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B Hjelle

Publications and source records attributed to B Hjelle.

At least 73 records · Page 4Linked to original sources
PubMed1994

Characterization of human antibody responses to four corners hantavirus infections among patients with hantavirus pulmonary syndrome.

Hantavirus pulmonary syndrome (HPS) is a human disease caused by a newly identified hantavirus, which we will refer to as Four Corners virus (FCV). FCV is related most closely to Puumala virus (PUU) and to Prospect Hill virus (PHV). Twenty-five acute HPS serum samples were tested for immunoglobulin G (IgG) and IgM antibody reactivities to FCV-encoded recombinant proteins in Western blot (immunoblot) assays. All HPS serum samples contained both IgG and IgM antibodies to the FCV nucleocapsid (N) protein. FCV N antibodies cross-reacted with PUU N and PHV N proteins. A dominant FCV N epitope was mapped to the segment between amino acids 17 and 59 (QLVTARQKLKDAERAVELDPDDVNKSTLQSRRAAVSALETKLG). All HPS serum samples contained IgG antibodies to the FCV glycoprotein-1 (G1) protein, and 21 of 25 serum samples contained FCV G1 IgM antibodies. The FCV G1 antibodies did not cross-react with PUU G1 and PHV G1 proteins. The FCV G1 type-specific antibody reactivity mapped to a segment between amino acids 59 and 89 (LKIESSCNFDLHVPATTTQKYNQVDWTKKSS). One hundred twenty-eight control serum samples were tested for IgG reactivities to the FCV N and G1 proteins. Nine (7.0%) contained FCV N reactivities, 3 (2.3%) contained FCV G1 reactivities, and one (0.8%) contained both FCV N and FCV G1 reactivities. The epitopes recognized by antibodies present in control serum samples were different from the epitopes recognized by HPS antibodies, suggesting that the control antibody reactivities were unrelated to FCV infections. These reagents constitute a type-specific assay for FCV antibodies.

Adolescent↗
PubMed1994

Prevalence of human T cell lymphotropic virus type II in American Indian populations of the southwestern United States.

We investigated the seroprevalence of human T cell lymphotropic virus type II (HTLV-II) using a screening enzyme-linked immunosorbent assay (ELISA) and immunoblot confirmation among the predominant tribes (Pueblo and Athapaskan) served by two large Indian Health Service facilities in New Mexico. Among persons being treated for sexually transmitted diseases, eight (3.2%) of 250 were seropositive for HTLV II, compared with eight (2.1%) of 385 women attending prenatal clinics. In a survey of unselected patients at one of the facilities, 15 (3.4%) of 446 were seropositive. Of 31 seropositive subjects, 25 were infected with HTLV-II and six infections could not be typed. Sera from nine (29%) of the 31 infected subjects had absorbance values less than the manufacturer's cutoff in the ELISA. Both Pueblo and Athapaskan groups had similar overall seroprevalences, but women tended to have a slightly higher seroprevalence than men, and seroprevalence tended to increase with age. These data show that HTLV-II infection is present among diverse groups of American Indians in the southwestern United States. Present ELISA screening tests, such as those used in this study, lack sensitivity to HTLV-II infection unless a reduced absorbance cutoff is used.

Adolescent↗
PubMed1994

Emergence of hantaviral disease in the southwestern United States.

Hantaviruses are parasites of small mammals, predominantly peridomestic and commensal rodents. They have a worldwide distribution. Hantavirus-related illness occurs in rural areas where humans come into contact with rodents. In most cases human infection is manifested by one of a variety of acute illnesses involving hemorrhagic fever and renal disease. In May 1993, a cluster of patients with an acute pulmonary disease with high mortality was noted in the Four Corners region of the southwestern United States. Serologic and genetic studies indicated that the etiologic agent was a novel hantavirus. The uncertainty engendered by the emergence of a new disease with high mortality forced a rapid response by state and federal agencies and by the University of New Mexico Medical Center, Albuquerque, where most patients from this region were referred. Considerable progress has been made in identifying infected cases on clinical and laboratory grounds and in ensuring that appropriate supportive care is made available to patients as soon as they are suspected of having hantaviral infection. Cases of hantavirus pulmonary syndrome--both new and retrospectively diagnosed--are still being recognized throughout the western United States. Many important questions remain unanswered.

Adolescent↗
PubMed1994

Outbreak of Hantavirus pulmonary syndrome in the southwestern United States. Response of pathologists and other laboratorians.

