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B Hjelle

Publications and source records attributed to B Hjelle.

At least 55 records · Page 3Linked to original sources
PubMed1995

Nucleotide sequence analysis of the M genomic segment of El Moro Canyon hantavirus: antigenic distinction from four corners hantavirus.

El Moro Canyon hantavirus (ELMC, previously known as HMV-1) is associated with the western harvest mouse Reithrodontomys megalotis. The interpretation that ELMC is a novel hantavirus was based upon comparisons of the nucleotide sequence of the S genomic segment with those of other hantaviruses. We now show that the ELMC M genome, like the S genome, is genetically similar to but distinct from that of Four Corners hantavirus (FC). The ELMC M genome is 3801 nt in length and encodes a glycoprotein precursor of 1139 amino acids. The G1 and G2 genes are 71 and 73.1% identical to those of FC and the corresponding glycoproteins are 73.5 and 82.3% identical. A portion of the G1 glycoprotein of ELMC that is homologous to an important linear epitope of FC differs from the FC epitope by 10 of 31 residues. That domain and flanking sequences were expressed in Escherichia coli. G1 antibodies from 3 of 19 FC-infected patients showed cross-reactivity with ELMC by Western blot assay. The portion of the ELMC G1 antigen recognized by those antibodies is the region of homology to the FC epitope. These data support our previous interpretation that ELMC is distinct from FC and other hantaviruses.

Amino Acid Sequence↗
PubMed1995

Prevalence and geographic genetic variation of hantaviruses of New World harvest mice (Reithrodontomys): identification of a divergent genotype from a Costa Rican Reithrodontomys mexicanus.

We recently described a novel hantavirus (HMV-1) of the western harvest mouse Reithrodontomys megalotis. Screening of 181 additional specimens of Reithrodontomys from the United States and Mexico, including samples of R. mexicanus, R. sumichrasti, and R. gracilis of Costa Rica, for antibodies to hantavirus nucleocapsid protein revealed a widespread enzootic of hantavirus infection. Genetic analyses of 7 S genomes of Reithrodontomys-associated hantaviruses demonstrated that the enzootic of HMV-1 extends from central Mexico into the southwestern United States. A presumed deer mouse hantavirus was found in an R. megalotis animal in Mexico. A highly divergent HMV-1-like virus, tentatively called HMV-2, was identified in a Costa Rican R. mexicanus. These data suggest a longstanding radiation of hantaviruses among New World harvest mice. We identify possible opportunities for genetic exchange among hantaviruses of related rodent hosts.

Animals↗
PubMed1995

Phylogenetically distinct hantavirus implicated in a case of hantavirus pulmonary syndrome in the northeastern United States.

Hantavirus pulmonary syndrome (HPS) is an acute respiratory illness with high mortality. It is caused by a newly described New World hantavirus known as Four Corners virus (FCV). Nearly all cases of HPS have occurred in the western United States. The etiologic agents in those cases have been closely related to each other, based upon comparisons of their genetic sequences. We have molecularly cloned the S genomic segment of a hantavirus (Rl-1) implicated in a case on HPS in the northeastern United States. Nucleotide sequence analysis shows that the Rl-1 virus has many similarities to FCV, but is clearly distinct from the western forms of that virus. These data suggest that HPS can be caused by multiple agents that together form a distinctive evolutionary clade.

Adult↗
PubMed1995

Genotypic characteristics of HTLV-II isolates from Amerindian and non-Indian populations.

The Amerindian human T-cell lymphotropic virus type II isolate HTLV-IIG12 has been demonstrated to be an HTLV-IIb with several unique features, including several restriction enzyme site changes, a distinctive pre-gag region, a stop codon within the pol gene, and an extended Tax protein. In this study, HTLV-II isolates from Amerindian and non-Indian populations were characterized by restriction enzyme site analysis to determine the prevalent HTLV-II subtype. In addition, DNA amplification by the polymerase chain reaction and Southern blot analyses were used to probe for the HTLV-IIG12 pre-gag region. Our results showed that of 13 Guaymi Indian isolates subtyped, all were HTLV-IIb, and that approximately one third of 17 isolates had the unique pre-gag region. While other HTLV-II-infected groups contained both HTLV-IIa and HTLV-IIb isolates, none of these isolates showed evidence of the distinctive HTLV-IIG12 pre-gag region. Lastly, DNA sequence analysis was used to determine the prevalence of the stop codon within the pol gene open reading frame. These analyses revealed that the occurrence of a stop codon within this sequence appeared to be characteristic of most HTLV-IIb subtypes. These results further our understanding of the genetic variations and evolution of the HTLV-II viruses within the endemically infected Amerindian populations, as well as U.S. intravenous drug users and other non-Indian populations.

