Reisen William K, Lothrop Hugh D, Wheeler Sarah S, Kennsington Marc, Gutierrez Arturo, Fang Ying, Garcia Sandra, Lothrop Branka
Arbovirus Research Unit, Center for Vectorborne Diseases, School of Veterinary Medicine, University of California, Old Davis Rd., Davis, CA 95616, USA.
J Med Entomol. 2008 May;45(3):494-508. doi: 10.1603/0022-2585(2008)45[494:pwnvta]2.0.co;2.
West Nile virus (family Flaviviridae, genus Flavivirus, WNV) invaded the Colorado Desert biome of southern California during summer 2003 and seemed to displace previously endemic St. Louis encephalitis virus (family Flaviviridae, genus Flavivirus, SLEV, an antigenically similar Flavivirus in the Japanese encephalitis virus serocomplex). Western equine encephalomyelitis virus (family Togaviridae, genus Alphavirus, WEEV), an antigenically distinct Alphavirus, was detected during 2005 and 2006, indicating that conditions were suitable for encephalitis virus introduction and detection. Cross-protective "avian herd immunity" due to WNV infection possibly may have prevented SLEV reintroduction and/or amplification to detectable levels. During 2003-2006, WNV was consistently active at wetlands and agricultural habitats surrounding the Salton Sea where Culex tarsalis Coquillett served as the primary enzootic maintenance and amplification vector. Based on published laboratory infection studies and the current seroprevalence estimates, house sparrows, house finches, and several Ardeidae may have been important avian amplifying hosts in this region. Transmission efficiency may have been dampened by high infection rates in incompetent avian hosts, including Gamble's quail, mourning doves, common ground doves, and domestic pigeons. Early season WNV amplification and dispersal from North Shore in the southeastern portion of the Coachella Valley resulted in sporadic WNV incursions into the urbanized Upper Valley near Palm Springs, where Culex pipiens quinquefasciatus Say was the primary enzootic and bridge vector. Although relatively few human cases were detected during the 2003-2006 period, all were concentrated in the Upper Valley and were associated with high human population density and WNV infection in peridomestic populations of Cx. p. quinquefasciatus. Intensive early mosquito control during 2006 seemed to interrupt and delay transmission, perhaps setting the stage for the future reintroduction of SLEV.
西尼罗河病毒(黄病毒科,黄病毒属,WNV)于2003年夏季侵入南加利福尼亚的科罗拉多沙漠生物群落,似乎取代了先前流行的圣路易斯脑炎病毒(黄病毒科,黄病毒属,SLEV,日本脑炎病毒血清复合体中一种抗原性相似的黄病毒)。西部马脑炎病毒(披膜病毒科,甲病毒属,WEEV,一种抗原性不同的甲病毒)在2005年和2006年被检测到,这表明当地条件适合脑炎病毒的传入和检测。WNV感染产生的交叉保护性“禽群免疫”可能阻止了SLEV的再次传入和/或扩增到可检测水平。在2003年至2006年期间,WNV在索尔顿海周边的湿地和农业栖息地持续活跃,致倦库蚊是主要的动物源性维持和扩增媒介。根据已发表的实验室感染研究和当前的血清流行率估计,家麻雀、家朱雀和几种鹭科鸟类可能是该地区重要的禽类扩增宿主。包括鳞斑鹑、哀鸽、彩鸽和家鸽在内的无感染能力的禽类宿主感染率较高,可能降低了传播效率。西尼罗河病毒在科切拉谷东南部北岸的早期扩增和传播导致其偶尔侵入棕榈泉附近城市化的上谷地区,致倦库蚊是主要的动物源性和桥梁媒介。尽管在2003年至2006年期间检测到的人类病例相对较少,但所有病例都集中在上谷地区,并且与高人口密度以及致倦库蚊周围人群中的西尼罗河病毒感染有关。2006年早期的强化蚊虫控制似乎中断并延迟了传播,这可能为未来SLEV的再次传入奠定了基础。