During late spring and early summer of 1993, national and international media called worldwide attention to a cluster of deaths in the southwestern United States. These patients succumbed to a rapidly progressive severe respiratory distress syndrome. After notification of state and national health agencies in mid-May, a major effort was launched to determine the cause of this often fatal respiratory distress syndrome, to advise the public on safety measures, and to determine the method of spread of this "mystery illness." Within weeks of recognition of the early cases, the Centers for Disease Control and Prevention announced the probable agent, a Hantavirus. This report details the response of pathologists, medical technologists, and other laboratory scientists to this new viral epidemic, with emphasis on activities that occurred within New Mexico.

Adolescent↗
PubMed1993

Human T-cell leukemia virus type II infection frequently goes undetected in contemporary US blood donors.

Serologic screening for human T-cell leukemia virus type I (HTLV-I) infection was begun in US blood banks with the licensure of enzyme-linked immunosorbent assays (ELISA) in December 1988. We examined the donation histories of the first 60 Western blot (WB)-confirmed HTLV-I/II positive donors to one blood center and found 8 had made 16 previous donations that scored negative on the screening ELISA. All 16 donations had ELISA absorbance below the cutoff for a positive assay, but still well above that of the average donation (17.6% +/- 5.7% of the cutoff). In a more extensive study, 17 donations from a total of 61,752 at six blood centers were both ELISA-positive and WB-positive for HTLV-I (4) or HTLV-II (13), and 218 samples had ELISA absorbance greater than 50% of the ELISA cutoff. One hundred seventy-eight of the 218 were tested further by WB and 11 were found positive. All 11 positives were confirmed by polymerase chain reaction; 10 had HTLV-II and 1 had HTLV-I. Thus, the HTLV-I-based screening ELISA missed at least 10 of 23, or 43% (95% confidence interval, 23% to 66%), of HTLV-II infections, compared with 1 of 5, or 20%, of HTLV-I infections.

Blood Donors↗
PubMed1993

Spastic ataxia associated with human T-cell lymphotropic virus type II infection.

Human T-cell lymphotropic virus type one (HTLV-1) is associated with tropical spastic paraparesis or HTLV-I--associated myelopathy. We report 2 women with a spastic ataxic illness similar to HTLV-I--associated myelopathy infected solely with HTLV-II. Identification of HTLV-II infection was made serologically, by polymerase chain reaction, and by viral culture (in 1 woman). One woman, treated with 200 mg of danazol orally, three times daily, had pronounced improvement in ambulation, nocturnal spasticity, and nighttime urinary frequency. It appears that infection with HTLV-II may cause an illness similar to HTLV-I--associated myelopathy, but distinguished by the presence of ataxia.

Antibodies, Monoclonal↗
PubMed1993

Endemic human T cell leukemia virus type II infection in southwestern US Indians involves two prototype variants of virus.

Human T cell leukemia virus (HTLV) type II is endemic in certain American Indians, and high rates of infection occur in intravenous drug users (IVDUs). North American IVDUs are infected with two distinct variants, HTLV-IIa and -IIb. If IVDUs became infected as a result of interaction with members of an American Indian population, both viral forms should be demonstrable in such populations. Nucleotide sequence analysis of 630 bases of the env gene encoding the gp21 protein was done on DNA from 12 New Mexico Indians (8 Pueblo, 4 Navajo). All samples were typical subtype a or b viruses. Seven of the 8 Pueblo and 2 of 4 Navajo had subtype b; the rest had subtype a. The results are compatible with an indigenous New World origin for both subtypes of HTLV-II.

Adult↗
PubMed1992

Chronic neurodegenerative disease associated with HTLV-II infection.

Although human T-cell leukemia virus (HTLV) type I is known to cause a number of diseases, there has been no convincing evidence of pathological changes after infection with the related virus, HTLV-II. We have found an endemic focus of HTLV-II infection among members of an American Indian population in New Mexico, USA. We set out to determine the pathological consequences of HTLV-II infection in this population and identified two sisters (aged 59 and 46 years) with a disease superficially resembling the myeloneuropathy induced by HTLV-I. These women had a syndrome similar to the olivopontocerebellar atrophy variant of multiple system atrophy, and HTLV-II infection was confirmed by western blot and the polymerase chain reaction. Thus, HTLV-II may, like HTLV-I, cause a progressive neurodegenerative disease.

Ataxia↗
PubMed1992

Sequence variation of functional HTLV-II tax alleles among isolates from an endemic population: lack of evidence for oncogenic determinant in tax.