Base Sequence↗
PubMed1995

Nucleotide sequence and restriction fragment length polymorphism analysis of the long terminal repeat of human T cell leukemia virus type II.

Molecular studies have demonstrated the existence of two major subtypes of human T cell leukemia virus type II: HTLV-IIa and HTLV-IIb. In attempts to further classify this family of viruses we have carried out nucleotide sequence and restriction fragment length polymorphism (RFLP) analysis of the long terminal repeat (LTR), a region that has been shown in previous studies to have the greatest intra- and intersubtype genomic divergence. Analysis of the nucleotide sequences suggested the existence of distinct phylogenetic groups in each subtype and, on the basis of predicted differences in restriction endonuclease sites, RFLP analysis allowed the identification of four groups within the IIa subtype (a1-a4) and six within the IIb subtype (b1-b6). Nucleotide sequence analysis also suggested the possible existence of HTLV-II quasispecies. However, this appeared not to be significant, and preliminary studies suggest that these would not be expected to influence the results of RFLP analysis appreciably. The validity of the RFLP method was demonstrated in an analysis of 36 randomly chosen samples from HTLV-II seropositive blood donors from the New York City Blood Center, where it could be shown that all could be successfully classified. Moreover, the RFLP analysis correctly matched the viruses in donors and recipients of contaminated blood in four situations in which HTLV-II was inadvertently transmitted by transfusion. RFLP analysis of the LTR appears to be a rapid and reliable method by which to identify HTLV-II infection. This should prove useful in studies of the epidemiology and the characterization of viruses present both in nonindigenous and indigenous populations.

Base Sequence↗
PubMed1995

Cross-neutralization of hantaviruses with immune sera from experimentally infected animals and from hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome patients.

Plaque-reduction neutralization tests were done with eight of nine known representative hantaviruses and immune sera from experimentally infected animals and from patients with hemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS). Results obtained with animal sera demonstrated each virus to be antigenically unique. Neutralization with the HPS patient sera was highest with Sin Nombre (SN) virus and to a lesser extent with Black Creek Canal (BCC) virus. Sera from Korean HFRS patients reacted best with Hantaan virus, but cross-reactivity with all other viruses except Thottapalayam (TPM) virus was also observed. Sera from Swedish HFRS patients reacted best with Puumala virus but cross-reacted with Prospect Hill, SN, and BCC viruses and to a lesser extent with all of the other viruses except TPM virus.

Animals↗
PubMed1995

Isla Vista virus: a genetically novel hantavirus of the California vole Microtus californicus.

Prospect Hill virus (PH) was isolated from a meadow vole (Microtus pennsylvanicus) in 1982, and much of its genome has been sequenced. Hantaviruses of other New World microtine rodents have not been genetically characterized. We show that another Microtus species (the California vole M. californicus) from the United States is host to a genetically distinct PH-like hantavirus, Isla Vista virus (ILV). The nucleocapsid protein of ILV differs from that of PH by 11.1% and a portion of the G2 glycoprotein differs from that of PH by 19.6%. ILV antibodies were identified in five of 33 specimens of M. californicus collected in 1975 and 1994-1995. Enzymatic amplification studies showed that 1975 and 1994-1995 ILV genomes were highly similar. Secondary infection of Peromyscus californicus was identified in Santa Barbara County, California. A long-standing enzootic of a genetically distinct hantavirus lineage is present in California voles.

Animals↗
PubMed1995

Molecular linkage of hantavirus pulmonary syndrome to the white-footed mouse, Peromyscus leucopus: genetic characterization of the M genome of New York virus.

The complete M segment sequences of hantaviruses amplified from tissues of a patient with hantavirus pulmonary syndrome in the northeastern United States and from white-footed mice, Peromyscus leucopus, from New York were 99% identical and differed from those of Four Corners virus by 23%. The serum of this patient failed to recognize a conserved, immunodominant epitope of the Four Corners virus G1 glycoprotein. Collectively, these findings indicate that P. leucopus harbors a genetically and antigenically distinct hantavirus that causes hantavirus pulmonary syndrome.

