Search PubMed⌕ Search

Biomedical subjects

C J Peters

Publications and source records attributed to C J Peters.

At least 145 records · Page 8Linked to original sources
PubMed1996

Evidence against person-to-person transmission of hantavirus to health care workers.

Unusual, primarily pulmonary, manifestations of hantaviral illness occurring in the southwestern United States raised the possibility of person-to-person transmission of a recently recognized hantavirus, Sin Nombre virus. To determine whether such transmission had occurred among health care workers (HCWs) exposed to patients with confirmed hantavirus pulmonary syndrome, we evaluated HCWs who had cared for patients with hantavirus pulmonary syndrome or who had processed specimens from these patients. Information about exposure to these patients and about recent illnesses was obtained via a standardized questionnaire. Serum specimens were tested for IgM and IgG antibodies to hantaviruses with use of ELISAs. Of the 396 HCWs, 266 (67%) reported that they had been exposed to patients with hantavirus pulmonary syndrome or to their body fluids or that they had processed laboratory specimens from these patients. Although 108 (27%) of the HCWs reported fever, myalgias, or respiratory illnesses during the 3 months before the serum specimens were obtained, hantavirus antibodies were not detected in any HCW. These data suggest that person-to-person transmission of Sin Nombre virus is unlikely to occur in health care settings.

Adolescent↗
PubMed1996

Evidence against infection with hantaviruses among forest and park workers in the southwestern United States.

To determine if individuals with extensive exposure to rodent habitats were infected with Sin Nombre hantavirus (SNV), we evaluated forest and park service personnel from the region of endemicity in the southwestern United States. Information about work and recreational activities, including exposure to rodents and a history of recent illnesses, was obtained via a standardized questionnaire. Serum specimens were also collected. Of 140 participating workers, 84 (60%) were primarily engaged in outdoor work activities, 14 (10%) were office-based supervisors, and 42 (30%) were office workers. Of the 140 employees, 89 (64%) reported repeated exposures to rodents, rodent nests, and/or rodent droppings; 22 (16%) reported trapping or handling wild rodents. Hantavirus antibodies were not detected in any park employee. These data suggest that transmission of SNV is a rare event even among persons in the southwestern United States who have a high level of exposure to this virus. Although park employees and visitors in this region are at low risk of infection with SNV, these persons should continue to use recommended measures for risk reduction.

Animals↗
PubMed1996

Hantavirus pulmonary syndrome: the first 100 US cases.

In the spring of 1993, hantavirus pulmonary syndrome (HPS) "emerged" in the southwestern United States, where a multiagency investigation led to the rapid description of this new clinical entity and its etiology. Analysis of the first 100 US cases identified showed that the disease was distributed in 21 states, had gone unrecognized since at least 1959, and had a distinct spring-early summer seasonality. Of the infected persons, 54% were male; 63% were Caucasian, 35% were Native American, and 2% were African American. The average age of case-patients was 34.9 years, and 8 were children or adolescents aged < or = 16 years. The overall case-fatality rate was 52%. There was a 91% concordance among serologic, immunohistochemical, and molecular results. HPS in the United States is caused by at least three newly described pathogenic hantaviruses, each of which has a distinct rodent host, and cases of HPS have been recently recognized in Canada and South America. National surveillance of this sporadic disease remains essential for further defining the epidemiology and clinical spectrum.

Adolescent↗
PubMed1996

Direct genetic detection of Dobrava virus in Greek and Albanian patients with hemorrhagic fever with renal syndrome.

Blood samples were collected from an Albanian and a Greek patient with hemorrhagic fever with renal syndrome and tested by reverse transcriptase-polymerase chain reaction. The genetic detection assay amplified hantavirus-specific DNA fragments from RNA extracted from the blood of the patients; nucleotide sequence analysis revealed that the causative agent of the disease was Dobrava virus. These findings suggest that Dobrava virus (which was originally isolated from the lungs of an Apodenws flavicollis mouse in Slovenia) is endemic throughout the Balkan States and causes overt human disease.

Adult↗
PubMed1996

Khabarovsk virus: a phylogenetically and serologically distinct hantavirus isolated from Microtus fortis trapped in far-east Russia.

