Cross-reactive, cell-mediated immunity and protection of chickens from lethal H5N1 influenza virus infection in Hong Kong poultry markets
Cross-reactive, cell-mediated immunity and protection of chickens from lethal H5N1 influenza virus infection in Hong Kong poultry markets
复制标题
DOI：
10.1128/jvi.75.6.2516-2525.2001
复制
发表时间：
2001-03-01
影响因子：
5.4
通讯作者：
Webster, RG
中科院分区：
文献类型：
--
作者：
Seo, SH;Webster, RG
1997年，由鸡传染给人类的H5N1禽流感病毒导致18例确诊感染。尽管携带致命的H5N1流感病毒，但香港家禽市场的大多数鸡没有出现疾病迹象。此时，H9N2流感病毒正在市场上共同传播。我们研究了H9N2流感病毒在保护鸡免受致命的H5N1流感病毒感染中的作用。在中和或血凝抑制试验中，感染H9N2流感病毒的鸡血清与H5N1流感病毒没有交叉反应。大多数在3至70天前感染H9N2流感病毒的鸡在H5N1流感病毒的致命攻击中存活下来，但受感染的禽类在其粪便中释放H5N1流感病毒。将感染了H9N2流感病毒的近交系鸡（B-2/B-2）的T淋巴细胞或CD8(+) T细胞过继转移到初交系鸡（B2/B2）身上，可以保护它们免受致命的H5N1流感病毒的感染。体外细胞毒性试验表明，感染H9N2流感病毒的鸡的T淋巴细胞或CD8(+) T细胞以剂量依赖的方式识别感染H5N1或H9N2流感病毒的靶细胞。我们的研究结果表明，H9N2流感病毒诱导的交叉反应性细胞免疫保护了1997年香港市场上的鸡免受H5N1流感病毒的致命感染，但允许病毒在粪便中脱落。我们的研究结果首次表明，交叉反应性细胞免疫可以改变活禽市场禽类感染禽流感病毒的结果，并为H5N1流感病毒的延续创造条件。
In 1997, avian H5N1 influenza virus transmitted from chickens to humans resulted in 18 confirmed infections. Despite harboring lethal H5N1 influenza viruses, most chickens in the Hong Kong poultry markets showed no disease signs. At this time, H9N2 influenza viruses were cocirculating in the markets. We investigated the role of H9N2 influenza viruses in protecting chickens from lethal H5N1 influenza virus infections. Sera from chickens infected with an H9N2 influenza virus did not cross-react with an H5N1 influenza virus in neutralization or hemagglutination inhibition assays. Most chickens primed with an H9N2 influenza virus 3 to 70 days earlier survived the lethal challenge of an H5N1 influenza virus, but infected birds shed H5N1 influenza virus in their feces. Adoptive transfer of T lymphocytes or CD8(+) T cells from inbred chickens (B-2/B-2) infected with an H9N2 influenza virus to naive inbred chickens (B2/B2) protected them from lethal H5N1 influenza virus. In vitro cytotoxicity assays showed that T lymphocytes or CD8(+) T cells from chickens infected with an H9N2 influenza virus recognized target cells infected with either an H5N1 or H9N2 influenza virus in a dose-dependent manner. Our findings indicate that cross-reactive cellular immunity induced by H9N2 influenza viruses protected chickens from lethal infection with H5N1 influenza viruses in the Hong Kong markets in 1997 but permitted virus shedding in the feces. Our findings are the first to suggest that cross-reactive cellular immunity can change the outcome of avian influenza virus infection in birds in live markets and create a situation for the perpetuation of H5N1 influenza viruses.