosts.

High Pathogenicity of Influenza A (H10N8) Virus in Mice.

Three human cases of H10N8 virus infections were initially reported in China in late 2013 and early 2014, two of which were fatal. This was the first time the H10N8 subtype has been detected in humans, and the pathogenicity of this virus remains under characterized. We first assessed its pathogenicity by infecting BALB/c mice with two H10N8 isolates, A/Jiangxi-Donghu/346-1/2013 and A/Chicken/Jiangxi/102/2013. The human isolate (H346-1) demonstrated stronger capability of replication and induced higher cytokine response in vivo than the chicken isolate (C102). In addition, H346-1 was fatal to mice, while all mice (N = 14) in C102-infected group survived during the infection course without weight loss. We hypothesized that the 627K mutation in the PB2 gene (PB2-K627) in H346-1 was associated with high pathogenicity in mice. Taken together, this study based on mouse model provides some insight into understanding the pathogenicity of the emerging viruses in mammals.

Cause of death in hospitalized patients with laboratory-confirmed influenza / Causa de muerte en pacientes hospitalizados con gripe confirmada por laboratorio

Background: We analyzed the underlying cause of death recorded in hospitalized patients with laboratory-confirmed influenza. Methods: The present study included all patients with a laboratory-confirmed diagnosis of influenza during the influenza seasons 2009-2010 to 2013-2014 who were attended to in hospital and died. Their underlying cause of death according to the International Classification of Diseases 10th Revision was obtained from the Navarre Mortality Registry. Results: Among 49 patients studied, the underlying causes of death were 35% influenza, 4% pneumonia, 14% other respiratory diseases, 10% circulatory disease and 37% other causes. Conclusions: Non-cardiorespiratory causes accounted for a third of deaths in patients with confirmed influenza, thus all-cause mortality should be considered in estimating the full burden of influenza mortality (AU)

Fundamento: La mortalidad por gripe no se conoce bien porque la mayoría de las personas que mueren por gripe no se confirman por laboratorio. Analizamos la causa básica de muerte registrada en los pacientes hospitalizados con gripe confirmada por laboratorio. Métodos: Se incluyeron todos los pacientes con diagnóstico de gripe por laboratorio que habían sido atendidos en el hospital y murieron durante las temporadas 2009-2010 a 2013-2014 en Navarra. La causa básica demuerte se obtuvo del Registro de Mortalidad. Resultados: Entre los 49 pacientes estudiados, la causa básica de muerte fue en el 35% gripe, en el 4% neumonía, en el 14% otras enfermedades respiratorias, en el 10% enfermedades cardiovasculares y en el 37% otras causas. Conclusiones: Un tercio de las muertes en pacientes con gripe confirmada se asignaron a causas no cardiorrespiratorias. Deberían tenerse en cuenta todas las causas para estimar la carga total de la mortalidad por gripe (AU)

Clinical characteristics of human infection with a novel avian-origin influenza A(H10N8) virus.

BACKGROUND: Novel influenza A viruses of avian-origin may be the precursors of pandemic strains. This descriptive study aims to introduce a novel avian-origin influenza A (H10N8) virus which can infect humans and cause severe diseases. METHODS: Collecting clinical data of three cases of human infection with a novel reassortment avian influenza A (H10N8) virus in Nanchang, Jiangxi Province, China. RESULTS: Three cases of human infection with a new reassortment avian influenza A(H10N8) virus were described, of which two were fatal cases, and one was severe case. These cases presented with severe pneumonia that progressed to acute respiratory distress syndrome (ARDS) and intractable respiratory failure. CONCLUSION: This novel reassortment avian influenza A (H10N8) virus in China resulted in fatal human infections, and should be added to concerns in clinical practice.