White D J, Means R G, Birkhead G S, Bosler E M, Grady L J, Chatterjee N, Woodall J, Hjelle B, Rollin P E, Ksiazek T G, Morse D L
New York State Department of Health, Bureau of Communicable Disease Control, Albany, NY, USA.
Arch Intern Med. 1996 Apr 8;156(7):722-6.
A case of hantavirus pulmonary syndrome with possible exposure in New York and/or Rhode Island was confirmed in February 1994.
To conduct four studies to determine the historical and geographic distribution of human and small-mammal infection with hantaviruses in New York State.
Enzyme-linked immunosorbent assays were performed on serum samples obtained from 130 humans during a 1978 babesiosis survey, 907 small mammals collected in New York State since 1984, 12 rodents collected in 1994 near the residences of the patients with hantavirus pulmonary syndrome, and 76 New York patients with acute respiratory distress syndrome-like illness (as suspected cases of hantavirus pulmonary syndrome).
None of the human serum samples from the 1978 serosurvey showed evidence of hantavirus exposure by enzyme-linked immunosorbent assay. Statewide historical serum samples from white-footed mice showed evidence of Sin Nombre virus infection in 12.0% (97/809) and Seoul-like virus infection in 9.6% (78/809). Site-specific seropositivity rates were as high as 48.5% with Sin Nombre virus during 1 year (1984). Two of 12 mice captured near the residences of a human patient were positive for Sin Nombre virus by enzyme-linked immunosorbent assay, yet were negative for viral RNA by polymerase chain reaction. None of the patients with suspected hantavirus pulmonary syndrome was serologically reactive for Sin Nombre virus.
We provide serologic evidence of small-mammal infection with hantaviruses in New York State as long ago as 1984. Human cases of hantavirus pulmonary syndrome are rare in New York, and data indicate that transmission to humans is probably infrequent. A unique set of host, agent, and environmental factors may be necessary to cause hantavirus pulmonary syndrome in humans.
1994年2月确诊了一例汉坦病毒肺综合征病例,该患者可能在纽约和/或罗德岛接触过汉坦病毒。
开展四项研究,以确定纽约州人类和小型哺乳动物感染汉坦病毒的历史和地理分布。
对1978年巴贝斯虫病调查期间从130名人类身上采集的血清样本、1984年以来在纽约州收集的907只小型哺乳动物、1994年在汉坦病毒肺综合征患者住所附近捕获的12只啮齿动物以及76名患有急性呼吸窘迫综合征样疾病(疑似汉坦病毒肺综合征病例)的纽约患者进行酶联免疫吸附测定。
1978年血清学调查的人类血清样本中,通过酶联免疫吸附测定均未显示出接触汉坦病毒的证据。来自白足鼠的全州历史血清样本显示,12.0%(97/809)有辛诺柏病毒感染证据,9.6%(78/809)有首尔样病毒感染证据。在某一年(1984年),辛诺柏病毒的特定地点血清阳性率高达48.5%。在一名人类患者住所附近捕获的12只小鼠中,有2只通过酶联免疫吸附测定显示辛诺柏病毒呈阳性,但通过聚合酶链反应检测病毒RNA呈阴性。疑似汉坦病毒肺综合征的患者中,没有一例对辛诺柏病毒血清学反应呈阳性。
我们提供了早在1984年纽约州小型哺乳动物感染汉坦病毒的血清学证据。纽约州人类汉坦病毒肺综合征病例罕见,数据表明该病毒向人类的传播可能不常见。可能需要一组独特的宿主、病原体和环境因素才会导致人类感染汉坦病毒肺综合征。