Human T-cell leukemia-lymphoma virus type II (HTLV-II) has been isolated from patients with hairy cell leukemia (HCL). We previously described a population with longstanding endemic HTLV-II infection, and showed that there is no increased risk for HCL in the affected groups. We thus have direct evidence that the endemic form(s) of HTLV-II cause HCL infrequently, if at all. By comparison, there is reason to suspect that the viruses isolated from patients with HCL had an etiologic role in the disease in those patients. One way to reconcile these conflicting observations is to consider that isolates of HTLV-II might differ in oncogenic potential. To determine whether the structure of the putative oncogenic determinant of HTLV-II, tax2, might differ in the new isolates compared to the tax of the prototype HCL isolate, MO, four new functional tax cDNAs were cloned from new isolates. Sequence analysis showed only minor (0.9-2.0%) amino acid variation compared to the published sequence of MO tax2. Some codons were consistently different from published sequences of the MO virus, but in most cases, such variations were also found in each of two tax2 clones we isolated from the MO T-cell line. These variations rendered the new clones more similar to the tax1 of the pathogenic virus HTLV-I. Thus we find no evidence that pathologic determinants of HTLV-II can be assigned to the tax gene.

Alleles↗
PubMed1992

Identification of immunodominant epitopes in envelope glycoprotein of human T lymphotropic virus type II.

A series of synthetic peptides derived from the envelope glycoprotein of human T lymphotropic virus type II (HTLV-II) was used in an enzyme immunoassay to determine the immunodominant epitopes of envelope glycoprotein. Of the 11 synthetic peptides spanning the external glycoprotein of HTLV-II (gp52) and the 3 from the transmembrane protein (gp21), 3 peptides from gp52 (termed Env-20(85-102), Env-202(173-209), and Env-203(219-256] reacted with most of the polymerase chain reaction-confirmed HTLV-II specimens (83, 95, and 76%, respectively); all other peptides reacted minimally with these specimens. Env-202(173-209) reacted with a greater percentage (91 to 100%) of specimens from different risk groups, including intravenous drug users (n = 30), North American Indians (n = 13), Guaymi Indians from Panama (n = 22), and routine U.S. blood donors (n = 34), when compared with Env-20(85-102) (73 to 100%) or Env-203(219-256) (68 to 83%). Furthermore, Env-20(85-102) and Env-202(173-209) had some reactivity (8-25%) with sera from HTLV-I-infected individuals, whereas Env-203(219-256) reacted with 58% of HTLV-I specimens. We conclude that peptides Env-20(85-102) and Env-202(173-209) represent the type-specific immunodominant epitopes of HTLV-II external glycoprotein.

Amino Acid Sequence↗
PubMed1992

Immune responsiveness to the immunodominant recombinant envelope epitopes of human T lymphotropic virus types I and II in diverse geographic populations.

The heterogeneity of immune responsiveness to the immunodominant epitopes of human T lymphotropic virus (HTLV) types I (MTA-1(162-209)) and II (K-55(162-205)) were determined in natural infections with HTLV-I and -II from diverse geographic areas (n = 285). Of the HTLV-I specimens confirmed by polymerase chain reaction (PCR), all North American (n = 37) and Peruvian (n = 19) specimens reacted with MTA-1. Of HTLV-II specimens confirmed by PCR, 44 (96%) of 46 from North American blood donors, 28 (97%) of 29 from native Americans, and all from intravenous drug users (n = 29) reacted with K-55. Specimens from other geographic areas (Peru, 30; Brazil, 4; Mexico, 10; Italy, 5; Somalia, 13; Ethiopia, 17; Japan, 32; and Jamaica, 15) all reacted either with MTA-1 or K-55. By synthetic peptide-based serologic typing, all of these specimens could be typed as HTLV-I or -II. In addition to the direct implications of these findings for diagnostic purposes, these data provide indirect evidence for the conservation of immunodominant HTLVenv epitopes in diverse geographic populations.

Africa↗
PubMed1992

Spontaneous proliferation of HTLV-II-infected peripheral blood lymphocytes: HLA-DR-driven, IL-2-dependent response.

Peripheral blood lymphocytes obtained from HTLV-II-infected persons (n = 13) and cultured in the absence of exogenous stimulator demonstrated augmented spontaneous proliferation (17,672 +/- 5,498 cpm) when compared with cells from healthy donors (1,921 +/- 1,306 cpm). Removal of non-T population did not abrogate the proliferative response of patients' PBMC, suggesting that the proliferation is not related to the autologous mixed lymphocyte reaction. Addition of recombinant interleukin-2 (rIL-2; 0.1 U/ml) to spontaneously proliferating cultures from HTLV-II-infected persons resulted in a 3- to 4-fold increase in proliferation (61,985 +/- 16,003); in contrast, PBMC from controls demonstrated 38- to 42-fold increase in their proliferative capacity in response to rIL-2 (77,256 +/- 13,044). Antibodies to both IL-2 receptor and HLA-DR were able to inhibit the spontaneous proliferation of PBMC from HTLV-II-infected persons in a dose-dependent manner. Furthermore, addition of cyclosporin A, which preferentially blocks accumulation of IL-2 mRNA, also inhibited spontaneous proliferation in a dose-dependent manner. These observations suggest that the spontaneous proliferation of HTLV-II-infected PBMC is at least in part an HLA-DR-driven, IL-2-dependent event, which is not analogous to the AMLR.

