Viruses Genomes - ANDES VIRUS
Andes virus
causes hantavirus pulmonary syndrome (HPS)
Andes virus, one of five hantaviruses known to cause hantavirus pulmonary syndrome (HPS), emerged in 1995 in southwestern Argentina. Hantaviruses are serologically related, rodent-borne viruses, which, when transmitted from their natural hosts to humans, cause an acute illness
Since 1995 HPS cases have been reported in several American countries including Argentina, Bolivia, Brazil, Canada, Chile, Panama, Paraguay, United States, and Uruguay . Andes virus has been responsible for most of the 400 plus cases recorded in Argentina, Chile, and Uruguay. Infection occurs primarily by the respiratory route via aerosolised virus in rodent excreta. Field investigations have identified sigmodontine rodents as the host of the respiratory hantaviruses, the rodents are lifelong carriers of the virus and are not subject to infection from it.
A family outbreak of HPS in April 1995 near El Bolson, in southwestern Argentina, where two of three affected individuals died, led to the initial characterization of the putative agent. A limited sequence analysis of viral cDNA amplified from autopsy tissues (case AH-1) indicated that the HPS-associated virus, named Andes virus, represented a new member of the hantavirus genus. The Andes virus genome is comprised of 3 parts, small, medium and large. Researchers have confirmed the unique nature of Andes virus by sequencing the entire small segment and the more variable region of G1-encoding (glycoprotein envelope) medium segment. They report the genetic characterization of two HPS-associated viral RNAs in autopsy tissues of individuals affected in Esquel (Argentina) and in Chile. A comparison of the sequences to the corresponding sequences of other hantaviruses reveals that Andes virus variants circulate east and west of the Andes mountains.
HPS begins as a nonspecific feverish symptoms, sharing many of its initial symptoms with other more common viral infections.
Patients then quickly develop noncardiogenic pulmonary edema, respiratory failure, and shock. The overall case fatality
rate of HPS is approximately 40 percent.
References:
Virus Res. 1997 Jul;50(1):77-84
Emerg Infect Dis. 2002 Apr;8(4):437-9
http://www.cdc.gov/ncidod/EID/vol8no4/01-0300.htm
http://www.aafp.org/afp/20020915/1015.html
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