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      Genetic Analysis of Viruses Associated with Emergence of Rift Valley Fever in Saudi Arabia and Yemen, 2000-01

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          Abstract

          The first confirmed Rift Valley fever outbreak outside Africa was reported in September 2000, in the Arabian Peninsula. As of February 2001, a total of 884 hospitalized patients were identified in Saudi Arabia, with 124 deaths. In Yemen, 1,087 cases occurred, with 121 deaths. Laboratory diagnosis of Rift Valley fever virus (RVFV) infections included virus genetic detection and characterization of clinical specimens by reverse transcription-polymerase chain reaction, in addition to serologic tests and virus isolation. Genetic analysis of selected regions of virus S, M, and L RNA genome segments indicated little genetic variation among the viruses associated with disease. The Saudi Arabia and Yemen viruses were almost identical to those associated with earlier RVF epidemics in East Africa. Analysis of S, M, and L RNA genome segment sequence differences showed similar phylogenetic relationships among these viruses, indicating that genetic reassortment did not play an important role in the emergence of this virus in the Arabian Peninsula. These results are consistent with the recent introduction of RVFV into the Arabian Peninsula from East Africa.

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          Climate and satellite indicators to forecast Rift Valley fever epidemics in Kenya.

          All known Rift Valley fever virus outbreaks in East Africa from 1950 to May 1998, and probably earlier, followed periods of abnormally high rainfall. Analysis of this record and Pacific and Indian Ocean sea surface temperature anomalies, coupled with satellite normalized difference vegetation index data, shows that prediction of Rift Valley fever outbreaks may be made up to 5 months in advance of outbreaks in East Africa. Concurrent near-real-time monitoring with satellite normalized difference vegetation data may identify actual affected areas.
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            Rift Valley fever virus L segment: correction of the sequence and possible functional role of newly identified regions conserved in RNA-dependent polymerases.

            The sequence of Rift Valley fever virus L segment that we published in a previous paper was erroneous in the 3'-terminal region of the antigenomic RNA molecule. Here, we have shown that the L segment is in fact 6404 nucleotides long and encodes a polypeptide of 237.7K in the viral complementary sense. Sequence comparisons performed between the RNA-dependent RNA polymerases of 22 negative-stranded RNA viruses revealed the existence of two novel regions located at the amino termini of the proteins and conserved only in the polymerases of bunya- and arenaviruses. In the region conserved in all RNA-dependent polymerases, corresponding to the so-called 'polymerase module', we identified a new motif, designated premotif A, common to all RNA-dependent polymerases, as well as amino acids located in the region between motifs preA and A which are strictly conserved for segmented negative-stranded RNA viruses. Using the recently released coordinates of human immunodeficiency virus reverse transcriptase and the alignment between all RNA-dependent polymerases in the 'polymerase module', we have determined the position of the conserved residues in these polymerases and discuss their possible functions in light of the available structural information.
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              Laguna Negra virus associated with HPS in western Paraguay and Bolivia.

              A large outbreak of hantavirus pulmonary syndrome (HPS) recently occurred in the Chaco region of Paraguay. Using PCR approaches, partial virus genome sequences were obtained from 5 human sera, and spleens from 5 Calomys laucha rodents from the outbreak area. Genetic analysis revealed a newly discovered hantavirus, Laguna Negra (LN) virus, to be associated with the HPS outbreak and established a direct genetic link between the virus detected in the HPS cases and in the C. laucha rodents, implicating them as the primary rodent reservoir for LN virus in Paraguay. Virus isolates were obtained from two C. laucha, and represent the first successful isolation of a pathogenic South American hantavirus. Analysis of the prototype LN virus entire S and M and partial L segment nucleotide and deduced amino acid sequences showed that this virus is unique among the Sigmodontinae-borne clade of hantaviruses. Analysis of PCR fragments amplified from a serum sample from a Chilean HPS patient, who had recently traveled extensively in Bolivia (where C. laucha are known to occur), revealed an LN virus variant that was approximately 15% different at the nucleotide level and identical at the deduced amino acid level relative to the Paraguayan LN virus. These data suggest that LN virus may cause HPS in several countries in this geographic region.
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                Author and article information

                Journal
                Emerg Infect Dis
                Emerging Infect. Dis
                EID
                Emerging Infectious Diseases
                Centers for Disease Control and Prevention
                1080-6040
                1080-6059
                December 2002
                : 8
                : 12
                : 1415-1420
                Affiliations
                [* ]Centers for Disease Control and Prevention, Atlanta, Georgia, USA
                []Emory University, Atlanta, Georgia, USA
                []Ministry of Health, Riyadh, Saudi Arabia
                [§ ]National Institute of Virology, Johannesburg, South Africa
                Author notes
                Address for correspondence: Stuart T. Nichol, Mailstop G14, Special Pathogens Branch, Division of Viral and Rickettsial Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA; fax: 404-639-1118; e-mail: stn1@ 123456cdc.gov
                Article
                02-0195
                10.3201/eid0812.020195
                2738516
                12498657
                6c363d0c-63db-4b9e-b5cc-74578ff0143e
                History
                Categories
                Research

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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