高致病性H5N1型禽流感

目的:高致病性H5N1型禽流感在亚洲的持续爆发引起了人们对全球流感大流行的担心。截至2006年2月,已有160多人被证实感染了H5N1型禽流感,80多人已死亡。本文对H5N1型禽流感的起源,传播,预防及治疗,以及可能的流行情况进行了综述。

An Overview of the Highly Pathogenic H5N1 Influenza Virus

Since the first human case of H5N1 avian influenza virus infection was reported in 1997, this highly pathogenic virus has infected hundreds of people around the world and resulted in many deaths. The ability of H5N1 to cross species boundaries, and the presence of polymorphisms that enhance virulence, present challenges to developing clear strategies to prevent the pandemic spread of this highly pathogenic avian influenza (HPAI) virus. This review summarizes the current understanding of, and recent research on, the avian influenza H5N1 virus, including transmission, virulence, pathogenesis, clinical characteristics, treatment and prevention.

H5N1 influenza viruses： outbreaks and biological properties

All known subtypes of influenza A viruses are maintained in wild waterfowl, the natural reservoir of these viruses. Influenza A viruses are isolated from a variety of animal species with varying morbidity and mortality rates. More importantly, influenza A viruses cause respiratory disease in humans with potentially fatal outcome. Local or global outbreaks in humans are typically characterized by excess hospitalizations and deaths. In 1997, highly pathogenic avian influenza viruses of the H5N1 subtype emerged in Hong Kong that transmitted to humans, resulting in the first documented cases of human death by avian influenza virus infection. A new outbreak started in July 2003 in poultry in Vietnam, Indonesia, and Thailand, and highly pathogenic avian H5N1 influenza viruses have since spread throughout Asia and into Europe and Africa. These viruses continue to infect humans with a high mortality rate and cause worldwide concern of a looming pandemic. Moreover, H5N1 virus outbreaks have had devastating effects on the poultry industries throughout Asia. Since H5N1 virus outbreaks appear to originate from Southern China, we here examine H5N1 influenza viruses in China, with an emphasis on their biological properties.

Pathogenecity of Avian Influenza Virus H5N2： A Report from Western Iran

Influenza type A, is an avian disease with a complicated ecology and transmission routes in verity of avian and mammalian species. The present study aimed to demonstrate the characteristic, clinical and experimental features as well as pathogenecity of Avian Influenza Virus H5N2 through a laboratory-based experiment in western Iran. A post-mortem examination of experimentally chickens was undertaken in 2007. Overall 25 local native chickens including 15 layers and 10 roosters suspected with AI infection as well as 50 experimental chickens were studied. The virus was isolated from the embryonated specific pathogen-free （SPF） chicken eggs. There was an embryo mortality rate of 71% within 48 hours post inoculation （PI）. Hemagglutinin （HA） inhibition titres against AIV subtype H5N2 in the layers ranged from 4.20 to 4.75 （acute） and 6.21 to 7.82 （convalescent）. Accumulated mucous in trachea of the dissected birds, congested lungs, atrophied bursa, haemorrhagic cecal tonsils and inflamed thymus were the main clinical symptoms. Thickened and infected air sacs, pre hepatitis and enteritis signs were also observed, in experimental birds, the eyes＇ colour became red and the eyelashes were almost double in diameters after being infected. The AI virus found in the present study was classified as a highly pathogenic avian influenza.

Conservation of T cell epitopes between seasonal influenza viruses and the novel influenza A H7N9 virus

A novel avian influenza A(H7N9) virus recently emerged in the Yangtze River delta and caused diseases, often severe, in over 130 people. This H7N9 virus appeared to infect humans with greater ease than previous avian influenza virus subtypes such as H5N1 and H9N2. While there are other potential explanations for this large number of human infections with an avian influenza virus, we investigated whether a lack of conserved T-cell epitopes between endemic H1N1 and H3N2 influenza viruses and the novel H7N9 virus contributes to this observation. Here we demonstrate that a number of T cell epitopes are conserved between endemic H1N1 and H3N2 viruses and H7N9 virus. Most of these conserved epitopes are from viral internal proteins. The extent of conservation between endemic human seasonal influenza and avian influenza H7N9 was comparable to that with the highly pathogenic avian influenza H5N1. Thus, the ease of inter-species transmission of H7N9 viruses(compared with avian H5N1 viruses) cannot be attributed to the lack of conservation of such T cell epitopes. On the contrary, our findings predict significant T-cell based cross-reactions in the human population to the novel H7N9 virus. Our findings also have implications for H7N9 virus vaccine design.