Disease relevance of Hantavirus

• These studies provide a basic understanding of hantavirus-directed cellular responses that are likely to differentiate pathogenic and nonpathogenic hantaviruses, contribute to HFRS and HPS pathogenesis, and provide insight into disease mechanisms and potential therapeutic interventions [1].
• Infection with HPS-associated hantaviruses, NY-1 and Sin Nombre virus (SNV), is inhibited by antibodies to beta3 integrins and by the beta3-integrin ligand, vitronectin [2].
• Pathogenic hantaviruses [New York-1 virus (NY-1V) and Hantaan virus (HTNV)] bind immobilized beta3 polypeptides containing the PSI domain, and human (but not murine) beta3 polypeptides inhibit hantavirus infectivity [3].
• Generation of a recombinant cytomegalovirus for expression of a hantavirus glycoprotein [4].
• Inhibition of bunyaviruses, phleboviruses, and hantaviruses by human MxA protein [5].

Psychiatry related information on Hantavirus

• Here we show that infection of cynomolgus macaques by wild-type Puumala hantavirus resulted in typical signs of HFRS including lethargy, anorexia, proteinuria, and/or hematuria, in addition to cytokine (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha), C-reactive protein, creatinine, and nitric oxide responses [6].

High impact information on Hantavirus

• Utility of emergency, telephone-based national surveillance for Hantavirus pulmonary syndrome. Hantavirus Task Force [7].
• Pathogenic hantaviruses bind plexin-semaphorin-integrin domains present at the apex of inactive, bent alphavbeta3 integrin conformers [3].
• Because all hantaviruses induced >23 IFN-stimulated genes at late times p.i., pathogenic hantaviruses appear to suppress early cellular IFN responses that are activated by nonpathogenic hantaviruses [1].
• Intravenous ribavirin for hantavirus pulmonary syndrome: safety and tolerance during 1 year of open-label experience. Ribavirin Study Group [8].
• Most strikingly, the antiviral MxA protein, which interferes with hantavirus replication, was already induced 16 h after infection with TULV [9].

Chemical compound and disease context of Hantavirus

• Hantavirus prevalence in the IX Region of Chile [10].
• Tyrosine residues direct the ubiquitination and degradation of the NY-1 hantavirus G1 cytoplasmic tail [11].
• RGD tripeptides, which are required for many integrin-ligand interactions, are absent from all hantavirus G1 and G2 surface glycoproteins, and GRGDSP peptides did not inhibit hantavirus infectivity [12].
• Phylogenetic analysis confirmed that SNV-like hantaviruses are widely distributed in Peromyscus species rodents throughout North America. Classic SNV is the major cause of HPS in North America, but other Peromyscine-borne hantaviruses, e.g., New York and Monongahela viruses, are also associated with HPS cases [13].
• Neopterin concentrations were slightly lower in five females with low titers of antibodies against local B1 hantavirus strain (P < 0.05) [14].

Biological context of Hantavirus

• These findings implicate integrins as cellular receptors for hantaviruses and indicate that hantavirus pathogenicity correlates with integrin usage [2].
• This study reports completion of the genetic characterization of the entire genome of Sin Nombre (SN) virus (NMH10) detected in autopsy tissues from a patient who died of hantavirus pulmonary syndrome (HPS) [15].
• These results reveal a possible mechanism by which hantavirus infection and a TH1 immune response can cooperate to synergistically enhance chemokine expression by HMVEC-Ls and trigger immune-mediated increases in vascular permeability [16].
• The hantavirus ITAM coprecipitated Lyn, Syk, and ZAP-70 kinases from T or B cells, while mutagenesis of the ITAM abolished these interactions [17].
• Nucleotide sequence analysis of the M genomic segment of El Moro Canyon hantavirus: antigenic distinction from four corners hantavirus [18].

Anatomical context of Hantavirus

• Infection of human umbilical vein endothelial cells and Vero E6 cells by the HFRS-causing hantaviruses Hantaan (HTN), Seoul (SEO), and Puumala (PUU) is inhibited by antibodies to alphavbeta3 integrins and by the integrin ligand vitronectin [12].
• Sin Nombre virus (SNV) is a major representative of the New World hantaviruses and the most common cause of hantavirus pulmonary syndrome (HPS) with high mortality in North America. Unlike other members of the family Bunyaviridae which mature in the Golgi complex, New World hantaviruses have been previously reported to mature at the cell surface [19].
• The prevalence of antibodies against glomerular basement membrane (GBM) antigens in sera from 47 patients with serologically verified hantavirus (Puumala serotype) infection were investigated [20].
• In the present study, we have demonstrated that the embryonic fibroblastic cells from a feral-origin strain (SPR) expressed 74 kDa Mx2 protein, which prevented the accumulation of viral transcripts and proteins of hantaviruses when the Mx2 gene was constitutively expressed in transfected Vero cells [21].

Gene context of Hantavirus

• Andes virus S segment was found to be 1876 nucleotides in length and to encode the nucleocapsid protein (N), 428 amino acids in length [22].
• Association of the nucleocapsid protein of the Seoul and Hantaan hantaviruses with small ubiquitin-like modifier-1-related molecules [23].
• The L protein contains all the polymerase motifs and structural domains found in other hantavirus polymerases [24].
• In recent years important progress has been made studying the nucleocapsid (N) protein of hantaviruses [25].
• Analyses of complete nucleocapsid protein and glycoprotein precursor sequences indicated that the isolates are strains of a novel hantavirus (proposed name "Maporal") which is phylogenetically most closely related to the viruses known to cause hantavirus pulmonary syndrome in southern South America [26].

Analytical, diagnostic and therapeutic context of Hantavirus

• Seroprevalence study of hantavirus antibodies in Pima Indians with renal disease [27].
• In May 1993, an outbreak of hantavirus pulmonary syndrome (HPS) occurred in the southwestern United States. A case-control study determined risk factors for HPS [28].
• The high levels of expression obtained, specific serological reactivity with immune sera and the low level of biological containment required for production of this protein all suggest a significant advantage over authentic viral antigen for diagnosis of hantavirus infection [29].
• Sequence analysis of virus genome N-, G1-, and G2-encoding fragments showed this to be a novel hantavirus, Choclo virus [30].
• OBJECTIVE: a new 5 min rapid test, POC PUUMALA (Erilab Ltd, Finland), for detecting IgM antibodies to PUUV was evaluated and compared with the commercially available Hantavirus (Puumala) IgM ELISA test (Progen, Germany) [31].

References