Two hantavirus strains, MF43 and MF113, isolated from Microtus fortis trapped in the Khabarovsk region of far-eastern Russia, were analysed by direct nucleotide sequencing of PCR generated fragments of the M and S segments, by immunofluorescence and by focus reduction neutralization tests (FRNT). The nucleotide sequences revealed that the two isolates were closely related to each other but distinct from all other hantaviruses. Phylogenetic analysis of the M and S segments showed that the MF strains form a separate branch in the Hantavirus tree, positioned between the branches of Prospect Hill and Puumala viruses. The strains were shown to be serologically distinct from the other hantavirus serotypes by FRNT using immune rabbit sera. Puumala virus was the closest relative, both genetically and serologically. We propose that this new hantavirus serotype should be named Khabarovsk (KBR).

Animals↗
PubMed1996

Characterization of Oliveros virus, a new member of the Tacaribe complex (Arenaviridae: Arenavirus).

Oliveros virus is an agent isolated in cell culture from Bolomys obscurus (Rodentia, Muridae, Sigmodontinae) captured on the central Argentine pampa. Oliveros virus was shown to be related to members of the Tacaribe complex of the family Arenaviridae by immunofluorescent antibody (IFA) tests, electrophoretic pattern of viral proteins, and morphology as observed by electron microscopy. It was distinct from 12 other arenaviruses by a combination of plaque-reduction neutralization tests, comparison of endpoint titers among cross-IFA tests, and comparison of viral RNA sequence data. This agent is the third new arenavirus from South America described within the last three years.

Animals↗
PubMed1996

Prevalence of antibodies to arenaviruses in rodents from the southern and western United States: evidence for an arenavirus associated with the genus Neotoma.

The objectives of this study were to extend our knowledge of the geographic distribution and rodent host range of arenaviruses in North America. Sera from wild rodents collected from the southern and western United States were tested for antibody against Tamiami, Pichinde, Junin, and lymphocytic choriomeningitis viruses, using an indirect fluorescent antibody test. Antibody to at least one arenavirus was found in 220 (3.1%) of 7,106 rodents tested. The antibody-positive animals included Mus musculus from Florida and Texas; Neotoma albigula from Arizona, Colorado, and New Mexico; N. fuscipes and N. lepida from California: N. mexicana from Arizona, New Mexico, and Utah; N. stephensi from Arizona and New Mexico; and Oryzomys palustris and Sigmodon hispidus from Florida. Sigmodon hispidus seropositive for Tamiami virus were found only in Florida (156 [27.0%] of 578 tested), although 463 hispid cotton rats from outside that state were examined. High-titered antibodies to Tamiami virus were present in sera from S. hispidus, (geometric mean antibody titer [GMAT] of 1:792), whereas sera from Neotoma spp. reacted at high titer to both Tamiami (GMAT = 1:905) and Pichinde (GMAT = 1:433) viruses. The results suggest that arenaviruses are widely distributed in the southern United States and that one or more indigenous arenaviruses are associated with Neotoma spp. in North America.

Animals↗
PubMed1996

Lessons learned from the hantaviruses and other hemorrhagic fever viruses.

In recent years, numerous previously known infections pathogens and their associated diseases have been recognized. Among these newly identified agents are the viruses that cause the hemorrhagic fevers, including Sin Nombre virus, the etiologic agent of the 1993 outbreak of hantavirus pulmonary syndrome in the American Southwest. Epidemiologic and laboratory investigations of the hemorrhagic fevers and their etiologic agents provide lessons that may be used collectively as a paradigm of the nature of emerging and re-emerging infectious diseases.

Bunyaviridae↗
PubMed1996

Retrospective diagnosis of hantavirus pulmonary syndrome, 1978-1993: implications for emerging infectious diseases.

