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B Hjelle

Publications and source records attributed to B Hjelle.

At least 37 records · Page 2Linked to original sources
PubMed1999

Hantavirus (Bunyaviridae) infections in rodents from Orange and San Diego counties, California.

During a screening program to determine the extent of hantavirus activity in Orange and San Diego Counties, California, serum samples from 2,365 rodents representing nine genera and 15 species were tested for hantavirus antibodies. A reverse transcription-polymerase chain reaction on selected seropositive rodents was used to identify the specific hantavirus. Rodents positive for Sin Nombre virus (SNV) antibodies by Western blot included 86 (9.1%) of 948 deer mice (Peromyscus maniculatus), four (1.5%) of 275 California mice (Peromyscus californicus), one (0.5%) of 196 cactus mice (Peromyscus eremicus), 51 (12.2%) of 417 harvest mice (Reithrodontomys megalotis), and five (12.5%) of 40 California voles (Microtus californicus). All other specimens tested were negative for hantavirus antibodies. There was a correlation between age and sex of the reservoir host and prevalence of SNV antibody, especially among male deer mice and harvest mice. Few seasonal trends in antibody prevalence were observed and continued maintenance of SNV and El Moro Canyon virus was found at several foci over a 4-5-year period. Isla Vista virus was also found in voles and represents the first recorded in Orange County. Microhabitat selection on the part of these rodents based on plant density, plant height, and availability of food plants may explain, to some extent, all of the hantavirus-positive foci throughout the study area over a broad geographic range and the lack of antibody-positive rodents in dense chaparral, woodland, and riparian areas. The majority of rodents positive for SNV was identified from localities along coastal bluffs and the foothills of the Santa Ana Mountains, where trap success was high and P. maniculatus represented 43% of all rodents collected. Several residential, commercial, and industrial sites exist in these areas and the potential health risk should not be overlooked. This study represents an in-depth analysis of the prevalence, host distribution, and characteristics of rodent populations infected by three hantaviruses within a small, well-defined, geographic area.

Animals↗
PubMed1998

Serologic survey for hantavirus infection in domestic animals and coyotes from New Mexico and northeastern Arizona.

OBJECTIVE: To determine whether animals had serologic evidence of infection with Sin Nombre virus (SNV). DESIGN: Prospective serosurvey. SAMPLE POPULATION: Serum samples were obtained from 145 cats, 85 dogs, 120 horses, and 24 cattle between April 1993 and August 1994 and 54 coyotes between December 1994 and February 1995. PROCEDURE: Serum samples were analyzed by western immunoblot assays for reaction with SNV nucleocapsid antigen. Samples with reactivity to SNV nucleocapsid proteins were used to probe multiple-antigen blots containing recombinant fusion proteins derived from prototypic hantaviruses. Lung tissue or blood clots were used in nested reverse-transcriptase polymerase chain reaction assays for a 320-nucleotide portion of the SNV G1 gene. RESULTS: Sera from 4 of 145 (2.8%) cats and 4 of 85 (3.5%) dogs had trace reactivity to full-length SNV-encoded nucleocapsid proteins. All samples from horses, cattle, and coyotes were nonreactive. Sera from cats and dogs that had trace IgG-antibody reactivity to nucleocapsid proteins were then tested for IgG-antibody reactivity to nucleocapsid proteins of prototypic hantaviruses. One cat had multiple cross-reactivities with these hantaviruses, consistent with exposure to a hantavirus; however, epitope mapping studies did not support this conclusion. Reverse-transcriptase polymerase chain reaction studies of blood clots or lung tissue from 2 animals that had weak reactivity to SNV failed to amplify any hantavirus sequence. CLINICAL IMPLICATIONS: Domestic animals, particularly dogs and cats, as well as coyotes do not appear to have a major role in the maintenance and transmission of SNV.

Animals↗
PubMed1998

Tissue distribution of hantavirus antigen in naturally infected humans and deer mice.