Amino Acid Sequence↗
PubMed1995

Antibody responses to Four Corners hantavirus infections in the deer mouse (Peromyscus maniculatus): identification of an immunodominant region of the viral nucleocapsid protein.

Antibody responses to Four Corners hantavirus (FCV) infections in the deer mouse (Peromyscus maniculatus) were characterized by using FCV nucleocapsid protein (N), glycoprotein 1 (G1), and glycoprotein 2 (G2) recombinant polypeptides in Western immunoblot assays. Strong immunoglobulin G reactivities to FCV N were observed among FCV-infected wild P. maniculatus mice (n = 34) and in laboratory-infected P. maniculatus mice (n = 11). No immunoglobulin G antibody reactivities to FCV G1 or G2 linear determinants were detected. The strongest N responses were mapped to an amino-proximal segment between amino acids 17 and 59 (QLVTARQKLKDAERAVELDPDDVNKSTLQSRRAAVSALETKLG). FCV N antibodies cross-reacted with recombinant N proteins encoded by Puumala, Seoul, and Hantaan viruses.

Amino Acid Sequence↗
PubMed1995

Hantaviruses: clinical, microbiologic, and epidemiologic aspects.

Hantaviruses comprise a genus of the family Bunyaviridae. Bunyaviruses are enveloped viruses with a negative-sense, tripartite RNA genome. Hantaviruses are etiologic agents for two acute and severe illnesses of man, hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Each hantavirus is primarily associated with a single rodent host species or genus, and is transmitted to man through accidental inhalation or ingestion of virus-contaminated rodent excreta. The distribution of hantaviruses is worldwide. HFRS is caused by infection with Hantaan, Seoul, Dobrava/Belgrade, and Puumala hantaviruses, all of which are enzootic in murid rodents of Old World origin. HPS is caused by any of several hantavirus species associated with indigenous New World rodents of the subfamily Sigmodontinae, family Muridae. HFRS and HPS have numerous common epidemiologic, clinical, and laboratory characteristics. Common features include fever, myalgia, thrombocytopenia, neutrophilia, and a profound capillary leak syndrome associated with hypotension, decreased cardiac output, and shock. Worldwide, HPS is much less common than HFRS but is associated with a higher mortality rate. Recovery from hantavirus disease is generally complete, although chronic renal insufficiency may be a rare sequel of HFRS.

Animals↗
PubMed1995

Hantavirus pulmonary syndrome: clinical, diagnostic, and virologic aspects.

Hantavirus pulmonary syndrome is an acute pneumonitis with a high mortality rate that is caused by a newly recognized hantavirus. Four Corners virus (also known as Muerto Canyon virus and Sin Nombre virus) is enzootic among deer mice (Peromyscus maniculatus). Incidental transmission to humans can result in a disease characterized by rapidly progressive respiratory insufficiency, diffuse noncardiogenic pulmonary edema, vascular volume contraction with hemoconcentration, lactic acidosis, depressed cardiac output, and cardiac dysrhythmias preterminally. The onset of pulmonary edema is preceded by a prodrome of fever and severe myalgias. Characteristic laboratory abnormalities include thrombocytopenia, leukocytosis with prevalent immature myeloid cells, and the presence of immunoblastic lymphocytes in the peripheral blood. Agent-specific diagnosis is based on the detection of Four Corners virus-specific antibodies in serum by Western blot assays and the detection of Four Corners virus RNA in peripheral blood mononuclear cells by the reverse transcriptase-polymerase chain reaction. Effective treatment depends on the rapid institution of intensive care support.

Adolescent↗
PubMed1994

Genetic evidence for a hantavirus enzootic in deer mice (Peromyscus maniculatus) captured a decade before the recognition of hantavirus pulmonary syndrome.

