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      Hantavirus in African Wood Mouse, Guinea

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          Abstract

          Hantaviruses are rodentborne, emerging viruses that cause life-threatening human diseases in Eurasia and the Americas. We detected hantavirus genome sequences in an African wood mouse ( Hylomyscus simus) captured in Sangassou, Guinea. Sequence and phylogenetic analyses of the genetic material demonstrate a novel hantavirus species, which we propose to name "Sangassou virus."

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          Hantaviruses: a global disease problem.

          Hantaviruses are carried by numerous rodent species throughout the world. In 1993, a previously unknown group of hantaviruses emerged in the United States as the cause of an acute respiratory disease now termed hantavirus pulmonary syndrome (HPS). Before than, hantaviruses were known as the etiologic agents of hemorrhagic fever with renal syndrome, a disease that occurs almost entirely in the Eastern Hemisphere. Since the discovery of the HPS-causing hantaviruses, intense investigation of the ecology and epidemiology of hantaviruses has led to the discovery of many other novel hantaviruses. Their ubiquity and potential for causing severe human illness make these viruses an important public health concern; we reviewed the distribution, ecology, disease potential, and genetic spectrum.
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            Hantaviruses: immunology, treatment, and prevention.

            Hantaviruses are rodent-borne bunyaviruses that are associated with two main clinical diseases in humans: hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. It has been suggested that host-related immune mechanisms rather than direct viral cytopathology may be responsible for the principal abnormality (vascular dysfunction) in these syndromes. This review summarizes the current knowledge on hantaviral host immune responses, immune abnormalities, laboratory diagnosis, and antiviral therapy as well as the current approaches in vaccine development.
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              Persistent Sin Nombre virus infection in the deer mouse (Peromyscus maniculatus) model: sites of replication and strand-specific expression.

              To address Sin Nombre (SN) virus persistence in deer mice, we sacrificed experimentally infected deer mice at eight time points from day 21 to day 217 postinoculation (p.i.) and examined their tissues for viral nucleocapsid (N) antigen expression and both negative-strand (genomic) and positive-strand (replicative/mRNA) viral S segment RNA titers. All the animals that we inoculated developed persistent infections, and SN virus could be isolated from tissues throughout the course of infection. The transition from an acute to a persistent pattern of infection appeared to occur between days 60 and 90 p.i. Beginning on day 60 p.i., the heart, brown adipose tissue (BAT), and lung retained antigen expression and genomic viral RNA the most frequently. We found a statistically significant association among the presence of replicative RNA in the heart, lung, and BAT, widespread antigen expression (in > or =5 tissues), and RNA viremia. Of these three tissues, the heart retained negative-strand RNA and viral N antigen the most consistently (in 25 of 26 animals). During persistence, there were two distinct patterns of infection: restricted versus disseminated tissue involvement. Mice with the restricted pattern exhibited N antigen expression in or =5 tissues, neutralizing antibody titers of 1:160 to 1:20,480, replicative RNA in the heart, lung, and BAT at a high frequency, and RNA viremia. Virus could be isolated consistently only from mice that demonstrated the disseminated pattern. The heart, lung, and BAT are important sites for the replication and maintenance of SN virus during persistent infection.
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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
                May 2006
                : 12
                : 5
                : 838-840
                Affiliations
                [* ]Charité Medical School, Berlin, Germany;
                []Slovak Academy of Sciences, Bratislava, Slovak Republic;
                []Museum National d'Histoire Naturelle, Paris, France;
                [§ ]Philipps University, Marburg, Germany;
                []Severtsov Institute of Ecology and Evolution, Moscow, Russia;
                [# ]Viral Hemorrhagic Fever Project, Conakry, Guinea
                Author notes
                Address for correspondence: Detlev H. Krüger, Institute of Virology, Helmut-Ruska-Haus, University Hospital Charité Medical School, Campus Charité Mitte, Schumannstr. 20-21, D-10117 Berlin, Germany; email: detlev.kruger@ 123456charite.de
                Article
                05-1487
                10.3201/eid1205.051487
                3374458
                16704849
                44590ce4-1d50-41a0-98f2-14bb24643d81
                History
                Categories
                Dispatch
                Dispatch

                Infectious disease & Microbiology
                dispatch,africa,rna sequence analysis,hantavirus
                Infectious disease & Microbiology
                dispatch, africa, rna sequence analysis, hantavirus

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