OBJECTIVE: To investigate the occurrence of unrecognized cases of hantavirus pulmonary syndrome preceding the detection of the 1993 outbreak in the southwestern United States and the initial description of the syndrome. DESIGN: Retrospective clinicopathologic and immunohistologic study. PATIENTS: Eighty-two patients who died prior to April 1993 with histologically unexplained noncardiogenic pulmonary edema. METHODS: Clinicopathologic review and immunohistochemical evaluation of autopsy tissues for evidence of hantaviral infection. RESULTS: Twelve retrospective fatal cases of hantavirus pulmonary syndrome were identified through clinicopathologic review and immunohistochemical testing of tissues. Patients' ages ranged from 16 to 49 years. The earliest identified case occurred in 1978, 15 years prior to the outbreak of hantavirus pulmonary syndrome in the southwestern United States. Immunohistochemical testing showed widespread deposition of hantaviral antigens, primarily within endothelial cells, similar to the pattern observed with current hantavirus pulmonary syndrome cases. CONCLUSIONS: Although hantavirus pulmonary syndrome was first recognized in 1993, the findings from this study document the earlier existence of this disease. These findings underscore the need for systematic archiving and analysis of clinical information and specimens from patients with diseases of unknown etiology to facilitate the study of new clinical entities and their associated etiologic agents.

Adolescent↗
PubMed1995

Naturally occurring Sin Nombre virus genetic reassortants.

Genetic reassortment has been shown to play an important role in the evolution of several segmented RNA viruses and in the epidemiology of associated diseases. Sin Nombre (SN) virus is the cause of hantavirus pulmonary syndrome throughout the western United States. Like other hantaviruses, it possesses a genome consisting of three negative-sense RNA segments, S, M, and L. Recent analysis has demonstrated the presence of at least three different hantaviruses in Nevada and eastern California, including SN, Prospect Hill-like, and El Moro Canyon-like viruses. In addition, two distinct lineages of SN virus can be found in Peromyscus maniculatus rodents (sometimes in close proximity) trapped at study sites in this region. Data obtained by phylogenetic analysis of sequence differences detected among the S, M, and L genome segments of these SN viruses are consistent with reassortment having taken place between SN virus genetic variants. The results suggest that M (and to a lesser extent S or L) genome segment flow occurs within SN virus populations in P. maniculatus in this region. No reassortment was detected between SN virus and other hantavirus types present in the area. This finding suggests that as genetic distance increases, the frequency of formation of viable reassortants decreases, or that hantaviruses which are primarily maintained in different rodent hosts rarely have the opportunity to genetically interact.

Animals↗
PubMed1995

Genetic and serologic analysis of Black Creek Canal virus and its association with human disease and Sigmodon hispidus infection.

Black Creek Canal (BCC) virus is a newly identified virus associated with hantavirus pulmonary syndrome (HPS) in the southeastern United States. Nucleotide sequences were determined for the complete S and M and partial L genomic segments of a BCC virus isolate. Phylogenetic analysis indicates that each of the virus segments is unique, and there is no evidence of genetic reassortment having occurred between this and other previously characterized hantaviruses. All hantavirus-seropositive, wild-caught Sigmodon hispidus which were tested by polymerase chain reaction for the presence of BCC virus RNA were found to be positive, consistent with a chronic virus infection. This finding, together with serologic evidence, confirms S. hispidus as the primary rodent reservoir of this virus. Nucleotide sequence analysis of these PCR products indicates that BCC virus is genetically diverse and may pose a public health threat throughout much of the extensive range of this rodent species. Immunoprecipitation analysis demonstrated the presence of G1-, G2-, and N-specific antibodies in sera from BCC virus-infected patients with HPS and naturally infected S. hispidus. Comparison of the patterns of protein immunoprecipitation obtained with human acute- and convalescent-phase sera suggests that G1- and G2-specific antibodies increase relative to N-specific antibodies during the course of infection. The ratio of G1 to N protein immunoprecipitation by rodent or human acute-phase sera allowed differentiation of BCC and Sin Nombre virus infections.

Amino Acid Sequence↗
PubMed1995

Ultrastructural characteristics of Sin Nombre virus, causative agent of hantavirus pulmonary syndrome.