Adult↗
PubMed1992

Primary isolation of human T-cell leukemia-lymphoma virus types I and II: use for confirming infection in seroindeterminate blood donors.

We describe the use of an immunofluorescence assay and coculture to confirm human T-cell leukemia-lymphoma virus (HTLV) infection. Peripheral blood mononuclear cells from 32 of 32 seropositive donors were positive in the immunofluorescence assay, and 63% of their cocultures produced p24 antigen. Specific antibodies distinguished HTLV type I (HTLV-I) from HTLV-II. HTLV-I or HTLV-II was isolated from donors with indeterminate serologic test results.

Antibodies, Monoclonal↗
PubMed1991

Serologic distinction between human T-lymphotropic virus (HTLV) type I and HTLV type II.

In November 1988, the Food and Drug Administration approved reagents for serologic screening for human T-lymphotropic virus type I (HTLV-I) infection in blood donors and patients suspected of having HTLV-I-related illnesses. These reagents are able to detect HTLV type II (HTLV-II), a close relative of HTLV-I with no known pathologic effect. The distinction between the two forms of HTLV is important to the donor and to any recipient of blood containing HTLV. The application to sera from 38 seropositive blood donors and 2 recipients (37 "confirmed" positive and 3 indeterminate by Western blot) of two methods (Western blot and peptide enzyme immunoassay) for serologic distinction between HTLV-I and -II is described. These results were compared to those from polymerase chain reaction (PCR) analysis of HTLV proviral DNA obtained from donor peripheral blood mononuclear cells. The peptide enzyme immunoassay was found to be less sensitive than the Western blot, but completely concordant with PCR results when differential reactivity could be established. The Western blot pattern showed complete diagnostic concordance with the samples with confirmed-positive serologic tests, but was incorrect in two HTLV-II-infected donors with indeterminate serologic tests. Thirty-three (89%) of the 37 individuals from this predominantly Native American and Hispanic group of blood donors were found to have HTLV-II. These findings confirm and extend previous reports that HTLV-I infection may be less common, and HTLV-II infection more common, than previously believed. The peptide enzyme immunoassay can provide most individuals who have positive results with the HTLV-I/II screening test with serologic distinction between HTLV-I and HTLV-II.

Blood Donors↗
PubMed1991

Incidence of hairy cell leukemia, mycosis fungoides, and chronic lymphocytic leukemia in first known HTLV-II-endemic population.

Unlike human T cell leukemia-lymphoma virus type I (HTLV-I), HTLV-II has not been convincingly linked to a malignancy. In the first 10 months of serologic screening for HTLV-I/II among blood donors in New Mexico in 1988-1989, HTLV-I/II infection was found in 27 donors. HTLV-I/II infection was present in 1.0%-1.6% of American Indian and 0.16%-0.27% of Hispanic donors compared with 0.009%-0.06% of non-Hispanic white donors. HTLV-II was identified by DNA amplification in 12 of 13 samples from Indian and Hispanic seropositive donors. Despite apparent endemic HTLV-II infection in these populations, New Mexico Tumor Registry data showed that the incidences of hairy cell leukemia, mycosis fungoides, and chronic lymphocytic leukemia were comparable among the three ethnic groups. A population with endemic HTLV-II infection has been identified, and there is no evidence of increased risk for these three malignancies in the endemic groups.

Blood Donors↗
PubMed1991

Human T-cell leukemia/lymphoma viruses. Life cycle, pathogenicity, epidemiology, and diagnosis.

Human T-cell leukemia/lymphoma virus type I (HTLV-I) was discovered in 1980, and it subsequently was found to be the cause of adult T-cell leukemia/lymphoma. A progressive neurologic disease known as tropical spastic paraparesis, or HTLV-I-associated myelopathy, has also been linked to infection with HTLV-I. A related virus, HTLV type II (HTLV-II), has been isolated from patients with hairy-cell leukemia, but it has not been proved to be the cause of any disease. In late 1988, US blood banks began screening all blood donations for antibodies to HTLV-I/II. This program has resulted in the identification of many unexpectedly seropositive blood donors and provided much information about the prevalence of HTLV-I/II in the United States. In this article, I review the replication of these agents, as well as their pathogenesis, diagnosis, and mechanisms of spread.

Deltaretrovirus↗