The Sin Nombre virus (SNV) is the etiologic agent of hantavirus pulmonary syndrome in humans but does not cause disease in chronically infected deer mice (Peromyscus maniculatus), the natural host. In this study, murine antiserum raised against recombinant SNV nucleocapsid protein was utilized to localize viral antigen immunohistochemically in tissues from both humans (n = 20; 11 positive, 9 negative) and deer mice (n = 6; 4 positive, 2 negative). Viral infection status was confirmed by Western blot or reverse transcriptase-polymerase chain reaction. SNV antigen was detected in pulmonary and cardiac endothelium in both species, but positive cells in deer mice were rare. Other deer mouse tissues, including kidney, were negative; in contrast, vascular elements of several tissues from infected humans were positive, with strong staining of renal endothelium. The paucity of positive cells in chronically infected mice suggests a low virus burden compared with that of acutely infected humans.

Animals↗
PubMed1998

High prevalence of hantavirus infection in Indian communities of the Paraguayan and Argentinean Gran Chaco.

Serologic evidence of past infection with a Sin Nombre-like hantavirus(es) was demonstrated in 78 (40.4%) of 193 Indians living in western Paraguay and in 38 (17.1%) of 222 Indians inhabiting the Salta province of northern Argentina. In both populations seroprevalence increased with age, with the most striking increase occurring at 18 years of age in the Paraguayan population and at 35 years of age in the Salta population. The peak prevalences in both populations (66.6% and 44.0%, respectively) were seen in Indians > 53 years old. Although no sex difference was observed in the Paraguayan Indians, in the Salta population seroprevalence was greater in males than in females. Familiar clustering of the infection was observed. The data indicate that the Indian populations of the Gran Chaco are frequently exposed to and survive infection with a Sin Nombre-like virus(es). Possible explanations of this novel epidemiology are discussed.

Adolescent↗
PubMed1997

Rapid and specific detection of Sin Nombre virus antibodies in patients with hantavirus pulmonary syndrome by a strip immunoblot assay suitable for field diagnosis.

To develop a rapid antibody test for Sin Nombre hantavirus (SNV) infection for diagnosis of hantavirus pulmonary syndrome (HPS) in field settings where advanced instrumentation is not available, a strip immunoblot assay bearing four immobilized antigens for SNV and a recombinant nucleocapsid protein antigen of Seoul hantavirus (SEOV) was prepared. The SNV antigens included a full-length recombinant-expressed nucleocapsid (N) protein (rN), a recombinant-expressed G1 protein (residues 35 to 117), and synthetic peptides derived from N (residues 17 to 59) and G1 (residues 55 to 88). On the basis of the observed reactivities of hantavirus-infected patient and control sera, we determined that a positive assay requires reactivity with SNV or SEOV rN antigen and at least one other antigen. Isolated reactivity to either viral rN antigen is indeterminate, and any pattern of reactivity that does not include reactivity to an rN antigen is considered indeterminate but is unlikely to represent hantavirus infection. Fifty-eight of 59 samples from patients with acute SNV-associated HPS were positive according to these criteria, and one was initially indeterminate. Four of four samples from patients with HPS due to other hantaviruses were positive, as were most samples from patients with SEOV and Puumala virus infections. Of 192 control serum samples, 2 (1%) were positive and 2 were indeterminate. Acute SNV infection was distinguishable from remote SNV infection or infection with hantaviruses other than SNV by the presence of G1 peptide antigen reactivities in the former. The strip immunoblot assay shows promise for the detection of SNV antibodies early in the course of HPS.

Antibodies, Viral↗
PubMed1997

Serological diagnosis of hantavirus infections by an enzyme-linked immunosorbent assay based on detection of immunoglobulin G and M responses to recombinant nucleocapsid proteins of five viral serotypes.

