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Biomedical subjects

C J Peters

Publications and source records attributed to C J Peters.

At least 163 records · Page 9Linked to original sources
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

Complete genetic characterization and analysis of isolation of Sin Nombre virus.

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). The large (L) genome segment was found to be 6,562 nucleotides in length and encoded a putative L polymerase that was 2,153 amino acids in length. No evidence of segment reassortment with other well-characterized hantaviruses was obtained. The sequence of the entire S, M, and L genome segments of SN virus (strain NMR11) isolated from a mouse (trapped in the residence of the patient infected with SN virus [NMH10]) by passage two times in Peromyscus maniculatus and then by five passages in E6 Vero cells was determined and compared with that of the virus detected in autopsy tissues. Only 16 nucleotide differences were detected between the virus genomes, and none of these resulted in virus protein amino acid substitutions. Determination of the exact 5'- and 3'-terminal sequences of all genome segments of SN virus and representatives of other serologic groups in the Hantavirus genus, family Bunyaviridae, showed the existence of conserved nucleotide domains that may be involved in important regulatory mechanisms, such as RNA encapsidation, polymerase binding, and control of transcription and replication.

Amino Acid Sequence↗
PubMed1995

A newly recognized virus associated with a fatal case of hantavirus pulmonary syndrome in Louisiana.

Genetic analysis of virus detected in autopsy tissues of a fatal hantavirus pulmonary syndrome-like case in Louisiana revealed the presence of a previously unrecognized hantavirus. Nucleotide sequence analysis of PCR fragments of the complete S and M segments of the virus amplified from RNA extracted from the tissues showed the virus to be novel, differing from the closest related hantavirus, Sin Nombre virus, by approximately 30%. Both genome segments were unique, and there was no evidence of genetic reassortment with previously characterized hantaviruses. The primary rodent reservoir of Sin Nombre virus, the deer mouse Peromyscus maniculatus, is absent from Louisiana. Thus, the virus detected in Louisiana, referred to here as Bayou virus, must possess a different rodent reservoir.

Base Sequence↗
PubMed1995

Identification of a new North American hantavirus that causes acute pulmonary insufficiency.

In May 1993, a pulmonary disease syndrome with novel clinical and epidemiologic features was identified in the southwestern United States. Healthy young adults developed a febrile prodrome followed by the rapid onset of often lethal acute respiratory distress. Although an infectious disease was suspected, intensive investigations initially failed to identify the causative agent. Multiple specialized microbiology laboratories at the National Center for Infectious Diseases (Centers for Disease Control and Prevention) applied classic serologic and culture methods as well as recently developed molecular biological techniques to samples collected from field investigations of the patients. Serologic tests detected the presence of an active immune response to a hantavirus. Reverse transcription and polymerase chain reaction amplification of RNA extracted from human tissues used primers designed from sequences of known hantaviruses to demonstrate genomic sequences of a novel hantavirus. Immunohistochemistry showed the presence of hantavirus antigens in the endothelium of lung tissues from patients and provided the final pathogenetic link to this group of viruses. These methods were concordantly positive in virtually all samples available from 18 patients with compatible clinical histories identified between January and July 1993. Test results of control subjects and searches for other agents in identified cases were negative. This newly recognized hantavirus causes a novel syndrome of acute pulmonary edema and shock; the pathogenesis is related to the presence of virus antigens in the pulmonary capillaries. The virus may be an important cause of severe and fatal disease presenting as adult respiratory distress syndrome in otherwise healthy persons.

Antibodies, Viral↗
PubMed1995

Short report: isolation and partial characterization of a Puumala virus from a human case of nephropathia epidemica in France.

Puumala (PUU) virus (Bunyaviridae: Hantavirus), the etiologic agent of nephropathia epidemica (NE), the mid form of hemorrhagic fever with renal syndrome, is enzootic in Europe and has been known to occur in France since 1983. We report the first isolation of PUU virus in France and western Europe from a case of NE acquired in France. The virus was isolated from a serum collected in the acute phase of the clinical course by successive blind passages in Vero E6 cells. Serologic typing using monoclonal antibodies confirmed the identity of the virus as PUU. The sequence of an 832-nucleotide fragment of the virus medium RNA segment obtained by the polymerase chain reaction (PCR) also classified it as a PUU virus. The sequence of this isolate from a human case in France is closely related to the sequence of a PUU virus obtained by the PCR from a German patient.

Adult↗
PubMed1994

Genome structure and variability of a virus causing hantavirus pulmonary syndrome.