To determine if the emergence of hantavirus pulmonary syndrome in the United States was a consequence of recent amino-acid altering mutations and/or genetic reassortment with pathogenic hantaviruses, we examined lung and spleen tissues from seropositive deer mice trapped in August 1983 in Mono County, California, for hantaviral RNA by reverse transcriptase-directed polymerase chain reaction. Alignment and comparison of 1485 nucleotides of the S and M genomic segments enzymatically amplified from these tissues indicated that these deer mice harbored a hantavirus which was genetically similar, differing by less than 2% at the deduced amino-acid level, to the hantavirus implicated in cases of hantavirus pulmonary syndrome occurring in the Four-Corners region of New Mexico, Arizona, Utah, and Colorado in 1993. The peromyscine rodent-borne hantaviruses were, in turn, genetically distinct from other well-characterized hantaviruses, diverging by approximately 30% from Prospect Hill and Puumala viruses at the nucleotide and amino acid levels. Phylogenetic analysis using the maximum parsimony, neighbor-joining, and unweighted pair-group methods indicated that the Peromyscus-derived hantavirus shared a common ancestry with arvicolid rodent-borne hantaviruses. Overall congruency of the phylogenetic trees based on the S and M genomic sequences supported the evolutionary position of the peromyscine rodent-borne hantaviruses. Our data also establish the existence of a hantavirus enzootic in deer mice long before the recognition of hantavirus pulmonary syndrome in the United States.

Amino Acid Sequence↗
PubMed1994

Detection of Muerto Canyon virus RNA in peripheral blood mononuclear cells from patients with hantavirus pulmonary syndrome.

To determine if Muerto Canyon Virus (MCV) RNA is present in the peripheral blood of patients with hantavirus pulmonary syndrome, a reverse transcriptase-polymerase chain reaction (RT-PCR) assay for MCV RNA was used on blood samples from 20 seropositive case-patients. RNA was prepared from peripheral blood mononuclear cells (PBMC) or blood clot (or both) from 19 and from plasma from 11 case-patients. All 12 blood clot, all 13 PBMC, and 8 of 11 plasma preparations produced an MCV amplification product after RT-PCR with primers from the G2 gene. All of 5 PBMC RNA preparations tested were positive using unnested primers in S segment. Nucleotide sequences were determined for 16 G2 amplimers and 4 S segment amplimers, verifying that unique MCV cDNA sequences were amplified. Viral RNA became undetectable in 5 of 7 convalescent samples tested but was present up to day 23 of illness in 2 case-patients.

Base Sequence↗
PubMed1994

Dominant glycoprotein epitope of four corners hantavirus is conserved across a wide geographical area.

A newly identified hantavirus, tentatively called Four Corners virus (FCV), was found to be the aetiological agent of a 1993 outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States. Immunodominant epitopes of 43 and 31 amino acids were identified in the nucleocapsid protein and G1 glycoprotein, respectively. The G1 genes of different hantaviruses are highly divergent, suggesting that geographically diverse FCVs might fail to cross-react owing to antigenic drift. We now show that the immunodominant epitope of G1 is conserved among 18 FCVs from a broad geographical area, despite extensive nucleotide sequence heterogeneity. Antibodies from all 45 HPS patients, separated by more than 3000 km were shown to be reactive with the dominant G1 epitope. Evidence for limited cross-reactivity between the G1 antigen of a novel hantavirus of the cotton rat and that of FCV is presented.

Amino Acid Sequence↗
PubMed1994

A novel hantavirus associated with an outbreak of fatal respiratory disease in the southwestern United States: evolutionary relationships to known hantaviruses.

Four Corners hantavirus (FCV) is the tentative name of the suspected etiologic agent of the newly identified hantavirus-associated respiratory distress syndrome (HARDS). The identification in HARDS patients of serum immunoglobulin M and immunoglobulin G antibodies that cross-reacted with Hantaan, Seoul, and Puumala virus antigens first suggested that FCV is a hantavirus. Limited nucleotide sequence data from the FCV glycoprotein-2 (G2) confirmed that FCV is a hantavirus and showed that it is most closely related to Prospect Hill and Puumala viruses. We have molecularly cloned approximately 95% of the sequences of the M and S segments of the FCV genome encoding the envelope glycoproteins and nucleocapsid protein N from the lungs of a patient with HARDS. The nucleotide sequence has been determined for 2,632 bases. The nucleotide sequence data show that FCV is a new member of the Puumala virus and Prospect Hill virus division of the hantavirus genus. Phylogenetic tree analyses indicate that the M and S segments have evolved in parallel. Therefore, the novel pathogenic activity of FCV is not likely to be the result of recent reassortment of segments from less pathogenic viruses.

Amino Acid Sequence↗