Worldwide, hantaviruses cause more than 100,000 human infections annually. Rapid and accurate methods are important both in monitoring acute infections and for epidemiological studies. We and others have shown that the amino termini of hantavirus nucleocapsid proteins (Ns) are sensitive tools for the detection of specific antibodies in hantavirus disease. Accordingly, we expressed truncated Ns (amino acids 1 to 117) in Escherichia coli from the five hantaviruses known to be pathogenic to man; Hantaan (HTN), Seoul (SEO), Dobrava (DOB), Sin Nombre (SN), and Puumala (PUU) viruses. In order to obtain pure antigens for use in an enzyme-linked immunosorbent assay (ELISA), the recombinant proteins were purified by polyhistidine-metal chelate affinity chromatography. Polyclonal animal antisera and a panel of serum specimens from hantavirus-infected individuals from Scandinavia, Slovenia, Russia, Korea, China, and the United States were used to evaluate the usefulness of the method. With both human and animal sera, it was possible to designate the antibody response into two groups: those with HTN, SEO, and DOB virus reactivity on the one hand and those with SN and PUU virus reactivity on the other. In sera from Scandinavia, European Russia, and the United States, the antibody response was directed mainly to the PUU and SN virus group. The sera from Asia reacted almost exclusively with the HTN, SEO, and DOB types of viruses. This was true for both the immunoglobulin M (IgM) and IgG antibody responses, indicating that this type of discrimination can be done during the acute phase of hantavirus infections. Both the HTN, SEO, and DOB virus and the PUU and SN virus types of antibody response patterns were found in patients from the Balkan region (Solvenia).

Animals↗
PubMed1997

Rio Mamore virus: genetic characterization of a newly recognized hantavirus of the pygmy rice rat, Oligoryzomys microtis, from Bolivia.

Human hantavirus disease occurs throughout much of South America. The rodent hosts and the specific etiologic agent(s) are largely unknown, but many reported cases occurred within the habitation ranges of oryzomine rodents (rice rats). We have identified a genetically novel hantavirus (Rio Mamore virus [RM]) of the pygmy rice rat Oligoryzomys microtis in Bolivia. The complete sequence of the small (S) genome and the partial sequence of the medium (M) genome are described. This virus is closely related to the newly identified human pathogen Andes virus from Patagonia. To facilitate improved diagnosis of hantavirus infections in South America, we have expressed the complete nucleocapsid protein of RM in Escherichia coli and affinity-purified it for use in an ELISA and Western blot assays for antibodies to RM.

Amino Acid Sequence↗
PubMed1996

Human and rodent hantavirus infection in New York State: public health significance of an emerging infectious disease.

BACKGROUND: A case of hantavirus pulmonary syndrome with possible exposure in New York and/or Rhode Island was confirmed in February 1994. OBJECTIVE: To conduct four studies to determine the historical and geographic distribution of human and small-mammal infection with hantaviruses in New York State. METHODS: Enzyme-linked immunosorbent assays were performed on serum samples obtained from 130 humans during a 1978 babesiosis survey, 907 small mammals collected in New York State since 1984, 12 rodents collected in 1994 near the residences of the patients with hantavirus pulmonary syndrome, and 76 New York patients with acute respiratory distress syndrome-like illness (as suspected cases of hantavirus pulmonary syndrome). RESULTS: None of the human serum samples from the 1978 serosurvey showed evidence of hantavirus exposure by enzyme-linked immunosorbent assay. Statewide historical serum samples from white-footed mice showed evidence of Sin Nombre virus infection in 12.0% (97/809) and Seoul-like virus infection in 9.6% (78/809). Site-specific seropositivity rates were as high as 48.5% with Sin Nombre virus during 1 year (1984). Two of 12 mice captured near the residences of a human patient were positive for Sin Nombre virus by enzyme-linked immunosorbent assay, yet were negative for viral RNA by polymerase chain reaction. None of the patients with suspected hantavirus pulmonary syndrome was serologically reactive for Sin Nombre virus. CONCLUSIONS: We provide serologic evidence of small-mammal infection with hantaviruses in New York State as long ago as 1984. Human cases of hantavirus pulmonary syndrome are rare in New York, and data indicate that transmission to humans is probably infrequent. A unique set of host, agent, and environmental factors may be necessary to cause hantavirus pulmonary syndrome in humans.

Adolescent↗
PubMed1996

HTLV-I and HTLV-II Tax: differences in induction of micronuclei in cells and transcriptional activation of viral LTRs.