A previously unrecognized disease, hantavirus pulmonary syndrome, was described following an outbreak of severe, often lethal, pulmonary illness in the southwestern United States in May-June, 1993. We have now studied the morphologic features of the causative agent, Sin Nomber virus (SNV), by thin section electron microscopy and immunoelectron microscopy of infected Vero E6 cells. SNV virions were roughly spherical and had a mean diameter of 112 nm. They had a rather dense envelope and closely apposed fine surface projections, 7 nm in length. Filamentous nucleocapsids were present within virions. Viral inclusion bodies were present in the cytoplasm of infected cells; these appeared granular or filamentous, depending on the plane of section. All of these characteristics were similar to published descriptions of other hantaviruses; however, unlike all other hantaviruses and virtually all other member viruses of the family Bunyaviridae which bud upon smooth intracytoplasmic membranes, SNV budding occurred almost entirely upon the plasma membrane of infected cells. Virus budding was associated with the formation of long 28 nm diameter tubular projections. Occasional elongated 47 nm diameter virus-like particles were seen to bud upon intracytoplasmic membranes. As shown by immunoelectron microscopy, viral antigens were localized over virions, inclusions, and tubular projections associated with virion morphogenesis.

Animals↗
PubMed1995

Detection and sequence confirmation of Sin Nombre virus RNA in paraffin-embedded human tissues using one-step RT-PCR.

Sin Nombre virus (SNV) is the causative agent of hantavirus pulmonary syndrome (HPS). SNV RNA can be detected in fresh or frozen autopsy tissue samples by reverse transcriptase polymerase chain reaction (RT-PCR), and virus antigens can be identified by immunohistochemistry. A method was developed for demonstration of SNV RNA in formalin-fixed, paraffin-embedded tissues by RT-PCR. Virus genomes were detected in 8 of 12 (66.7%) fixed human tissue samples that were positive by immunohistochemistry, and RT-PCR prior to tissue fixation. By comparison with nucleotide sequences determined previously in fresh or frozen tissues of the same patients, identical genomic sequences were obtained, proving the authenticity of the PCR products. The study demonstrates that detection of SNV RNA in formalin-fixed, paraffin-embedded archival tissue by RT-PCR is feasible. This method allows retrospective studies on the phylogenetic epidemiology of SNV in North America.

Base Sequence↗
PubMed1995

Genetic characterization of a human isolate of Puumala hantavirus from France.

PUU90-13 is a strain of Puumala (PUU) virus (family Bunyaviridae: genus Hantavirus) isolated from a human in northeastern France (Rollin et al., 1995). This report describes the full-length sequences of the small (S) and medium (M) genomic RNAs of PUU90-13. The terminal sequences of both the S and M genomic RNAs were found to be conserved and imperfectly complementary. The S RNA of PUU90-13 is 1847 nt in length and contains the nucleocapsid (N) protein gene and a potential overlapping open reading frame (ORF-2) previously described in other hantaviruses. Statistical analysis of the third base substitution frequency in the N ORFs of PUU90-13 and other PUU viruses suggests that the ORF-2 is functional. The M RNA is 3681 nt in length and encodes the glycoprotein precursor. Both genomic segments share the highest degree of nucleotide and amino acid sequence identity with PUUBerkel, a PUU virus from Germany. Phylogenetic analyses of sequences from both segments indicate that PUU90-13 occupies a distinct Western European PUU virus lineage that it shares with PUUBerkel. Both PUU90-13 and PUUBerkel lack a potential N-linked glycosylation site found on the G2 glycoprotein of other PUU viruses.

Amino Acid Sequence↗
PubMed1995

Evaluation of the magnitude of the 1993 hantavirus outbreak in the southwestern United States.

In May 1993, an outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States was caused by the previously unrecognized Sin Nombre virus (SNV). Most HPS patients had an influenza-like prodrome, followed by rapid onset of pulmonary edema (fatality rate, 52%). To define the magnitude of the outbreak, patients with milder illnesses who sought medical care in the outbreak area during the outbreak period were assessed for infection with SNV. Of 299 study subjects, 43 had illnesses similar to the HPS prodrome. One laboratory finding, thrombocytopenia, was highly discriminatory between non-HPS patients (1%) and confirmed HPS patients (71%; P < .001) during the prodrome phase. No study subject had serologic evidence (IgM antibodies) of recent SNV infection. Five had IgG titers consistent with a previous hantavirus infection: 3 of these 5 were among the 43 patients who had illnesses similar to the HPS prodrome (P < .05). These data provide evidence that mild illness is rarely caused by SNV.

Adolescent↗