A previously unrecognized hantavirus (family Bunyaviridae) has recently been detected and shown to be associated with a severe respiratory illness with high mortality, termed hantavirus pulmonary syndrome (HPS). This disease has now been identified throughout the western United States. We present nucleotide sequence characterization of the three RNA segments composing the HPS virus genome and address the question of the apparent emergence of this highly lethal virus. No evidence of genetic reassortment with previously recognized hantaviruses was found, each RNA segment being unique and approximately 30% different at the nucleotide level to the segments of the closest relative, Prospect Hill virus. These findings, together with the observed extensive genetic diversity of HPS viruses and examples of geographic clustering of distinct virus genotypes, suggest that HPS and associated virus have likely existed undetected for many years. The virus genome M segment was determined to be 3696 nucleotides in length and encode G1 and G2 proteins, 652 and 488 amino acids in length. The S segment was found to be 2059 nucleotides in length and to encode a nucleocapsid protein, 428 amino acids in length. S segment analysis also revealed an unusually long noncoding region with numerous repeats and evidence for a potential NSS protein encoded in an overlapping frame.

Amino Acid Sequence↗
PubMed1994

Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. The Hantavirus Study Group.

BACKGROUND: In May 1993 an outbreak of severe respiratory illness occurred in the southwestern United States. A previously unknown hantavirus was identified as the cause. In Asia hantaviruses are associated with hemorrhagic fever and renal disease. They have not been known as a cause of human disease in North America. METHODS: We analyzed clinical, laboratory, and autopsy data on the first 17 persons with confirmed infection from this newly recognized strain of hantavirus. RESULTS: The mean age of the patients was 32.2 years (range, 13 to 64); 61 percent were women, 72 percent were Native American, 22 percent white, and 6 percent Hispanic. The most common prodromal symptoms were fever and myalgia (100 percent), cough or dyspnea (76 percent), gastrointestinal symptoms (76 percent), and headache (71 percent). The most common physical findings were tachypnea (100 percent), tachycardia (94 percent), and hypotension (50 percent). The laboratory findings included leukocytosis (median peak cell count, 26,000 per cubic millimeter), often with myeloid precursors, an increased hematocrit, thrombocytopenia (median lowest platelet count, 64,000 per cubic millimeter), prolonged prothrombin and partial-thromboplastin times, an elevated serum lactate dehydrogenase concentration, decreased serum protein concentrations, and proteinuria. Rapidly progressive acute pulmonary edema developed in 15 of the 17 patients (88 percent), and 13 patients, all of whom had profound hypotension, died (case fatality rate, 76 percent). Increases in the hematocrit and partial-thromboplastin time were predictive of death. CONCLUSIONS: Infection with a newly described hantavirus causes the hantavirus pulmonary syndrome, which is characterized by a brief prodromal illness followed by rapidly progressive, noncardiogenic pulmonary edema.

Adolescent↗
PubMed1994

Characterization of filoviruses based on differences in structure and antigenicity of the virion glycoprotein.

Eight different filovirus isolates, representing major episodes of filovirus hemorrhagic disease, were propagated for structural and antigenetic analyses of their glycoprotein (GP). Carbohydrate analysis revealed that N- and O-glycosylation are features of filovirus GPs. Oligosaccharide side chains differed in their sialylation pattern and seemed to be cell line-dependent. Marburg virus (MBG) isolates are clearly distinguished from Ebola (EBO) and Reston viruses by a lack of terminal sialic acids when propagated in E6 and MA-104 cells. It was also determined that GP-specific antisera failed to show any cross-reactivity between MBG isolates and other filoviruses. These data, together with prior findings, indicate that the genus Filovirus can be divided into a MBG group and EBO group.

Animals↗
PubMed1994

Hantavirus pulmonary syndrome in California: report of two cases and investigation.

We report two cases of hantavirus pulmonary syndrome that were probably acquired in California. Genetic analysis of tissue specimens from one of the patients revealed that the virus isolated is a variant of the strain (Sin Nombre virus) identified in the outbreak of hantavirus pulmonary syndrome that occurred in the Four Corners region of the southwestern United States in 1993. In addition to presenting the clinical features of the two cases, we discuss the possible risk factors for infection.

Adult↗
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

Genetic identification of a new Puumala virus strain causing severe hemorrhagic fever with renal syndrome in Germany.

A severe case of suspected hemorrhagic fever with renal syndrome (HFRS) was recently identified in northwestern Germany. A genetic detection assay was designed that identified hantavirus-specific RNA in the patient's clinical specimens by reverse transcriptase-polymerase chain reaction amplification of virus S and M genome segments. Phylogenetic analysis of the nucleotide sequences demonstrated that this virus belonged to the Puumala (PUU) group, with the closest relationship to a PUU isolate from Finland. Within the group, this virus formed a separate lineage. This finding represents the first genetic characterization of a hantavirus causing severe HFRS in Germany. The data suggest that PUU viruses circulating in western European countries are genetically distinct from their northeastern counterparts. Comparison of deduced amino acid sequences demonstrated a loss of a potential N-glycosylation site in the G2 protein compared with other PUU viruses.