Human T-cell leukemia virus (HTLV) types I and II are highly related viruses that differ in disease manifestations. HTLV-I has been linked unmistakably to adult T-cell leukemia-lymphoma. On the other hand, there is little evidence that prior infection with HTLV-II increases risk for lymphoproliferative disorders. Both viruses encode homologous transcriptional-activating proteins (respectively designated as Tax1 and Tax2) which have been suggested to be important mediators of viral pathogenesis. Previously, we reported that Tax1 is a potent inducer of micronuclei formation in cells. Here, we present evidence that Tax2 lacks micronuclei inductive ability. We contrast this phenotypic difference between Tax1 and Tax2 at the cellular level with their similarities at the molecular level in transcriptional activation.

Amino Acid Sequence↗
PubMed1996

Genetic variants of human T-lymphotrophic virus type II in American Indian groups.

The human T-lymphotropic virus type II (HTLV-II) is found in many New World Indian groups in North and South America and may have entered the New World from Asia with the earliest migration of ancestral Amerindians over 15,000 years ago. To characterize the phylogenetic relationships of HTLV-II strains infecting geographically diverse Indian populations, we used polymerase chain reaction to amplify HTLV-II sequences from lymphocytes of seropositive Amerindians from Brazil (Kraho, Kayapo, and Kaxuyana), Panama (Guaymi), and the United States (the Navajo and Pueblo tribes of the southwestern states and the Seminoles of Florida). Sequence analysis of a 780-base pair fragment (located between the env gene and the second exons of tax/rex) revealed that Amerindian viruses clustered in the same two genetic subtypes (IIa and IIb) previously identified for viruses from intravenous drug users. Most infected North and Central American Indians had subtype IIb, while HTLV-II infected members of three remote Amazonian tribes clustered as a distinct group within subtype IIa. These findings suggest that the ancestral Amerindians migrating to the New World brought at least two genetic subtypes, IIa and IIb. Because HTLV-II strains from Amazonian Indians form a distinct group within subtype HTLV-IIa, these Brazilian tribes are unlikely to be the source of IIa viruses in North American drug users. Finally, the near identity of viral sequences from geographically diverse populations indicate that HTLV-II is a very ancient virus of man.

Amino Acid Sequence↗
PubMed1996

Sequence analysis of the complete S genomic segment of a newly identified hantavirus isolated from the white-footed mouse (Peromyscus leucopus): phylogenetic relationship with other sigmodontine rodent-borne hantaviruses.

Four Corners (FC) or Sin Nombre virus, a hantavirus harbored by the deer mouse (Peromyscus maniculatus), is the principal etiologic agent of hantavirus pulmonary syndrome (HPS). Recently, a hantavirus, designated New York (NY) virus, isolated from a white-footed mouse (Peromyscus leucopus) captured on Shelter Island, New York, was molecularly linked to a fatal case of HPS occurring in the northeastern United States. To clarify the genetic and phylogenetic relationship between NY and FC viruses and other sigmodontine rodent-borne hantaviruses, we amplified and sequenced the entire S genomic segment of NY virus. The S segment of NY virus was 2078 nucleotides long, with an open reading frame of 1284 nucleotides in the virus complementary strand, capable of encoding a protein of 428 amino acids, and with a 752-nucleotide long 3'-noncoding region, comprised of numerous imperfect repeats. Pairwise analysis indicated that NY virus was more similar to FC virus than to other sigmodontine rodent-borne hantaviruses, differing from strains of FC virus by 16.6-17.8% and 7.0-8.2% at the nucleotide and amino acid levels, respectively. As determined by the maximum parsimony and neighbor-joining methods, NY virus formed a separate lineage from FC virus and was phylogenetically distinct from hantaviruses harbored by other sigmodontine rodents. Whether or not NY and FC viruses represent distinct viral species is unclear. Further analyses of hantaviruses harbored by white-footed mice are needed to clarify the genetic diversity and evolution of Peromyscus-borne hantaviruses.

Amino Acid Sequence↗
PubMed1996

Occupational exposure leading to hantavirus pulmonary syndrome in a utility company employee.

