HANTAAN VIRUS: Hantavirus Disease, Risk of Infection by Hantaviruses

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HANTAAN VIRUS: Hantavirus Disease

HANTAAN VIRUS: Hantavirus Disease, Risk of Infection by Hantaviruses

 Hantaviruses, any of several members of the virus family Bunyaviridae that infect vertebrates (animals with backbones, including humans). Unlike most members of this family, which are carried by mosquitoes, ticks, or flies, hantaviruses are carried by specific rodent hosts and are transmitted directly from host to host by virus-laden saliva, urine, and feces. Humans are infected through exposure to the dried excretions from infected rodents. Hantaviruses cause two different human diseases: hemorrhagic fever with renal syndrome, in which damage to the kidneys is common, and acute respiratory distress syndrome, in which damage to the lungs is common.

 Hantaviruses are spherical and are 90 to 100 nanometers (1 nanometer equals 1 billionth of a meter, or 4 x 10-8 inches) in diameter. They are composed of an envelope covered with spikes surrounding three protein-wrapped, circular pieces of ribonucleic acid (RNA). Although many hantaviruses have been identified recently, their true number and potential for causing disease is probably far greater than is presently thought.

 Acute respiratory distress syndrome is one of two human diseases caused by hantavirus. Dust containing virus-infected rodent feces becomes airborne and is inhaled. The virus embeds in the lungs where the infection begins. Flulike symptoms appear in about a week, followed by the collection of fluid and white blood cells in the lungs, causing respiratory failure, then death.

 The first human disease known to be due to a hantavirus infection was hemorrhagic fever with renal syndrome, identified in the early 1950s during the Korean War. Thousands of United Nations troops developed a mysterious disease marked by fever, headache, hemorrhage, and acute kidney failure. Despite much research, the cause remained unknown for 26 years until a new virus, named Hantaan virus, was isolated in Korea from field mice in 1976.

 Hemorrhagic fever with renal syndrome is widespread in the Far East, particularly in China and Korea. There are two seasonal disease peaks, associated with the harvesting of wheat in summer and of rice in late fall. During these times the host rodent populations peak and the fields are full of dust containing dried, virus-laden excrement. The disease is fatal in about 5 to 10 percent of cases. A milder form of the disease, caused by Seoul virus and transmitted by rats, occurs in Japan, Korea, China, and the United States, especially in seaports, where rats are common. Symptoms are less severe and include nephritis (inflammation of the kidneys).


 In 1993 a new hantavirus disease was recognized in the southwestern United States. The illness was at first referred to as Four Corners Disease, named for the area where the disease was first observed, where Arizona, New Mexico, Colorado, and Utah meet. The agent responsible was called the Sin Nombre (an area in New Mexico which in Spanish means “no name”) virus. The victims of the virus developed influenza-like symptoms—including fever, muscle aches, cough, and headache—which rapidly worsened. Fluid and white blood cells accumulated in the lungs, causing hypoxia (low blood-oxygen levels), shock, and, in many cases, death from a type of lung failure called acute respiratory distress syndrome, also known as hantavirus pulmonary syndrome. Within a short time, cases were found in other states. By the end of 1995, 123 cases, with a fatality rate of 51 percent, had been confirmed from 23 states. The disease was also identified in Canada, Brazil, Venezuela, and Argentina.

 The search for the cause of this mysterious disease began with typical epidemiological studies that involved interviewing survivors and people who came in contact with the victims. Blood samples from victims shared evidence of antibodies against hantaviruses, an indication that they had been exposed to hantavirus in the past, and that this earlier exposure had initiated an immune response. To prove which hantavirus was indeed the cause of the victims' death, scientists used the polymerase chain reaction (PCR). This technique is used to rapidly amplify DNA strands. Once amplified, specific methods are used to identify the specific virus. Scientists determined with certainty that hantavirus was present in the tissues of the victims and determined that the disease was caused by a previously unknown hantavirus. Hantavirus specimens from different areas were compared, revealing that several previously unknown viruses were active in the United States. The entire genetic structure of the Sin Nombre virus was determined, and diagnostic tests were created. The same methods are being used in attempts to develop a vaccine. (For a description of vaccines, See Immunization.)

 The primary host of Sin Nombre virus in the southwestern United States is the deer mouse, Peromyscus maniculatus. In large sections of this part of the country, 10 to 35 percent of deer mice are infected, and in certain areas about 80 percent of deer mice carry the virus.

 Sin Nombre virus, like other hantaviruses, does not cause disease in its rodent hosts. The virus is shed in the saliva, urine, and feces of these animals for many weeks and perhaps for the lifetime of the animal. Human infection occurs when dust containing infected dried rodent excretions is inhaled. Sin Nombre and the other newly discovered hantaviruses probably have long been present in the region of the western United States inhabited by deer mice. The virus was recognized in 1993 only because of the number and clustering of human cases, after two particularly wet winters and an abundant supply of rodent food caused an increase in rodent populations, which then led to a rise in the incidence of the disease.


 The risk of infection by hantaviruses can be reduced by preventing rodents from living in or near human dwellings. Rodent nests and droppings should be wetted down with a disinfectant before they are removed.

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