Amino Acid Sequence↗
PubMed1994

Rift Valley fever in rural northern Senegal: human risk factors and potential vectors.

To investigate past infection in and transmission of Rift Valley fever (RVF) virus to humans within an endemic focus, we undertook a retrospective cohort study of the seminomadic Peul people living in sub-Saharan northcentral Senegal. Residents of the rural settlement of Yonofere five years of age or older were studied during February-May 1989. Anti-RVF virus IgG was found in blood samples of 22.3% of 273 persons who responded to a standard questionnaire; none had IgM antibodies. Seropositivity was similar for males (25.4%) and females (21.1%), increased markedly with age for both sexes, and varied considerably among compounds (groups of huts) (0-37.5%). Risk factors for past RVF virus infection were nursing sick people, assisting animals during abortions/births, and treating sick animals. In all age groups, odds ratios (ORs) for RVF viral antibody among females who reported treating sick animals were three to six times greater than for those who did not. The ORs for males who reported assisting with animal births/abortions and nursing sick people were approximately five times those for males who did not. Serologic prevalence of RVF viral antibody among sheep averaged 30.1% overall (0.8% IgM), but varied among compounds (0-66.7%) in a manner different from that of humans. The seasonal abundance and relative density of potential mosquito vectors were estimated by monthly samples captured in Centers for Disease Control and Prevention-type traps. Mosquito abundance varied seasonally with rainfall (> 90% captures during four months). Species diversity was large (28 spp.), dominated by Aedes and Culex. Rift Valley fever virus was not isolated from 142 pools of 2,956 unengorged mosquitoes tested, although three other arboviruses were found. Results indicate that RVF is endemic in this region, people are at considerable risk of infection, and that a heretofore unrecognized mode of human infection under nonepizootic conditions may be transmission via contact with infected animals or humans.

Adolescent↗
PubMed1994

Cardiovascular and pulmonary responses to Pichinde virus infection in strain 13 guinea pigs.

In fatal human Lassa fever, severe hypotension, circulatory shock, and pulmonary edema develop as terminal events. We examined cardiovascular and respiratory functions in strain 13 guinea pigs infected with Pichinde virus, an animal model for studying human Lassa fever. Cardiovascular functions were studied in anesthetized and conscious guinea pigs, whereas pulmonary functions were measured only on animals under anesthesia. In anesthetized animals, cardiovascular disturbances were severe and progressive from postinoculation day (PID) 10. Cardiac output, measured by thermodilution, decreased 28 to 53% below baseline values from PID 10 to 12 and was accompanied by a gradual reduction of mean arterial blood pressure and heart rate. Although left ventricular systolic pressure decreased significantly, the left ventricular +dp/dtmax and -dp/dtmax decreased only slightly on PID 12. Similar depressed cardiovascular responses were observed in conscious animals infected with Pichinde virus. Changes included decreased cardiac output, heart rate, cardiac work, cardiac power, and stroke volume, as well as increased total peripheral resistance and prolonged mean transit time. We postulate that a global cardiovascular dysfunction with the involvement of right and left sides of the heart may be the main cause of irreversible circulatory deterioration and death during Pichinde virus infection in strain 13 guinea pigs.

Animals↗
PubMed1994

Prevalence of infection with Junin virus in rodent populations in the epidemic area of Argentine hemorrhagic fever.

We report the results of indirect fluorescent antibody screening for antibody to Junin virus in 1,101 sera from small mammals captured on two mark-recapture grids in the epidemic area of Argentine hemorrhagic fever. Twenty-six of 29 seropositive animals were the cricetid rodent Calomys musculinus, for a 30-month prevalence of 7.9% in that species. Combining these data with previously published data on antigen detection provided an estimated total prevalence of infection of 10.9% for this, the principal reservoir species. Other infected species included two cricetids, C. laucha and Bolomys obscurus, and a predatory carnivore, Galictis cuja. Approximately half of infected animals simultaneously carried serum antibody and antigen in blood and saliva, some for 29-61 days. Except for C. laucha, which was associated with crop habitats, seropositive animals were strongly associated with the relatively rare roadside and fence-line habitats. Seropositive C. musculinus were predominantly males in the oldest age and heaviest body mass classes, and seropositive males were twice as likely to have body scars as seronegative males. These observations suggest that most infections were acquired through horizontal transmission and that aggressive encounters among adult, male C. musculinus in relatively densely populated roadside and fence-line habitats are an important mechanism of transmission of Junin virus within reservoir populations.

Age Factors↗