Hantavirus pulmonary syndrome is a newly recognized rodent-borne zoonosis. We report a case of hantavirus pulmonary syndrome in an employee of a California utility company who was probably occupationally exposed to Sin Nombre virus. Environmental assessment and genetic comparison of the patient's hantavirus isolates to hantavirus isolates from rodents trapped at possible sites of exposure suggested that the patient contracted his infection at the work site. The study revealed a close correspondence between the patient's viral genotype and that from a rodent trapped at the work site. This report alerts the public health and medical community to the fact that employees of utility companies and similar industries may be an important risk group in areas where hantavirus is endemic and emphasizes the need to incorporate strategies for preventing exposure to hantavirus and other emerging infections into occupational safety protocols.

Animals↗
PubMed1996

Hantavirus pulmonary syndrome, renal insufficiency, and myositis associated with infection by Bayou hantavirus.

Hantaviruses are etiologic agents of hemorrhagic fever with renal syndrome, an acute illness characterized by acute renal insufficiency, proteinuria, and hemodynamic instability. Recently, a New World form of hantavirus disease, hantavirus pulmonary syndrome (HPS), was recognized; in this form, pulmonary edema is prominent, but renal insufficiency is generally lacking. HPS cases from the southeastern United States may be exceptional in that they have exhibited both pulmonary and renal manifestations. One case in Louisiana and one case in Florida were linked to infection by the distinct but closely related Bayou and Black Creek Canal hantaviruses, respectively. We report a nonfatal case of HPS caused by Bayou hantavirus that occurred in eastern Texas. Clinical manifestations included pulmonary and renal insufficiency and myositis, which had previously been observed in the patient from Florida. The occurrence of distinctive clinical abnormalities in HPS cases from the southeastern United States supports the concept that there are clinically significant differences between western and southeastern forms of HPS.

Adult↗
PubMed1996

Epidemiologic linkage of rodent and human hantavirus genomic sequences in case investigations of hantavirus pulmonary syndrome.

Sin Nombre virus (SNV) causes the zoonotic disease hantavirus pulmonary syndrome (HPS). Its mechanisms of transmission from rodent to human are poorly understood. It is possible that specific genetic signature sequences could be used to determine the probable site of each case-patient's exposure. Environmental assessments suggested 12 possible sites of rodent exposure for 6 HPS patients. Rodents were captured at 11 of the 12 sites and screened for SNV infection within 2 weeks of the patient's diagnosis. Viral sequences amplified from tissues of rodents at each site were compared with those from case-patients' tissues. Rodents bearing viruses with genetic sequence identity to case-patients' viruses across 2 genomic segments were identified in 4 investigations but never at >1 site. Indoor exposures to rodents were especially common at implicated sites. By distinguishing among multiple possible sites of exposure, viral genotyping studies can enhance understanding of the conditions associated with infection by SNV.

Animals↗
PubMed1996

Cocirculation of multiple hantaviruses in Texas, with characterization of the small (S) genome of a previously undescribed virus of cotton rats (Sigmodon hispidus).

An environmental and laboratory investigation was conducted after a fatal childhood case of hantavirus pulmonary syndrome occurred in Deaf Smith County, Texas in May 1995. A trapping campaign was conducted to identify possible rodent carriers. Six species of murid and heteromyid rodents were collected, and at least one hantavirus-seropositive specimen was found in each of the five murid species. Tissues from a selection of 11 seropositive specimens were examined by the polymerase chain reaction (PCR) and sequencing of viral genetic material. The predominant hantavirus was El Moro Canyon virus (ELMCV), which occurred in three of three harvest mice (Reithrodontomys megalotis) and in three of four deer mice (Peromyscus maniculatus) examined. Sin Nombre virus (SNV) was found in one deer mouse and one white-footed mouse (P. leucopus). A seropositive house mouse (Mus musculus) was negative by PCR. Two cotton rats (Sigmodon hispidus) were infected by a virus of novel genotype (Muleshoe virus [MULEV]) that bears closet resemblance to Bayou hantavirus. The sequence of the complete small genomic segment was determined for one MULEV, and high-level expression of its nucleocapsid protein was induced in Escherichia coli. Serologic studies indicated that the most likely etiologic agent in the human infection was SNV.

Adolescent↗